Acromegaly is a disorder that occurs when your body makes too much growth hormone (GH). Produced mainly in the pituitary gland, GH controls the physical growth of the body. In adults, too much of this hormone causes bones, cartilage, body organs, and other tissues to increase in size. Common changes in appearance include enlarged or swollen nose, ears, hands, and feet.
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How common is acromegaly?
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Acromegaly is rare. Scientists estimate that about 3 to 14 of every 100,000 people have been diagnosed as having acromegaly.1
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Who is more likely to develop acromegaly?
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Acromegaly is most often diagnosed in middle-aged adults, but symptoms can appear at any age. In children, too much growth hormone causes a condition called gigantism rather than acromegaly. Gigantism occurs when excess GH begins before the end of puberty, when children\u2019s growth plates fuse or close. Having too much GH before the growth plates close causes children to grow tall in height.
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What are the complications of acromegaly?
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Acromegaly is treatable in most people. But because symptoms come on slowly, health problems can develop before the disorder is diagnosed and treated.
People with acromegaly also have an increased risk for colon polyps, which may develop into colon cancer if not removed.
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Some people with acromegaly may have a genetic condition that can lead tumors to develop in different parts of their bodies. Increased GH can cause these other tumors to grow.
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Untreated, acromegaly can lead to serious health problems and early death. But when successfully treated, symptoms generally improve and may go away altogether. Life expectancy may return to normal.2
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What are the symptoms of acromegaly?
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Symptoms of acromegaly can vary from person to person. Common changes in physical appearance include
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hands and feet become larger and swollen\u2014you may notice a change in ring or shoe size, especially shoe width
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lips, nose, and tongue become larger
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bone changes: brow and lower jaw jut out, bridge of the nose gets bigger, and space between teeth increases
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skin becomes thick, coarse, and oily
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sweating and skin odor increase
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voice becomes deeper
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skin tags\u2014small, usually flesh-colored growths of skin that have a raised surface\u2014may get larger or darker
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Other common symptoms include
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headaches
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joint aches
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vision problems
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What causes acromegaly?
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Acromegaly develops when the pituitary gland releases too much GH into the body over a long period of time. When GH enters the blood, this signals the liver to produce another hormone, called insulin-like growth factor I (IGF-I). IGF-I is the hormone that actually causes bones and body tissue to grow. High levels of this hormone also cause changes in how the body processes blood glucose (blood sugar) and lipids (fats), which can lead to type 2 diabetes, high blood pressure, and heart disease.
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In more than 9 out of 10 cases, acromegaly is caused by a tumor in the pituitary gland, called a pituitary adenoma.3 More rarely, the cause may be a tumor in another part of the body.
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Although scientists don\u2019t know what causes these tumors to develop, genetic factors may play a role. In young adults, acromegaly has been linked to defects in certain genes.
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Pituitary tumors
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Pituitary tumors are almost always benign, or noncancerous. Some tumors grow slowly, and symptoms of too much GH may not be noticed for many years. Other tumors may grow rapidly.
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Depending on its size and location, the tumor may press against other pituitary tissue. Possible effects include
changes in thyroid hormone, which can affect weight, energy levels, hair, and skin
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decreases in cortisol, which can cause weight loss, dizziness, tiredness, low blood pressure, and nausea
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A tumor that grows large in size may also press against nearby parts of the brain. This can lead to other symptoms, such as headaches and vision problems.
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Some pituitary tumors that create growth hormone can also increase the levels of other hormones in the body. For example, the tumor may produce prolactin, the hormone that prompts the mammary glands to produce milk. This can lead to breast milk discharge in women.
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Nonpituitary tumors
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Rarely, acromegaly is caused by tumors located in the hypothalamus\u2014a small area of the brain near the pituitary gland, pancreas, lungs, or other parts of the chest or abdomen. Some of these tumors make growth hormone themselves. But more often, the tumors produce growth hormone-releasing hormone (GHRH), a hormone that signals the pituitary gland to make growth hormone.
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How do doctors diagnose acromegaly?
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Blood tests
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Doctors most often diagnose acromegaly by ordering two blood tests that help determine if your body is making too much GH.
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IGF test. Levels of GH in the blood can change throughout the day. A reliable way to track GH in the body is by measuring the level of IGF-I in the blood. In most cases, a high IGF-I level suggests that you have acromegaly.
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Oral glucose tolerance test. To confirm the diagnosis, your doctor will order an oral glucose tolerance test. For this test, you will drink a sugary liquid. A health professional will then test your blood every half hour for 2 hours to measure growth hormone levels. The sugar in the drink will normally cause GH levels to fall. But if your body is making too much of the hormone, these levels will not go down enough\u2014thereby confirming the diagnosis of acromegaly.
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Imaging tests
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If the blood tests confirm that your body is making too much GH, your doctor will conduct imaging tests to locate and measure the tumor that may be causing the problem. Two commonly used tests are
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Magnetic resonance imaging. The preferred test for viewing a pituitary tumor is the magnetic resonance imaging (MRI) scan. The MRI scan uses radio waves and magnets to create detailed images of your internal organs and soft tissues without x-rays.
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Computed tomography scan. If an MRI is not a good option for you (for example, if you have a pacemaker or other implant that has metal), your doctor may order a computed tomography (CT) scan instead. The CT scan uses a combination of x-rays and computer technology to create images of your organs and other internal parts of your body.
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If the imaging test doesn\u2019t find a pituitary tumor, your doctor will look for nonpituitary tumors as the cause of your high GH levels.
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How do doctors treat acromegaly?
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Treatment options include surgery, medicines, and radiation therapy. The goals of treatment are to control tumor size, return GH and IGF-I levels back to normal, improve symptoms, and manage related health problems. No single treatment is right for everyone. Your doctor will recommend a treatment plan that works for you, depending on factors such as your age, tumor size, severity of symptoms, GH and IGF-I levels, and health status.
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Surgery
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Doctors can remove most pituitary tumors using a method called transsphenoidal surgery. The operation is done through the nose and sphenoid sinus, a hollow space in the skull behind the nasal passages and below the brain. Two approaches to this surgery are
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with a microscope\u2014a magnifying tool
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with an endoscope\u2014a thin, lighted tube with a tiny camera
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In both approaches, the surgeon uses advanced MRI imaging to scan the area around the tumor before surgery. He or she then makes a small cut inside your nostril to view the area and remove the tumor using tiny, special tools. In microscopic surgery, the surgeon uses a microscope to magnify the area. In endoscopic surgery, an endoscope camera sends images to a television monitor instead. Risks and results are similar for both approaches.3
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When the tumor that is creating too much GH is not located in the pituitary gland, other types of surgery are used to remove the tumor. Removing these nonpituitary tumors also lowers GH levels and improves acromegaly symptoms.
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Risks. Complications from surgery can include bleeding, cerebrospinal fluid leaks, meningitis, sodium (salt) and water imbalance, and low levels of pituitary hormones.3
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Outcomes. The surgery is considered a success if blood levels of GH and IGF-I return to normal after 12 weeks. The cure rate right after surgery is about 85 percent for small tumors and 40 to 50 percent for large tumors.3
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When successful, the surgery relieves pressure on nearby areas of the brain and causes GH levels to drop right away. Soft tissue swelling may get better within a few days but facial changes may take longer to improve.
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Surgery is most successful in people with smaller pituitary tumors. Success largely depends on the skill and experience of the surgeon, as well as the location of the tumor. Even experienced surgeons may not be able to remove the tumor if it\u2019s too close to parts of the brain where surgery would be risky. However, surgeons may be able to remove part of the tumor.
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Postsurgery treatments. In most cases, levels of GH and IGF-I improve but don\u2019t go back to normal. If levels of these hormones are still too high or begin to rise again, you may need further treatment. Most often, this will involve taking medicines. In some cases, your doctor may recommend a second surgery.
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Medicines
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Currently, three types of medicines are used to treat acromegaly, but they are not a cure. The medicines may be used alone or in combination with each other.
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Somatostatin analogs. The medicines most often used to treat acromegaly are called somatostatin analogs (SSAs). These drugs curb the release of GH and may also reduce the size of the pituitary tumor. Several studies have shown that these drugs are safe and effective for long-term treatment. The medicines are delivered by injection, but scientists are currently studying other options, such as pills.4 The most common side effects of SSAs are cramps, gas, and diarrhea. These effects are usually mild and go away over time. Some people may develop gallstones that usually do not cause symptoms. Hair loss is possible and, in rare cases, permanent. Control of blood sugar usually improves but, rarely, may worsen.
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Dopamine agonists. These medicines inhibit GH production and tumor growth, but not as well as SSAs do. Dopamine agonists are most likely to work in people who have mild GH excess and those who have both acromegaly and hyperprolactinemia (too much of the hormone prolactin). The medicines are taken by mouth. Side effects can include nausea, stuffed nose, tiredness, headache, dizziness when standing, nightmares, and mood changes.
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Growth hormone-receptor antagonists. Unlike the other two medicines, GH-receptor antagonists do not stop the body from making too much GH. Instead, they block GH from signaling the body to make more IGF-I. The drug is taken in the form of a daily injection under the skin that patients can administer themselves. Side effects can include liver problems.
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Radiation therapy
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The third treatment option is radiation therapy, which uses high-energy x-rays or particle waves to kill tumor cells. This type of treatment may be recommended if surgery isn\u2019t possible or fails to remove all tumor tissue, and medicines are not an option or working for you.
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Stereotactic. The preferred type of radiation therapy is stereotactic radiation therapy, which uses 3-D imaging to precisely aim high doses of radiation to the tumor from various angles.3 The treatment can sometimes be done in a single session, reducing the risk of damage to nearby tissue. However, a single dose may not work for very large tumors and tumors located close to nerves that affect vision.
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Conventional. The second option is conventional radiation therapy, which also targets the tumor with external beams. This type of radiation therapy delivers small doses of radiation in a series of treatments over 4 to 6 weeks.
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As radiation treatment lowers GH and IGF-I levels over time, it may take years for this treatment to noticeably improve acromegaly symptoms. Your doctor is likely to prescribe medicines while you wait for GH and IGF-I levels to go back to normal and for symptoms to improve.
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All forms of radiation therapy cause other pituitary hormones to slowly decrease over time. About half of people treated with radiation therapy will need hormone replacement after treatment ends. Radiation can also impair a patient\u2019s fertility.
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Vision loss and brain injury are rare complications. Rarely, other types of tumors can develop many years later in areas that were in the path of the radiation beam.
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Clinical Trials for Acromegaly
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The NIDDK conducts and supports clinical trials in many diseases and conditions, including endocrine diseases. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.
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What are clinical trials for acromegaly?
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Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about disease and improve health care for people in the future.
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Researchers are studying many aspects of acromegaly and gigantism, such as
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use of medicine to treat gigantism in children and adolescents
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genetic factors that may cause pituitary tumors to develop, and how to treat the tumors and related complications in children and adults
What clinical studies for acromegaly are looking for participants?
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You can view a filtered list of clinical studies on acromegaly that are open and recruiting at www.ClinicalTrials.gov. You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the NIH does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.
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References
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Lisa Nachtigall, M.D., Harvard Medical School and Massachusetts General Hospital Neuroendocrine and Pituitary Tumor Center
Adrenal insufficiency is a disorder that occurs when the adrenal glands don\u2019t make enough of certain hormones. The adrenal glands are located just above the kidneys. Adrenal insufficiency can be primary, secondary, or tertiary. Primary adrenal insufficiency is often called Addison\u2019s disease.
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Adrenal insufficiency can affect your body\u2019s ability to respond to stress and maintain other essential life functions. With treatment, most people with adrenal insufficiency can have a normal, active life.
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Addison's disease
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Addison\u2019s disease occurs when the adrenal glands are damaged and can\u2019t make enough of the hormone cortisol and sometimes the hormone aldosterone.
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Secondary adrenal insufficiency
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Secondary adrenal insufficiency starts in the pituitary\u2014a pea-sized gland at the base of the brain. The pituitary makes adrenocorticotropin (ACTH), a hormone that tells the adrenal glands to make cortisol. If the pituitary doesn\u2019t make enough ACTH, the adrenal glands don\u2019t make enough cortisol. Over time, the adrenal glands can shrink and stop working.
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Tertiary adrenal insufficiency
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Tertiary adrenal insufficiency starts in the hypothalamus, a small area of the brain near the pituitary. The hypothalamus makes corticotropin-releasing hormone (CRH), a hormone that tells the pituitary to make ACTH. When the hypothalamus doesn\u2019t make enough CRH, the pituitary gland doesn\u2019t make enough ACTH. In turn, the adrenal glands don\u2019t make enough cortisol.
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What do adrenal hormones do?
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The adrenal glands make two main types of hormones: cortisol and aldosterone.
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Cortisol
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Cortisol is sometimes called the \u201cstress hormone\u201d because it helps your body respond to stress. Cortisol also helps
Cortisol belongs to a class of hormones called glucocorticoids.
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Aldosterone
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Aldosterone helps maintain the balance of the minerals sodium and potassium in your blood. Sodium and potassium work together to control the salt and water balance in your body and help keep blood pressure stable. Both help maintain normal nerve and muscle function. Potassium also helps your heartbeat stay regular.
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Aldosterone belongs to a class of hormones called mineralocorticoids.
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How common is adrenal insufficiency?
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Addison\u2019s disease is rare. In developed countries, it affects about 100 to 140 of every million people.1
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Secondary adrenal insufficiency is more common, affecting 150 to 280 people per million.2,3 Secondary and tertiary adrenal insufficiency are often grouped together, so no numbers for tertiary adrenal insufficiency by itself are available.
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Who is more likely to develop adrenal insufficiency?
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Women are more likely than men to develop Addison\u2019s disease.3 This condition occurs most often in people between the ages of 30 and 50,2 although it can occur at any age, even in children.
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Secondary adrenal insufficiency occurs in people with certain conditions that affect the pituitary.
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People who take glucocorticoid medicines, such as prednisone, for a long time and then stop are most likely to develop tertiary adrenal insufficiency. These medicines are used to treat medical conditions such as asthma, rheumatoid arthritis, lupus, cancer, and inflammation, among others.
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What are the complications of adrenal insufficiency?
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The most serious complication of adrenal insufficiency is called adrenal crisis. If not treated right away, adrenal crisis can cause death. Your body needs much more cortisol than usual during times of physical stress such as illness, serious injury, or surgery. The severe lack of cortisol at these times can cause life-threatening low blood pressure, low blood glucose, low blood sodium, and high blood potassium.
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Sometimes the lack of aldosterone in Addison\u2019s disease can cause hyponatremia. This condition occurs when you don\u2019t have enough sodium in your blood. Hyponatremia can cause confusion, fatigue, and muscle twitches and seizures. The lack of aldosterone can also cause hyperkalemia, or too much potassium. Mild hyperkalemia may not cause problems, but severe hyperkalemia can cause life-threatening changes in your heart rhythm.
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References
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Symptoms & Causes
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What are the symptoms of adrenal insufficiency?
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The most common symptoms of adrenal insufficiency are
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chronic, or long-lasting, fatigue
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muscle weakness
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loss of appetite
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weight loss
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abdominal pain
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Other symptoms of adrenal insufficiency can include
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nausea
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vomiting
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diarrhea
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low blood pressure that drops further when you stand up, causing dizziness or fainting
People with Addison\u2019s disease may also have darkening of their skin. This darkening is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes such as the lining of the cheek.
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Because symptoms of adrenal insufficiency come on slowly over time, they may be overlooked or confused with other illnesses. Sometimes symptoms appear for the first time during adrenal crisis. If you always feel tired, weak, or are losing weight, ask your health care professional if you might have adrenal insufficiency. Early treatment can help avoid an adrenal crisis.
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What causes adrenal insufficiency?
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Different types of adrenal insufficiency have different causes. The most common cause of adrenal insufficiency overall is suddenly stopping corticosteroids after taking them for a long time.
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Addison\u2019s disease
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Damage to the adrenal glands in Addison\u2019s disease is usually caused by autoimmune disease\u2014when your immune system attacks your body\u2019s own cells and organs. In developed countries, autoimmune disease causes 8 or 9 of every 10 cases of Addison\u2019s disease.4
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Certain infections can also cause Addison\u2019s disease. Tuberculosis (TB) can damage the adrenal glands and used to be the most common cause of Addison\u2019s disease. As treatment improved over the years, TB became a much less common cause. People with HIV/AIDS, whose weakened immune systems can\u2019t fight off infections that could cause Addison\u2019s disease, are also at risk.
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Less common causes of Addison\u2019s disease are
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cancer cells in the adrenal glands
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surgical removal of the adrenal glands to treat other conditions
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bleeding into the adrenal glands
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genetic disorders that affect the way the adrenal glands develop or function
Anything that affects the pituitary\u2019s ability to make ACTH can cause secondary adrenal insufficiency. The pituitary makes many different hormones, so ACTH may not be the only hormone that\u2019s lacking.
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Causes of secondary adrenal insufficiency include
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autoimmune disease
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pituitary tumors or infection
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bleeding in the pituitary
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genetic diseases that affect the way the pituitary gland develops or functions
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surgical removal of the pituitary to treat other conditions
The most common cause of tertiary adrenal insufficiency is suddenly stopping corticosteroids after taking them for a long time. Prescription doses of corticosteroids can cause higher levels of cortisol in your blood than your body normally makes. High levels in your blood for a long time cause the hypothalamus to make less CRH. Less CRH means less ACTH, which in turn causes the adrenal glands to stop making cortisol.
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Once you stop taking corticosteriods, your adrenal glands may be slow to start working again. To give them time to start making cortisol again, your doctor will gradually reduce your dose over a period of weeks or even months. Even so, your adrenal glands might not begin to work normally for many months. Your doctor should watch you carefully for symptoms of adrenal insufficiency.
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Tertiary adrenal insufficiency can also occur after Cushing\u2019s syndrome is cured. Cushing\u2019s syndrome is a hormonal disorder caused by high levels of cortisol in the blood for a long time. Sometimes Cushing\u2019s syndrome is caused by tumors, usually noncancerous, in the pituitary or adrenal glands that make too much ACTH or cortisol. Once the tumors are surgically removed, the source of excess ACTH or cortisol is suddenly gone. Your adrenal glands may be slow to start working again.
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Reference
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Diagnosis
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How do doctors diagnose adrenal insufficiency?
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Your doctor will review your symptoms and run tests to confirm that your cortisol levels are low.
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Review of symptoms
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In its early stages, adrenal insufficiency can be hard to diagnose since symptoms come on slowly. Your health care professional may suspect it after reviewing your medical history and symptoms. The next step is blood testing to see if your cortisol levels are too low and to help find the cause.
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Blood tests
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ACTH stimulation test
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The ACTH stimulation test is the test used most often to diagnose adrenal insufficiency. In this test, a health care professional will give you an intravenous (IV) injection of man-made ACTH, which is just like the ACTH your body makes. Your health care professional will take samples of your blood before and 30 minutes or 60 minutes after the injection. The cortisol levels in your blood samples are measured in a lab.
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The normal response after an ACTH injection is a rise in blood cortisol levels. People with Addison\u2019s disease and most people who have had secondary adrenal insufficiency for a long time have little or no increase in cortisol levels. The adrenal glands may be too damaged to respond to ACTH.
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The ACTH test may not be accurate in people who have had secondary adrenal insufficiency for a shorter time because their adrenal glands have not yet shrunk and can still respond to ACTH.
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Insulin tolerance test
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If the results of the ACTH stimulation test aren\u2019t clear or your doctor suspects a problem in the pituitary, you may have an insulin tolerance test (ITT). A health care professional will give you an IV injection of the hormone insulin, which lowers your levels of blood glucose. The dose is high enough to cause hypoglycemia, which occurs when your blood glucose level drops too low.
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Hypoglycemia causes physical stress, which normally triggers the pituitary to make more ACTH. A health care professional will draw your blood at the beginning of the test and again every half hour during the next 2 hours. If your cortisol levels are low, your pituitary isn\u2019t making enough ACTH, so your adrenal glands don\u2019t make enough cortisol. The ITT is the most reliable test to diagnose secondary adrenal insufficiency.
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Very low blood glucose levels can be dangerous, so a health care professional must be present at all times during this test to make sure blood glucose levels don\u2019t drop too low. The ITT isn\u2019t safe for people with heart disease, a history of seizures, and other serious illnesses.
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CRH stimulation test
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The CRH stimulation test is another option to help identify secondary insufficiency if the results of the ACTH test aren\u2019t clear. This test can also tell secondary from tertiary adrenal insufficiency.
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A health care professional will give you an IV injection of CRH and take samples of your blood before and 30, 60, 90, and 120 minutes after the injection to measure ACTH levels. If the pituitary is damaged, it won\u2019t make ACTH in response to the CRH injection. This result shows secondary adrenal insufficiency. A slow rise in ACTH levels suggests tertiary adrenal insufficiency.
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What tests do doctors use to find the cause of adrenal insufficiency?
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Once doctors diagnosis and identify the type of adrenal insufficiency, they may use blood and imaging tests to find the exact cause.
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Addison\u2019s disease
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Antibody blood tests
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A blood test can find antibodies that are present in autoimmune Addison\u2019s disease. Antibodies are proteins made by your immune system to protect your body from bacteria or viruses. In autoimmune Addison\u2019s disease, the antibodies mistakenly attack the adrenal glands. Most, but not all, people with autoimmune Addison\u2019s disease have these antibodies. If the test shows antibodies, you don\u2019t need further testing.
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Computed tomography (CT) scan
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CT scans use a combination of x-rays and computer technology to create images of your organs and other internal structures. A CT scan of the abdomen can find changes in your adrenal glands. In autoimmune Addison\u2019s disease, the glands are small or normal size and don\u2019t have other visible abnormalities.
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Enlarged adrenal glands or a buildup of calcium in the glands can occur when Addison\u2019s disease is caused by infection, bleeding in the adrenal glands, or cancer cells in the glands. However, these changes don\u2019t always occur in Addison\u2019s disease caused by TB.
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Tests for TB
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Tests to find TB include a chest x-ray, a urine test to look for the bacteria that causes TB, and a TB skin test. In the skin test, a health care professional injects a tiny amount of inactive TB bacteria under the skin of your forearm. If you develop a hard, raised bump or swelling on your arm, you have the TB bacteria in your body, even if you don\u2019t have active TB.
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Secondary and tertiary adrenal insufficiency
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Magnetic resonance imaging (MRI)
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MRI machines use radio waves and magnets to create detailed pictures of your internal organs and soft tissues without using x-rays. An MRI can look for changes in your pituitary and hypothalamus, such as large, noncancerous pituitary tumors.
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Treatment
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How do doctors treat adrenal insufficiency?
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Your doctor will prescribe hormone medicines to replace the hormones that your adrenal glands aren\u2019t making. You\u2019ll need higher doses during times of physical stress.
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Hormone replacement
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Cortisol is replaced with a corticosteroid, most often hydrocortisone, which you take two or three times a day by mouth. Less often, doctors prescribe prednisone or dexamethasone.
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If your adrenal glands aren\u2019t making aldosterone, you will take a medicine called fludrocortisone, which helps balance the amount of sodium and fluids in your body. People with secondary adrenal insufficiency usually make enough aldosterone, so they don\u2019t need to take this medicine.
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Your doctor will adjust the dose of each medicine to meet your body\u2019s needs.
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Treatment for adrenal crisis includes immediate IV injections of corticosteroids and large amounts of IV saline, a salt solution, with dextrose added. Dextrose is a type of sugar.
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Treatment in special situations
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Surgery
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If you\u2019re having any type of surgery that uses general anesthesia, you may have treatment with IV corticosteroids and saline. IV treatment begins before surgery and continues until you\u2019re fully awake after surgery and can take medicine by mouth. Your doctor will adjust the \u201cstress\u201d dose as you recover until you\u2019re back to your pre-surgery dose.
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Illness
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Talk with your doctor about how to adjust your dose of corticosteroids during an illness. You will need to increase your dose if you have a high fever. Once you recover, your doctor will adjust your dose back to your regular, pre-illness level. You will need immediate medical attention if you have a severe infection or diarrhea, or are vomiting and can\u2019t keep your corticosteroid pills down. Without treatment, in an emergency room if necessary, these conditions can lead to an adrenal crisis.
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Injury or other serious condition
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If you have a severe injury, you may need a higher, \u201cstress\u201d dose of corticosteroids right after the injury and while you recover. The same is true if you have a serious health condition such as suddenly passing out or being in a coma. Often, you must get these stress doses intravenously. Once you recover, your doctor will adjust your dose back to regular, pre-injury level.
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Pregnancy
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If you become pregnant and have adrenal insufficiency, you\u2019ll take the same dose of medicine as you did before pregnancy. However, if nausea and vomiting in early pregnancy make it hard to take medicine by mouth, your doctor may need to give you corticosteroid shots. During delivery, treatment is similar to that of people needing surgery. Following delivery, your doctor will slowly decrease your dose, and you\u2019ll be back to your regular dose about 10 days after your baby is born.
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Eating, Diet, & Nutrition
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What should I eat if I have adrenal insufficiency?
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Some people with Addison\u2019s disease who have low aldosterone can benefit from a high-sodium diet. A health care professional or a dietitian can recommend the best sodium sources and how much sodium you should have each day.
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High doses of corticosteroids are linked to a higher risk of osteoporosis\u2014a condition in which the bones become less dense and more likely to fracture. If you take corticosteroids, you may need to protect your bone health by getting enough dietary calcium and vitamin D. A health care professional or a dietitian can tell you how much calcium you should have based on your age. You may also need to take calcium supplements.
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Clinical Trials
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The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other components of the National Institutes of Health (NIH) conduct and support research into many diseases and conditions, including adrenal insufficiency.
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What are clinical trials for adrenal insufficiency?
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Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about disease and improve health care for people in the future.
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Researchers are studying many aspects of adrenal insufficiency to
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Learn more about conditions that affect the endocrine glands
Watch a video of NIDDK Director Dr. Griffin P. Rodgers explaining the importance of participating in clinical trials.
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What clinical trials for adrenal insufficiency are looking for participants?
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You can view a filtered list of clinical studies on adrenal insufficiency that are open and recruiting at www.ClinicalTrials.gov. You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the NIH does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.
\n \n \n
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Constantine Stratakis, M.D., D.Med. Sci., Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH
Cushing\u2019s syndrome is a disorder that occurs when your body makes too much of the hormone cortisol over a long period of time. Cortisol is sometimes called the \u201cstress hormone\u201d because it helps your body respond to stress. Cortisol also helps
The adrenal glands, two small glands on top of your kidneys, make cortisol.
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How common is Cushing\u2019s syndrome?
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Endogenous Cushing\u2019s syndrome is rare. \u201cEndogenous\u201d means something inside your body is causing the disorder rather than something outside your body, such as medicine. Estimates vary, ranging from about 40 to 70 people out of every million.1
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Who is more likely to have Cushing\u2019s syndrome?
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Cushing\u2019s syndrome most often affects adults, usually aged 30 to 50,1 but can also occur in children. Cushing\u2019s syndrome affects about three times as many women as men.2 In people who have type 2 diabetes and blood glucose levels that stay too high over time, along with high blood pressure, Cushing\u2019s syndrome may be the cause. People who take medicines called glucocorticoids, which are similar to cortisol, also can develop Cushing\u2019s syndrome. This type of Cushing\u2019s syndrome is called \u201cexogenous.\u201d More than 10 million Americans take glucocorticoids each year,3 but it\u2019s not known how many of them develop Cushing\u2019s syndrome.
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What are the complications of Cushing\u2019s syndrome?
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Cushing\u2019s syndrome can cause health problems such as
Although Cushing\u2019s syndrome can usually be cured, it can be fatal if not treated.
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What are the symptoms of Cushing\u2019s syndrome?
\n
Signs and symptoms of Cushing's syndrome vary. People who have very high levels of cortisol for a long time are likely to have clear signs of the disorder, including
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weight gain
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thin arms and legs
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a round face
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increased fat around the base of the neck
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a fatty hump between the shoulders
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easy bruising
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wide purple stretch marks, mainly on the abdomen, breasts, hips, and under the arms
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weak muscles
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Children with Cushing\u2019s syndrome tend to have obesity and grow more slowly than other children. Women may have excess hair on their face, neck, chest, abdomen, and thighs. Menstrual periods may become irregular or stop. Men may have decreased fertility with lowered interest in sex and may have erectile dysfunction.
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Not everyone with Cushing\u2019s syndrome has these symptoms, which can make it hard to detect.
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What causes Cushing\u2019s syndrome?
\n
The most common cause of Cushing\u2019s syndrome is the long-term, high-dose use of the cortisol-like glucocorticoids. These medicines are used to treat other medical conditions, such as asthma, rheumatoid arthritis, and lupus. Glucocorticoids are often injected into a joint to treat pain. Use of glucocorticoids also suppresses the immune system after an organ transplant to keep the body from rejecting the new organ.
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Other people develop endogenous Cushing\u2019s syndrome because their bodies make too much cortisol. Several types of tumors can cause the body to make excess cortisol.
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Pituitary tumors
\n
Pituitary tumors, also called pituitary adenomas, are noncancerous growths on the pituitary gland. The pituitary gland sits at the base of the brain and is about the size of a pea. The pituitary makes adrenocorticotropic hormone (ACTH) and other hormones. ACTH tells the adrenal glands to make cortisol. These pituitary tumors make too much ACTH, causing the adrenals to make too much cortisol.
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Pituitary tumors that make too much ACTH cause 8 out of 10 cases of Cushing\u2019s syndrome2 not caused by glucocorticoid medicines. Doctors call this type of Cushing\u2019s syndrome Cushing\u2019s disease.
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Ectopic ACTH-producing tumors
\n
Some tumors that develop outside the pituitary gland also can produce ACTH. This condition is called ectopic ACTH syndrome. Most often, these tumors occur in the lungs. Ectopic tumors also can occur in the pancreas, thyroid, and thymus\u2014a gland that helps build a healthy immune system. Ectopic tumors may be cancerous.
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Adrenal tumors
\n
Sometimes a tumor on the adrenal gland itself makes too much cortisol. Adrenal tumors are most often benign but sometimes are cancerous.
\n
How do doctors diagnose Cushing\u2019s syndrome?
\n
Cushing\u2019s syndrome can be hard to diagnose. Symptoms such as fatigue and weight gain can have many different causes. Cushing\u2019s syndrome may be mistaken for other conditions that have many of the same signs, such as polycystic ovary syndrome or metabolic syndrome. Your doctor will first want to rule out other conditions.
\n
Diagnosis is based on your medical history, a physical exam, and lab tests. Your doctor may ask if you are taking glucocorticoids or have had injections and rule that out before ordering lab tests.
\n
Doctors may use urine, saliva, or blood tests to diagnose Cushing\u2019s syndrome. Sometimes doctors run a follow-up test to find out if excess cortisol is caused by Cushing\u2019s syndrome or has a different cause.
\n
No one test is perfect, so doctors usually do two of the following tests to confirm a diagnosis:
\n
24-hour urinary free-cortisol test
\n
In this test, you will collect your urine over a 24-hour period. Your health care professional will send your urine sample to a lab to test cortisol levels. Higher than normal cortisol levels suggest Cushing\u2019s syndrome.
\n
Late-night salivary cortisol test
\n
This test measures the amount of cortisol in your saliva in the late evening. Normally, cortisol production drops just after we fall asleep. In Cushing\u2019s syndrome, cortisol levels don\u2019t drop. You can collect your saliva sample at home and return it to your health care professional or send it to a lab for testing.
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Low-dose dexamethasone suppression test (LDDST)
\n
In this test, you will take a low dose of dexamethasone, a type of glucocorticoid, usually around 11:00 p.m. A health care professional will draw your blood the following morning, usually around 8 a.m. Sometimes doctors use another type of LDDST test, in which you take dexamethasone every 6 hours for 48 hours. Your blood is drawn 6 hours after the last dose.
\n
Normally, cortisol levels in the blood drop after taking dexamethasone. Cortisol levels that don\u2019t drop suggest Cushing\u2019s syndrome.
\n \n
When one of the first blood tests show that your body has too much cortisol, your doctor may order a follow-up test, called the dexamethasone\u2013corticotropin-releasing hormone (dexamethasone-CRH) test.
\n
Dexamethasone\u2013CRH test
\n
The dexamethasone-CRH test shows whether excess cortisol is caused by Cushing\u2019s syndrome or by something else.
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Some people have high cortisol levels off and on but don\u2019t develop the long-term health effects of Cushing's syndrome. These people may have pseudo-Cushing's syndrome, a condition sometimes found in people who have depression or anxiety, drink too much alcohol, have diabetes with blood glucose levels that are often too high, or have obesity.
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This test combines the LDDST and a CRH stimulation test. CRH is a hormone made in the part of the brain called the hypothalamus. CRH tells the pituitary to make ACTH, which in turn tells the adrenals to make cortisol. When cortisol levels rise enough, they turn off the CRH signal, so ACTH and cortisol levels fall.
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You\u2019ll get a shot of CRH and take dexamethasone by mouth. If you have pseudo-Cushing\u2019s syndrome, the dexamethasone will decrease ACTH and cortisol levels and keep them from rising. Cortisol levels that are high just before the CRH shot or rise during this test suggest Cushing's syndrome.
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How do doctors find the cause of Cushing\u2019s syndrome?
\n
Once your doctor diagnoses Cushing\u2019s syndrome, other tests can help tell whether the source of the problem is pituitary, ectopic, or adrenal. Knowing the source is important in choosing the best type of treatment.
\n
Blood tests
\n
The first step is to measure ACTH levels in the blood. If ACTH levels are low, the cause is probably an adrenal tumor. People with adrenal tumors don\u2019t need further blood tests.
\n
If ACTH levels are normal or high, the cause is probably a pituitary or ectopic tumor.
\n
Other blood tests help tell pituitary tumors from ectopic tumors. Doctors usually do more than one test.
\n
CRH stimulation test. For this test, you\u2019ll get a shot of CRH. If you have a pituitary tumor, CRH will increase the ACTH and cortisol in your blood. This rarely happens in people with ectopic tumors.
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High-dose dexamethasone suppression test (HDDST). This test is the same as the LDDST, except it uses higher doses of dexamethasone. If the cortisol levels in your blood drop after taking a high dose of dexamethasone, you probably have a pituitary tumor. If your cortisol levels don\u2019t drop, you may have an ectopic tumor.
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Other tests
\n
Other tests look for tumors and help tell pituitary tumors from ectopic tumors.
\n
Imaging tests. Imaging tests show the size and shape of the pituitary and adrenal glands and look for tumors. If blood tests show that the tumor is ectopic, imaging tests can help locate the tumor. The most common imaging tests are the computerized tomography (CT) scan and magnetic resonance imaging (MRI).
\n \n
Petrosal sinus sampling. Pituitary tumors are usually small and may not show up in an imaging test. If an MRI doesn\u2019t show a pituitary tumor, you might have petrosal sinus sampling. This test is often the best way to tell pituitary from ectopic causes of Cushing's syndrome.
\n
Your doctor will draw samples of blood from your petrosal sinuses\u2014veins that drain the pituitary. At the same time, you will have a blood sample taken from a blood vessel far away from the pituitary. You will also get a shot of CRH, the hormone that causes the pituitary to release ACTH.
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Higher levels of ACTH in the blood from the petrosal sinuses than from the other blood vessel indicate a pituitary tumor. Similar levels of ACTH in all the blood samples suggest an ectopic tumor.
\n
How do doctors treat Cushing\u2019s syndrome?
\n
Treatment depends on the cause and may include surgery, radiation, chemotherapy, or cortisol-reducing medicines. If the cause is long-term use of glucocorticoids to treat another disorder, your doctor will gradually reduce your dosage to the lowest dose that will control that disorder. Sometimes disorders that doctors treat with glucocorticoids can be treated with a non-glucocorticoid medicine instead.
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Pituitary tumors
\n
The most common treatment for pituitary tumors is surgery to remove the tumor. Using a special microscope and fine instruments, a surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Your doctor will probably refer you to a center specializing in this type of surgery.
\n
The success, or cure, rate of this surgery can be as high as 90 percent when done by a highly experienced surgeon.4 If surgery fails or the cure doesn\u2019t last, surgery can be repeated, often with good results.
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After the surgeon removes the tumor, your pituitary won\u2019t make enough ACTH for a while. Your doctor will prescribe cortisol medicine since there\u2019s not enough ACTH to tell the adrenal glands to make enough cortisol. You may be able to stop cortisol medicine in 6 to 18 months.
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If surgery fails or isn\u2019t possible, radiation therapy is an option. One type of radiation therapy uses small doses of radiation to the pituitary over a 6-week period. Another type uses a single, high dose of radiation. Cortisol levels may not return to normal after radiation therapy for several years. Your doctor may prescribe medicines to bring cortisol levels back to normal until radiation therapy takes effect.
\n
Ectopic ACTH-producing tumors
\n
The first choice of treatment for ectopic tumors is to remove them surgically. If the tumor is cancerous and has spread, you may need chemotherapy, radiation therapy, or other cancer treatments. Medicines to reduce cortisol levels may also be part of your treatment. If other treatments fail, surgeons might have to remove the adrenal glands to control Cushing\u2019s syndrome.
\n
Adrenal tumors
\n
Surgery to remove the adrenal gland with the tumor is the most common treatment. Some rare diseases cause many nodules in both adrenal glands and require surgery to remove both glands. If you have both adrenal glands removed, you will need to take medicine for life to replace cortisol and other hormones the adrenal glands make.
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Clinical Trials
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The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other components of the National Institutes of Health (NIH) conduct and support research into many diseases and conditions.
\n
What are clinical trials, and are they right for you?
\n
Clinical trials are part of clinical research and at the heart of all medical advances. Clinical trials look at new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. Find out if clinical trials are right for you.
\n
What clinical trials are open?
\n
Clinical trials that are currently open and are recruiting can be viewed at www.ClinicalTrials.gov.
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References
\n \n
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
Graves\u2019 disease is an autoimmune disorder that can cause hyperthyroidism, or overactive thyroid. The thyroid is a small, butterfly-shaped gland in the front of your neck. Thyroid hormones control the way your body uses energy, so they affect nearly every organ in your body, even the way your heart beats.
\n
With Graves\u2019 disease, your immune system attacks your thyroid gland, causing it to make more thyroid hormones than your body needs. As a result, many of your body\u2019s functions speed up.
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How common is Graves\u2019 disease?
\n
Graves\u2019 disease affects nearly 1 in 100 Americans.1 About 4 out of 5 cases of hyperthyroidism in the United States are caused by Graves\u2019 disease.1
\n
Who is more likely to have Graves\u2019 disease?
\n
Graves\u2019 disease is more common in women and people older than age 30.2 You are more likely to develop the disease if you
problems with the menstrual cycle, fertility, and pregnancy
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eye discomfort and changes in vision
\n
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What are the symptoms of Graves\u2019 disease?
\n
Graves\u2019 disease often causes symptoms of hyperthyroidism. Graves\u2019 disease can also affect your eyes and skin. Symptoms can come and go over time.
\n
Hyperthyroidism
\n
Symptoms of hyperthyroidism can vary from person to person and may include5
\n Symptoms of hyperthyroidism may include trouble sleeping and fatigue. \n
Eye problems
\n
More than 1 in 3 people with Graves\u2019 disease develop an eye disease called Graves\u2019 ophthalmopathy (GO).6 GO occurs when your immune system attacks the muscles and other tissues around your eyes. Symptoms can include
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bulging eyes
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gritty, irritated eyes
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puffy eyes
\n
light sensitivity
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pressure or pain in the eyes
\n
blurred or double vision
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These symptoms can start before or at the same time as symptoms of hyperthyroidism. Rarely, GO can develop after Graves\u2019 disease has been treated. You can develop GO even if your thyroid function is normal. Most people have mild symptoms.
\n
Skin problems
\n
Rarely, people with Graves\u2019 disease develop a condition that causes the skin to become reddish and thick, with a rough texture. Called Graves\u2019 dermopathy or pretibial myxedema, the condition usually affects your shins but can also develop on the top of your feet and other parts of your body. Most cases are mild and painless.
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What causes Graves\u2019 disease?
\n
Researchers aren\u2019t sure why some people develop autoimmune disorders such as Graves\u2019 disease. These disorders probably develop from a combination of genes and an outside trigger, such as a virus.
\n
With Graves\u2019 disease, your immune system makes an antibody called thyroid-stimulating immunoglobulin (TSI) that attaches to your thyroid cells. TSI acts like thyroid-stimulating hormone (TSH), a hormone made in your pituitary gland that tells your thyroid how much thyroid hormone to make. TSI causes your thyroid to make too much thyroid hormone.
\n
How do doctors diagnose Graves\u2019 disease?
\n
Your doctor will take your medical history and perform a physical exam to look for signs of Graves\u2019 disease. To confirm a diagnosis of Graves\u2019 disease, your doctor may order one or more of these thyroid tests
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Blood tests. These tests can measure the levels of your thyroid hormones and also check for TSI.
\n
Radioactive iodine uptake test. This test measures the amount of iodine your thyroid is taking up from your bloodstream to make thyroid hormones. If your thyroid is taking up large amounts of iodine, you may have Graves\u2019 disease.
\n
Thyroid scan. This test, often done together with the radioactive iodine uptake test, shows how and where iodine is distributed in your thyroid. With Graves\u2019 disease, the iodine shows up throughout the gland. With other causes of hyperthyroidism such as nodules\u2014small lumps in the gland\u2014the iodine shows up in a different pattern.
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Doppler blood flow measurement. This test, also called Doppler ultrasound, uses sound waves to detect increased blood flow in your thyroid due to Graves\u2019 disease. Your doctor may order this test if radioactive iodine uptake is not a good option for you, such as during pregnancy or breastfeeding.
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How do doctors treat Graves\u2019 disease?
\n
Treating hyperthyroidism
\n
Hyperthyroidism is usually treated with medicines, radioiodine therapy, or thyroid surgery. Your doctor can help you identify the best option based on your age, health, symptoms, and other factors.
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Leonard Wartofsky, M.D., M.A.C.P., Washington Hospital Center and Georgetown University Hospital
large numbers of white blood cells, which are part of the immune system, build up in the thyroid
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the thyroid becomes damaged and can\u2019t make enough thyroid hormones
\n
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Thyroid hormones control how your body uses energy, so they affect nearly every organ in your body\u2014even the way your heart beats.
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\n The thyroid is a small gland in your neck that makes thyroid hormones. \n
\n
Does Hashimoto\u2019s disease have another name?
\n
Hashimoto\u2019s disease is also called Hashimoto\u2019s thyroiditis, chronic lymphocytic thyroiditis, or autoimmune thyroiditis.
\n
How common is Hashimoto\u2019s disease?
\n
The number of people who have Hashimoto\u2019s disease in the United States is unknown. However, the disease is the most common cause of hypothyroidism, which affects about 5 in 100 Americans.1
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Who is more likely to have Hashimoto\u2019s disease?
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Hashimoto\u2019s disease is 4 to 10 times more common in women than men.2 Although the disease may occur in teens or young women, it more often develops in women ages 30 to 50.3 Your chance of developing Hashimoto\u2019s disease increases if other family members have the disease.
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You are more likely to develop Hashimoto\u2019s disease if you have other autoimmune disorders, including4
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\n
celiac disease, a digestive disorder that damages the small intestine
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lupus, a chronic, or long-term, disorder that can affect many parts of the body
What are the symptoms of Hashimoto\u2019s disease?
\n
Many people with Hashimoto\u2019s disease have no symptoms at first. As the disease progresses, you may have one or more of the symptoms of hypothyroidism.
heavy or irregular menstrual periods or fertility problems
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slowed heart rate
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Hashimoto\u2019s disease causes your thyroid to become damaged. Most people with Hashimoto\u2019s disease develop hypothyroidism. Rarely, early in the course of the disease, thyroid damage may lead to the release of too much thyroid hormone into your blood, causing symptoms of hyperthyroidism.3
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Your thyroid may get larger and cause the front of the neck to look swollen. The enlarged thyroid, called a goiter, may create a feeling of fullness in your throat, though it is usually not painful. After many years, or even decades, damage to the thyroid may cause the gland to shrink and the goiter to disappear.
\n A health professional examines a woman's neck. \n
What causes Hashimoto\u2019s disease?
\n
Researchers don\u2019t know why some people develop Hashimoto\u2019s disease, but a family history of thyroid disease is common. Several factors may play a role, including2
some medicines used to treat bipolar disorder or other mental health problems
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iodine-containing medicines used to treat abnormal heart rhythm
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exposure to toxins, such as nuclear radiation
\n
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How do doctors diagnose Hashimoto\u2019s disease?
\n
Doctors diagnose Hashimoto\u2019s disease based on
\n
\n
medical history and physical exam. Your doctor will start by taking a medical history and performing a physical exam. In addition to asking about symptoms, the doctor will check your neck for a goiter, which some people with Hashimoto\u2019s disease can develop.
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blood tests. Your doctor will order one or more blood tests to check for hypothyroidism and its causes. Examples include tests for \n
\n
the thyroid hormones T4 (thyroxine) and T3 (triiodothyronine)
\n
thyroid-stimulating hormone, or TSH
\n
thyroid peroxidase antibodies (TPO), a type of thyroid antibody that is present in most people with Hashimoto\u2019s disease
\n
\n
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You probably won\u2019t need other tests to confirm you have Hashimoto\u2019s disease. However, if your doctor suspects Hashimoto\u2019s disease but you don\u2019t have antithyroid antibodies in your blood, you may have an ultrasound of your thyroid. The ultrasound images can show the size of your thyroid and other features of Hashimoto\u2019s disease. The ultrasound also can rule out other causes of an enlarged thyroid, such as thyroid nodules\u2014small lumps in the thyroid gland.
\n
How do doctors treat Hashimoto\u2019s disease?
\n
How your doctors treat Hashimoto\u2019s disease usually depends on whether the thyroid is damaged enough to cause hypothyroidism. If you don\u2019t have hypothyroidism, your doctor may choose to simply check your symptoms and thyroid hormone levels regularly.
\n
\n You will take levothyroxine to replace the hormone your thyroid no longer makes. \n
\n
The medicine levothyroxine, which is identical to the natural thyroid hormone thyroxine (T4), is the recommended way to treat hypothyroidism. Prescribed in pill form for many years, this medicine is now also available as a liquid and in a soft gel capsule.2 These newer formulas may be helpful to people with digestive problems that affect how the thyroid hormone pill is absorbed.
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Some foods and supplements can affect how well your body absorbs levothyroxine. Examples include grapefruit juice, espresso coffee, soy, and multivitamins that contain iron or calcium.1,6 Taking the medicine on an empty stomach can prevent this from happening. Your doctor may ask you to take the levothyroxine in the morning, 30 to 60 minutes before you eat your first meal.
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Your doctor will give you a blood test about 6 to 8 weeks after you begin taking the medicine and adjust your dose if needed. Each time you change your dose, you\u2019ll have another blood test. Once you\u2019ve reached a dose that\u2019s working for you, your doctor will likely repeat the blood test in 6 months and then once a year.
\n
Never stop taking your medicine or take a higher dose without talking with your doctor first. Taking too much thyroid hormone medicine can cause serious problems, such as atrial fibrillation or osteoporosis.5
\n
Your hypothyroidism can be well-controlled with thyroid hormone medicine, as long as you take the medicine as instructed by your doctor and have regular follow-up blood tests.
\n
How does eating, diet, and nutrition affect Hashimoto\u2019s disease?
\n
The thyroid uses iodine, a mineral in some foods, to make thyroid hormones. However, if you have Hashimoto\u2019s disease or other types of autoimmune thyroid disorders, you may be sensitive to harmful side effects from iodine. Eating foods that have large amounts of iodine\u2014such as kelp, dulse, or other kinds of seaweed, and certain iodine-rich medicines\u2014may cause hypothyroidism or make it worse. Taking iodine supplements can have the same effect.
\n
Talk with members of your health care team about
\n
\n
what foods and beverages to limit or avoid
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whether you take iodine supplements
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any cough syrups you take that may contain iodine
\n
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However, if you are pregnant, you need to take enough iodine because the baby gets iodine from your diet. Too much iodine can cause problems as well, such as a goiter in the baby. If you are pregnant, talk with your doctor about how much iodine you need.
\n
Researchers are looking at other ways in which diet and supplements\u2014such as vitamin D and selenium\u2014may affect Hashimoto\u2019s disease.2 However, no specific guidance is currently available.3
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Clinical Trials for Hashimoto\u2019s Disease
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The NIDDK conducts and supports clinical trials in many diseases and conditions, including endocrine diseases. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.
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What are clinical trials for Hashimoto\u2019s disease?
\n
Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about Hashimoto\u2019s disease and improve health care for people in the future.
Watch a video of NIDDK Director Dr. Griffin P. Rodgers explaining the importance of participating in clinical trials.
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What clinical studies for Hashimoto\u2019s disease are looking for participants?
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You can find clinical studies on Hashimoto\u2019s disease at www.ClinicalTrials.gov. In addition to searching for federally funded studies, you can expand or narrow your search to include clinical studies from industry, universities, and individuals; however, the National Institutes of Health does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.
\n
References
\n \n
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
\n
The NIDDK would like to thank: Leonard Wartofsky, M.D., M.A.C.P., MedStar Georgetown University Hospital
Health Alert: Adrenal Crisis Causes Death in Some People Who Were Treated with hGH
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Doctors conducting the follow-up study of individuals treated with hGH looked at causes of death among recipients and found some disturbing news. Many more people have died from a treatable condition called adrenal crisis than from CJD. This risk does not affect every recipient. It can affect those who lack other hormones in addition to growth hormone. Please read on to find out if this risk applies to you. Death from adrenal crisis can be prevented.
\n
Adrenal crisis is a serious condition that can cause death in people who lack the pituitary hormone ACTH. ACTH is responsible for regulating the adrenal gland. Often, people are unaware that they lack this hormone and therefore do not know about their risk of adrenal crisis.
\n
Most people who were treated with hGH did not make enough of their own growth hormone. Some of them lacked growth hormone because they had birth defects, tumors or other diseases that cause the pituitary gland to malfunction or shut down. People with those problems frequently lack other key hormones made by the pituitary gland, such as ACTH, which directs the adrenal gland to make cortisol, a hormone necessary for life. Having too little cortisol can be fatal if not properly treated.
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Treatment with hGH does not cause adrenal crisis, but because a number of people lacking growth hormone also lack ACTH, adrenal crisis has occurred in some people who were treated with hGH. In earlier updates we have talked about how adrenal crisis can be prevented, but people continue to die from adrenal crisis, which is brought on by lack of cortisol. These deaths can be prevented. Please talk to your doctor about whether you are at risk for adrenal crisis.
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Why should people treated with hGH know about adrenal crisis? Among the people who received hGH, those who had birth defects, tumors, and other diseases affecting the brain lacked hGH and often, other hormones made by the pituitary gland. A shortage of the hormones that regulate the adrenal glands can cause many health problems. It can also lead to death from adrenal crisis. This tragedy can be prevented.
\n
What are adrenal hormones? The pituitary gland makes many hormones, including growth hormone and ACTH, a hormone which signals the adrenal glands to make cortisol, a hormone needed for life. If the adrenal gland doesn't make enough cortisol, replacement medications must be taken. The most common medicines used for cortisol replacement are: \n
\n
Hydrocortisone
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Prednisone
\n
Dexamethasone
\n
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What is adrenal crisis? Adrenal hormones are needed for life. The system that pumps blood through the body cannot work during times of physical stress, such as illness or injury, if there is a severe lack of cortisol (or its replacement). People who lack cortisol must take their cortisol replacement medication on a regular basis, and when they are sick or injured, they must take extra cortisol replacement to prevent adrenal crisis. When there is not enough cortisol, adrenal crisis can occur and may rapidly lead to death.
\n
What are the symptoms of lack of adrenal hormones? If you don't have enough cortisol or its replacement, you may have some of these problems: \n
\n
feeling weak
\n
feeling tired all the time
\n
feeling sick to your stomach
\n
vomiting
\n
no appetite
\n
weight loss
\n
When someone with adrenal gland problems has weakness, nausea, or vomiting, that person needs immediate emergency treatment to prevent adrenal crisis and possible death.
\n
Why are adrenal hormones so important? Cortisol (or its replacement) helps the body respond to stress from infection, injury, or surgery. The normal adrenal gland responds to serious illness by making up to 10 times more cortisol than it usually makes. It automatically makes as much as the body needs. If you are taking a cortisol replacement drug because your body cannot make these hormones, you must increase the cortisol replacement drugs during times of illness, injury, or surgery. Some people make enough cortisol for times when they feel well, but not enough to meet greater needs when they are ill or injured. Those people might not need cortisol replacement every day but may need to take cortisol replacement medication when their body is under stress. Adrenal crisis is extremely serious and can cause death if not treated promptly. Discuss this problem with your doctor to help decide whether you need more medication or other treatment to protect your health.
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How is adrenal crisis treated? People with adrenal crisis need immediate treatment. Any delay can cause death. When people with adrenal crisis are vomiting or unconscious and cannot take medicine, the hormones can be given as an injection. Getting an injection of adrenal hormones can save your life if you are in adrenal crisis. If you lack the ability to make cortisol naturally, you should carry a medical ID card and wear a Medic-Alert bracelet to tell emergency workers that you lack adrenal hormones and need treatment. This precaution can save your life if you are sick or injured.
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How can I prevent adrenal crisis? \n
\n
If you are always tired, feel weak, and have lost weight, ask your doctor if you might have a shortage of adrenal hormones.
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If you take hydrocortisone, prednisone, or dexamethasone, learn how to increase the dose when you become ill.
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If you are very ill, especially if you are vomiting and cannot take pills, seek emergency medical care immediately. Make sure you have a hydrocortisone injection with you at all times, and make sure that you and those around you (in case you're not conscious) know how and when to administer the injection.
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Carry a medical ID card and wear a bracelet telling emergency workers that you have adrenal insufficiency and need cortisol. This way, they can treat you right away if you are injured.
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Remember: Some people who lacked growth hormone may also lack cortisol, a hormone necessary for life. Lack of cortisol can cause adrenal crisis, a preventable condition that can cause death if treated improperly. Deaths from adrenal crisis can be prevented if patients and their families recognize the condition and are careful to treat it right away. Adrenal crisis is a medical emergency. Know the symptoms and how to adjust your medication when you are ill. Taking these precautions can save your life.
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
Human Growth Hormone & Creutzfeldt-Jakob Disease Resource List
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Nonprofit Organizations Offering Support and Information
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MAGIC (Major Aspects of Growth in Children) Foundation is a national, nonprofit organization that provides support and education about growth disorders in children and growth hormone deficiency in adults. Staff will help connect people who have similar interests or concerns.
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The Human Growth Foundation (HGF) is a nonprofit organization concerned with children\u2019s growth disorders and adult growth hormone deficiency. The HGF offers a brochure about adult growth hormone deficiency. The foundation also sponsors adult and pediatric Internet discussion forums to support the exchange of information about growth hormone deficiency and growth hormone replacement therapy. To subscribe, follow the instructions at www.hgfound.org.
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The Creutzfeldt-Jakob Disease (CJD) Foundation, Inc. was created in 1993 by two families who lost relatives to CJD and the neurologist who treated the patients. This nonprofit corporation seeks to promote awareness of CJD through research and education and to reach out to people who have lost loved ones to this illness. The CJD Foundation is on the web at cjdfoundation.org.
To conduct your own web search of the medical literature, see PubMed, a search engine of the National Library of Medicine\u2019s (NLM) MEDLINE database. In PubMed, you can read abstracts or summaries of many articles. Another useful web resource is the NLM\u2019s MedlinePlus, a directory of information resources that can help you research your health questions.
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The articles listed below are found in medical libraries. If you do not have access to a medical library, consult your local public librarian. Many public libraries will help you obtain copies of journal articles.
Honda H, Matsumoto M, Masahiro S, et al. Frequent detection of pituitary-derived PrPres in human prion diseases. J Neuropathol Exp Neurol. 2019;78(10):922-929.
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Peckeu L, Brandel JP, Welaratne A, et. al. Factors influencing the incubation of an infectious form of Creutzfeldt-Jakob disease. ClinInfect Dis. 2019;ciz692: https://doi.org/10.1093/cid/ciz692.
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Herv\u00e9 D, Porch\u00e9 M, Cabrejo L, et al. Fatal A\u03b2 cerebral amyloid angiopathy 4 decades after a dural graft at the age of 2 years. Acta Neuropathologica. 2018;135(5):801\u2013803.
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Jucker M, Walker LC. Propagation and spread of pathogenic protein assemblies in neurodegenerative diseases. Nature Neuroscience. 2018;21(10):1341\u20131349.
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Orr\u00fa CD, Soldau K, Cordano C, et al. Prion seeds distribute throughout the eyes of sporadic Creutzfeldt-Jakob disease patients. mBio. 2018;9(6):e02095-18.
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Purro SA, Farrow MA, Linehan J, et. al. Transmission of amyloid- \u03b2 protein pathology from cadaveric pituitary growth hormone. Nature. 2018;594;415-419
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Orr\u00fa CD, Yuan J, Appleby BS, et al. Prion seeding activity and infectivity in skin samples from patients with sporadic Creutzfeldt-Jakob disease. Science Translational Medicine. 2017;9(417).
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Ritchie DL, Adlard P, Peden AH, et al. Amyloid-\u03b2 accumulation in the CNS in human growth hormone recipients in the UK. Acta Neuropathologica. 2017;134(2): 221\u2013240.
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Ritchie DL, Barria MA, Peden AH, et al. UK Iatrogenic Creutzfeldt-Jakob disease: investigating human prion transmission across genotypic barriers using human tissue-based and molecular approaches. Acta Neuropathologica. 2017;133(4):579\u2013595.
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Coulthart MB, Geschwind MD, Qureshi S, et al. A case cluster of variant Creutzfeldt-Jakob disease linked to the Kingdom of Saudi Arabia. Brain. 2016;139(Pt 10):2609-2616.
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Hughson AG, Race B, Kraus A, et al. Inactivation of prions and amyloid seeds with hypochlorous acid. PLoS Pathog. 2016;12(9):e1005914.
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Jaunmuktane Z, Mead S, Ellis M, et al. Evidence for human transmission of amyloid-\u03b2 pathology and cerebral amyloid angiopathy. Nature. 2015;525(7568):247\u2013250.
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Orr\u00fa CD, Groveman BR, Hughson AG, et al. Rapid and sensitive RT-QuIC detection of human Creutzfeldt-Jakob disease using cerebrospinal fluid. MBio. 2015;6(1):e02451\u201314.
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Prusiner SB, Woerman, AL, Mordes, DA, et al. Evidence for \u03b1-synuclein prions causing multiple system atrophy in humans with parkinsonism. Proceedings of the National Academy of Sciences of the United States of America. 2015;112(38):E5308-5317.
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Orr\u00fa CD, Bongianni M, Tonoli G, et al. A test for Creutzfeldt-Jakob disease using nasal brushings. New England Journal of Medicine. 2014;371:519\u2013529.
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Appleby BS, Lu M, Bizzi A, et al. Iatrogenic Creutzfeldt-Jakob disease from commercial cadaveric human growth hormone. Emerging Infectious Diseases. 2013;19(4):682\u2013684.
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Irwin DJ, Abrams JY, Schonberger LB, et al. Evaluation of potential infectivity of Alzheimer and Parkinson disease proteins in recipients of cadaver-derived human growth hormone. JAMA Neurology. 2013;70(4):462\u2013468.
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Brown P, Brandel JP, Sato T, et al. Iatrogenic Creutzfeldt-Jakob disease, final assessment. Emerging Infectious Diseases. 2012;18(6):901\u2013907.
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Abrams JY, Schonberger LB, Belay ED, et al. Lower risk of Creutzfeldt-Jakob disease in pituitary growth hormone recipients initiating treatment after 1977. Journal of Clinical Endocrinology & Metabolism. 2011;96:E1666\u2013E1669. Abstract available at academic.oup.com/jcem/article/96/10/E1666/2836371.
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Creutzfeldt-Jakob disease surveillance in the UK. Twentieth annual report 2011. The National CJD Research & Surveillance Unit (NCJDRSU). www.cjd.ed.ac.uk/sites/default/files/report20b.pdf(PDF, 1.47 MB)
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Bell J, Parker KL, Swinford RD, Hoffman AR, Maneatis T, Lippe B. Long-term safety of recombinant human growth hormone in children. Journal of Clinical Endocrinology & Metabolism. 2010;95:167\u2013177.
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Boyd A, Klug GMJA, Schonberger LB, et al. Iatrogenic Creutzfeldt-Jakob disease in Australia: time to amend infection control measures for pituitary hormone recipients? Medical Journal of Australia. 2010;193:366\u2013369.
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Heath CA, Cooper SA, Murray K, et al. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Annals of Neurology. 2010;67(6):761\u2013770.
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Matsui Y, Satoh K, Mutsukura K, et al. Development of an ultra-rapid diagnostic method based on heart-type fatty acid binding protein levels in the CSF of CJD patients. Cellular and Molecular Neurobiology. 2010;30(7):991\u2013999.
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Tian HJ, Zhang JT, Lang SY, Wang XQ. MRI sequence findings in sporadic Creutzfeldt-Jakob disease. Journal of Clinical Neuroscience. 2010;17(11):1378\u20131380.
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Vranac T, Bresjanac M. Metabolic aspects of prion diseases: an overview. Current Drug Targets. 2010;11(10):1207\u20131217.
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Wilton P, Mattsson AF, Darendeliler F. Growth hormone treatment in children is not associated with an increase in the incidence of cancer: experience from KIGS (Pfizer International Growth Database). Journal of Pediatrics. 2010;157(2):265\u2013270.
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Lodi R, Parchi P, Tonon C, et al. Magnetic resonance diagnostic markers in clinically sporadic prion disease: a combined brain magnetic resonance imaging and spectroscopy study. Brain. 2009;132(10):2669\u20132679.
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Parchi P, Strammiello R, Notari S, et al. Incidence and spectrum of sporadic Creutzfeldt-Jakob disease variants with mixed phenotype and co-occurrence of PrPSc types: an updated classification. Acta Neuropathologica. 2009;118(5):659\u2013671.
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Quadrio I, Ugnon-Caf\u00e9 S, Dupin M, et al. Rapid diagnosis of human prion disease using streptomycin with tonsil and brain tissues. Laboratory Investigation. 2009;89(4):406\u2013413.
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Zerr K, Kallenberg K, Summers DM, et al. Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease. Brain. 2009;132(10):2659\u20132668.
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Zou S, Fang CT, Schonberger LB. Transfusion transmission of human prion diseases. Transfusion Medicine Reviews. 2008;22:58\u201369.
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Sanchez-Juan P, Cousens SN, Will RG, van Duijn CM. Source of variant Creutzfeldt-Jakob disease outside United Kingdom. Emerging Infectious Diseases. 2007;13:1166\u20131169.
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Ergun-Longmire B, Mertens AC, Mitby P, et al. Growth hormone treatment and risk of second neoplasms in the childhood cancer survivor. Journal of Clinical Endocrinology & Metabolism. 2006;91:3494\u20133498.
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
Hyperthyroidism, also called overactive thyroid, is when the thyroid gland makes more thyroid hormones than your body needs. The thyroid is a small, butterfly-shaped gland in the front of your neck. Thyroid hormones control the way the body uses energy, so they affect nearly every organ in your body, even the way your heart beats. With too much thyroid hormone, many of your body\u2019s functions speed up.
\n The thyroid is a small gland in your neck that makes thyroid hormones. \n
How common is hyperthyroidism?
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About 1 out of 100 Americans ages 12 years and older have hyperthyroidism.1
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Who is more likely to develop hyperthyroidism?
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Hyperthyroidism is more common in women and people older than 60.2 You are more likely to have hyperthyroidism if you
eat large amounts of food containing iodine, such as kelp
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use medicines that contain iodine
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use nicotine products3
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were pregnant within the past 6 months
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Is hyperthyroidism during pregnancy a problem?
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Mild hyperthyroidism during pregnancy is usually not a problem. But severe hyperthyroidism during pregnancy, when untreated, can affect both the mother and the baby. If you have hyperthyroidism and plan to get pregnant or become pregnant, work with your doctor to get the disease under control.
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\n Be sure your hyperthyroidism is under control before becoming pregnant. \n
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What are the complications of hyperthyroidism?
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Untreated, hyperthyroidism can cause serious health problems, including
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an irregular heartbeat that can lead to blood clots, stroke, heart failure, and other heart-related problems
In older adults, hyperthyroidism is sometimes mistaken for depression or dementia. Older adults may have different symptoms, such as loss of appetite or withdrawal from people, than younger adults with hyperthyroidism. You may want to ask your doctor about hyperthyroidism if you or your loved one shows these symptoms.
Graves\u2019 disease, the most common cause of hyperthyroidism, is an autoimmune disorder. With this disease, your immune system attacks the thyroid and causes it to make too much thyroid hormone.
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Overactive thyroid nodules
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Overactive thyroid nodules, or lumps in your thyroid, are common and usually not cancerous. However, one or more nodules may become overactive and produce too much thyroid hormone. Overactive nodules are found most often in older adults.
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Thyroiditis
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Thyroiditis is inflammation of your thyroid gland. Some types of thyroiditis can cause thyroid hormone to leak out of your thyroid gland into your bloodstream. As a result, you may develop symptoms of hyperthyroidism.
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The types of thyroiditis that can cause hyperthyroidism include
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subacute thyroiditis, which involves a painfully inflamed and enlarged thyroid.
painless thyroiditis, which is similar to postpartum thyroiditis, but occurs in the absence of pregnancy. Your thyroid may be enlarged. Experts think painless thyroiditis is probably an autoimmune condition.
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Thyroiditis can also cause symptoms of hypothyroidism, or underactive thyroid. In some cases, after your thyroid is overactive for a period of time, it may become underactive.
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Too much iodine
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Your thyroid uses iodine to make thyroid hormone. How much iodine you consume affects how much thyroid hormone your thyroid makes. In some people, consuming large amounts of iodine may cause the thyroid to make too much thyroid hormone.
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Some cough syrups and medicines, including some heart medicines, may contain a lot of iodine. Seaweed and seaweed-based supplements also contain a lot of iodine.
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Too much thyroid hormone medicine
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Some people who take thyroid hormone medicine for hypothyroidism may take too much. If you take thyroid hormone medicine, see your doctor at least once a year to have your thyroid hormone levels checked. You may need to adjust your dose if your doctor finds your thyroid hormone level is too high.
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Some other medicines may also interact with thyroid hormone medicine and raise hormone levels. If you take thyroid hormone medicine, ask your doctor about interactions when starting new medicines.
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Noncancerous tumor
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In some rare cases, a noncancerous tumor of the pituitary gland, located at the base of the brain, can cause hyperthyroidism.
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How do doctors diagnose hyperthyroidism?
\n A blood test might confirm a diagnosis of hyperthyroidism. \n
Your doctor will take a medical history and perform a physical exam. A hyperthyroidism diagnosis can\u2019t be based on symptoms alone because many of its symptoms are the same as those of other diseases. That\u2019s why your doctor may use several thyroid blood tests and imaging tests to confirm the diagnosis and find its cause.
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Because hyperthyroidism can cause fertility problems, women who have trouble getting pregnant often get tested for thyroid problems.
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How do doctors treat hyperthyroidism?
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Your doctor will treat your hyperthyroidism to bring your thyroid hormone levels back to normal. Treating the disease will prevent long-term health problems, and it will relieve uncomfortable symptoms. No single treatment works for everyone.
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Your treatment depends on what\u2019s causing your hyperthyroidism and how severe it is. When recommending a treatment, your doctor will consider
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your age
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possible allergies to or side effects of the medicines
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other conditions, such as pregnancy or heart disease
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whether you have access to an experienced thyroid surgeon
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Treatment options
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Hyperthyroidism is usually treated with medicines, radioiodine therapy, or thyroid surgery.
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Thanh D. Hoang, D.O., FACP, FACE, CAPTAIN (select), Walter Reed National Military Medical Center
Hypothyroidism, also called underactive thyroid, is when the thyroid gland doesn\u2019t make enough thyroid hormones to meet your body\u2019s needs. The thyroid is a small, butterfly-shaped gland in the front of your neck. Thyroid hormones control the way your body uses energy, so they affect nearly every organ in your body, even the way your heart beats. Without enough thyroid hormones, many of your body\u2019s functions slow down.
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\n The thyroid is a small gland in your neck that makes thyroid hormones. \n
\n
How common is hypothyroidism?
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Nearly 5 out of 100 Americans ages 12 years and older have hypothyroidism, although most cases are mild or have few obvious symptoms.1
\n
Who is more likely to develop hypothyroidism?
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Women are much more likely than men to develop hypothyroidism. The disease is also more common among people older than age 60.1
Left untreated, hypothyroidism during pregnancy can affect both mother and baby. However, thyroid medicines can help prevent problems and are safe to take during pregnancy. Many women taking thyroid hormone medicine need a higher dose during pregnancy, so contact your doctor right away if you find out you\u2019re pregnant.
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What are the complications of hypothyroidism?
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Hypothyroidism can contribute to high cholesterol. If you have high cholesterol, you should get tested for hypothyroidism. Rarely, severe untreated hypothyroidism may lead to myxedema coma, an extreme form of hypothyroidism in which the body\u2019s functions slow to a life-threatening point. Myxedema coma requires immediate medical treatment.
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What are the symptoms of hypothyroidism?
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Hypothyroidism has many symptoms that can vary from person to person. Some common symptoms of hypothyroidism include
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fatigue
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weight gain
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trouble tolerating cold
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joint and muscle pain
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dry skin or dry, thinning hair
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heavy or irregular menstrual periods or fertility problems
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slowed heart rate
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depression
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\n Dry, thinning hair is one of many symptoms that might indicate hypothyroidism. \n
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Because hypothyroidism develops slowly, you may not notice symptoms of the disease for months or even years.
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Many of these symptoms, especially fatigue and weight gain, are common and do not necessarily mean you have a thyroid problem.
congenital hypothyroidism, or hypothyroidism that is present at birth
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surgical removal of part or all of the thyroid
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radiation treatment of the thyroid
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some medicines
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Less often, hypothyroidism is caused by too much or too little iodine in the diet or by disorders of the pituitary gland or hypothalamus.1 Iodine deficiency, however, is extremely rare in the United States.
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Hashimoto\u2019s disease
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Hashimoto\u2019s disease, an autoimmune disorder, is the most common cause of hypothyroidism. With this disease, your immune system attacks the thyroid. The thyroid becomes inflamed and can\u2019t make enough thyroid hormones.
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Thyroiditis
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Thyroiditis, an inflammation of your thyroid, causes stored thyroid hormone to leak out of your thyroid gland. At first, the leakage increases your blood\u2019s hormone levels, leading to thyrotoxicosis, a condition in which thyroid hormone levels are too high. The thyrotoxicosis may last for many months. After that, your thyroid may become underactive and, over time, the condition may become permanent, requiring thyroid hormone replacement.
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Three types of thyroiditis can cause thyrotoxicosis followed by hypothyroidism.2
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Subacute thyroiditis involves a painfully inflamed and enlarged thyroid.
Silent thyroiditis is painless, even though your thyroid may be enlarged. Experts think it is probably an autoimmune condition.
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Congenital hypothyroidism
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Some babies are born with a thyroid that is not fully developed or does not work properly. If untreated, congenital hypothyroidism can lead to intellectual disability and growth failure\u2014when a baby doesn\u2019t grow as expected. Early treatment can prevent these problems. That\u2019s why most newborns in the United States are tested for hypothyroidism.
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Surgical removal of part or all of the thyroid
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When surgeons remove part of the thyroid, the remaining part may produce normal amounts of thyroid hormone. But some people who have this surgery may develop hypothyroidism. Removing the entire thyroid always results in hypothyroidism.
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Surgeons may remove part or all of the thyroid as a treatment for
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hyperthyroidism
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a large goiter
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thyroid nodules, which are noncancerous tumors or lumps in the thyroid that can produce too much thyroid hormone
Radioactive iodine, a common treatment for hyperthyroidism, gradually destroys thyroid cells. If you receive radioactive iodine treatment, you probably will eventually develop hypothyroidism. Doctors also treat people who have head or neck cancers with external radiation therapy, which can also damage the thyroid if it is included in the treatment.
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Medicines
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Some medicines can interfere with thyroid hormone production and lead to hypothyroidism, including certain
Several recently developed cancer medicines, in particular, can either affect the thyroid directly or affect it indirectly by damaging the pituitary gland.
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How do doctors diagnose hypothyroidism?
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\n A blood test might confirm a diagnosis of hypothyroidism. \n
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Your doctor will take your medical history and perform a physical exam. A hypothyroidism diagnosis can\u2019t be based on symptoms alone because many of its symptoms are the same as those of other diseases.1 That\u2019s why your doctor may use several thyroid blood tests and imaging tests to confirm the diagnosis and find its cause.
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Because hypothyroidism can cause fertility problems, women who have trouble getting pregnant often get tested for thyroid problems.
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How do doctors treat hypothyroidism?
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Hypothyroidism is treated by replacing the hormones that your own thyroid can no longer make. You will take levothyroxine, a thyroid hormone medicine identical to a hormone a healthy thyroid makes.3 Usually prescribed in pill form, this medicine is also available as a liquid and as a soft gel capsule. These newer formulas may help people with digestive problems to absorb the thyroid hormone. Your doctor may recommend taking the medicine in the morning before eating.
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Your doctor will give you a blood test about 6 to 8 weeks after you begin taking the medicine, adjusting your dose if needed. Each time your dose is adjusted, you\u2019ll have another blood test. Once you\u2019ve reached a dose that\u2019s working for you, your doctor will probably repeat the blood test in 6 months and then once a year.
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Your hypothyroidism most likely can be completely controlled with thyroid hormone medicine, as long as you take the recommended dose as instructed. Never stop taking your medicine without talking with your doctor first. Taking too much thyroid hormone medicine can cause serious problems, such as atrial fibrillation or osteoporosis.1
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How does eating, diet, and nutrition affect hypothyroidism?
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Your thyroid uses iodine to make thyroid hormones. However, if you have Hashimoto\u2019s disease or other types of autoimmune thyroid disorders, you may be sensitive to iodine\u2019s harmful side effects. Eating foods that have large amounts of iodine\u2014such as kelp, dulse, or other kinds of seaweed\u2014may cause or worsen hypothyroidism. Taking iodine supplements can have the same effect.
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Talk with members of your health care team
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about what foods to limit or avoid
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if you take iodine supplements
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about any cough syrups you take because they may contain iodine
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If you are pregnant, you need more iodine because the baby gets iodine from your diet. Talk with your doctor about how much iodine you need.
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Clinical Trials for Hypothyroidism
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The NIDDK conducts and supports clinical trials in many diseases and conditions, including endocrine diseases. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.
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What are clinical trials for hypothyroidism?
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Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about disease and improve health care for people in the future.
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Researchers are studying many aspects of hypothyroidism, such as
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understanding how the disease progresses, its clinical presentation, and genetics
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investigating how effective and safe levothyroxine is for people with chronic kidney disease
Watch a video of NIDDK Director Dr. Griffin P. Rodgers explaining the importance of participating in clinical trials.
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What clinical studies for hypothyroidism are looking for participants?
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You can view a filtered list of clinical studies on hypothyroidism that are open and recruiting at www.ClinicalTrials.gov. You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the National Institutes of Health does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.
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References
\n \n
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
\n
The NIDDK would like to thank: Thanh D. Hoang, D.O., FACP, FACE, CAPTAIN (select), Walter Reed National Military Medical Center, and Henry B. Burch, M.D., Program Director, Division of Diabetes, Endocrinology, and Metabolic Diseases, NIDDK
Multiple endocrine neoplasia type 1 (MEN1) is a rare genetic disorder that mainly affects the endocrine glands. Located in different parts of the body, these glands control the production of hormones that direct many body processes, including growth, digestion, and sexual function.
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Previously called Wermer\u2019s syndrome, MEN1 causes tumors to develop in the
People with MEN1 may also develop tumors\u2014usually benign (not cancerous)\u2014in other endocrine glands and body tissues, including the skin. Multiple tumors often develop at the same time in different tissues.
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How common is MEN1?
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MEN1 is a rare, inherited condition, occurring in about 1 in 30,000 people.1
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Who is more likely to develop MEN1?
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A family history of the disorder increases your risk. If one of your parents has the gene for MEN1, you have a 50 percent chance of inheriting the defective gene.
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MEN1 affects men and women equally. Although the disorder can affect all age groups, the first symptoms are typically linked to overactive parathyroid glands and often appear in people in their early 20s.2,3 Most people are diagnosed as having MEN1 in their 40s, when the disorder has started to affect other endocrine glands.
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What are the complications of having MEN1?
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MEN1 causes tumors to develop in endocrine glands and other parts of the body. Although most of these tumors are noncancerous, they can cause the affected glands to increase in size and become overactive, producing too much hormone. In some cases, a large tumor may cause a gland to become underactive or unable to produce enough hormone.
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Complications vary, depending on
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the location of the tumors
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the size of the tumors
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type of hormone(s) affected, if any
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whether or not the tumors are cancerous
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Some tumors are nonfunctioning, which means they don\u2019t produce hormones. When small, these tumors may not cause any complications.
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Parathyroid glands
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About 95 percent of people with MEN1 develop tumors in the parathyroid glands by age 50.2 These four pea-sized glands produce parathyroid hormone, which helps maintain the right balance of calcium and phosphorus in your body. Over time, MEN1 can affect all four glands.
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Hyperparathyroidism. MEN1-related tumors cause the parathyroid glands to become overactive, producing too much parathyroid hormone. This condition, called hyperparathyroidism, is the most common complication associated with MEN1. Excess parathyroid hormone causes calcium levels in your blood to rise too high. Complications can include bone loss and kidney stones.
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Pancreas and digestive tract
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About 40 percent of people with MEN1 develop cancers in the pancreas, duodenum, or other parts of the digestive tract.2 Many different types of small tumors may develop at the same time. Many of these tumors produce hormones, while others do not produce hormones. Some tumors may be cancerous.
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In people with MEN1, the two most common tumors of the digestive tract are
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Gastrinomas. These tumors produce the hormone gastrin, which causes the stomach to release acid that helps the stomach digest food. Too much gastrin can cause stomach ulcers and serious diarrhea, leading to a condition called Zollinger-Ellison syndrome. People with MEN1 often have many small gastrinomas\u2014most often in the duodenum but also in the pancreas. Over time, some of these tumors may become cancerous.
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Insulinomas. These tumors form only in the pancreas, in cells that produce the hormone insulin. Insulin controls levels of blood glucose (blood sugar) by moving glucose into the cells, where it can be used for energy. Insulinomas make too much insulin, leading to low blood sugar. These tumors are almost always noncancerous and can usually be removed with surgery.
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Other, more rare pancreatic tumors may also develop and cause other complications. These tumors include
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Glucagonomas. These tumors cause cells in the pancreas to produce too much of the hormone glucagon, which raises blood sugar.
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VIPomas. These tumors cause cells in the pancreas to produce a hormone called vasoactive intestinal peptide (VIP), which releases water into the intestine.
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Pituitary gland
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Nearly 1 in 3 people with MEN1 develop tumors in the front part of the pituitary gland, called the anterior lobe.2 Like other pituitary tumors, these growths are often small in size and are almost always benign.
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In people with MEN1, the two most common pituitary tumors are
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Prolactinomas. The most common pituitary tumor in people with MEN1, prolactinomas produce the hormone prolactin. Normally, this hormone signals women\u2019s breasts to produce milk during pregnancy and breastfeeding. Women with a prolactinoma may notice milk discharge from their breast(s) (called galactorrhea) when they are not pregnant or breastfeeding. Complications from having too much prolactin in the blood can include infertility and bone loss.
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Tumors that produce growth hormone (GH). GH-producing tumors are the second most common pituitary tumors in people with MEN1.4 Excess GH causes bones and other body tissues to grow larger in size, which can cause a condition called acromegaly. Related health problems can include arthritis, carpal tunnel syndrome, tumors of the colon or rectum, and heart disease.
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Some tumors may produce both prolactin and GH. Other, more rare pituitary tumors may produce other hormones, which can lead to different symptoms and complications. These hormones include cortisol, which helps your body respond to stress, and thyroid hormones that affect metabolism.
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Pituitary tumors that grow large in size may cause other problems, making it difficult for the pituitary gland to work properly. These tumors may prevent the pituitary gland from making enough hormones, leading to a condition called hypopituitarism. The tumors may also press against nearby brain tissues, causing headaches and/or vision problems.
\n
Other tumors
\n
MEN1 can also cause tumors in other parts of the body. Examples include
\n
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tumors in other endocrine glands, such as the adrenal glands
\n
carcinoid tumors\u2014slow-growing tumors most often found in the stomach, thymus, and lungs
\n
skin tumors and tumors under the skin, most commonly angiofibromas, lipomas (benign tumors made of fat cells), and collagenomas (tumors involving a protein in the skin called collagen)
Complications may vary, depending on the type, size, and location of the tumor.
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What are the symptoms of MEN1?
\n
MEN1 symptoms can differ from person to person, even among family members who have the disorder. The age at which signs or symptoms appear may also vary.
\n
Parathyroid tumors
\n
As MEN1 almost always affects the parathyroid glands, the most common early symptoms are related to excess parathyroid hormone. These symptoms are often mild and may not be noticed for years. They include
MEN1 is an inherited disorder most often caused by a mutation in the MEN1 gene. The gene provides instructions for producing a protein called menin, known to play a role in keeping cells from growing and dividing too fast.
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MEN1 is an autosomal dominant disorder. This means that only one parent needs to have the defective gene to pass the disorder on to a child. If one parent has the MEN1 gene, each child has a 1 in 2 (50%) chance of having the disorder. In about 1 in 10 cases, the mutation is not inherited from either parent but develops on its own. This is a natural, random process that can occur in anyone.4
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Every person in the family who has MEN1 syndrome shares the same mutation. By studying different families with MEN1, scientists have identified hundreds of different mutations of the MEN1 gene that can cause the disorder. If you have any of these mutations, you are considered a carrier of MEN1, even if you have no symptoms.
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Knowing if you are a carrier is important because, even without symptoms, you are very likely to develop some MEN1-related tumors in your lifetime. You may already have tumors developing that have not been detected if you have not had a thorough assessment, and you can still pass the disorder on to a child.
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If there is a known MEN1 mutation in your family and genetic testing shows that you don\u2019t carry it, then you don\u2019t have MEN1 syndrome. You are unlikely to develop MEN1-related tumors in your lifetime and you won\u2019t pass the disorder on to any children.
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How do doctors diagnose MEN1?
\n
Your doctor will diagnose you as having MEN1 if you meet one of these three criteria5
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two or more MEN1-related tumors (tumors in parathyroid glands, pituitary gland, and pancreas, or other part of the digestive tract)
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one MEN1-related tumor and a first-degree relative (a parent, brother or sister, or child) who has been clinically diagnosed as having MEN1
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a MEN1 mutation, even if you have no signs or symptoms of MEN1
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Genetic testing for MEN1 mutation
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Genetic testing will help you find out if you have a gene mutation known to cause MEN1. Testing is recommended for5
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people who have two or more MEN1-related endocrine tumors or other signs or symptoms of MEN1
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all first-degree relatives of a person who has the MEN1 gene mutation
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An early diagnosis will help you monitor your symptoms and address problems before they become serious. Genetic testing for a known familial mutation may be appropriate starting as early as age 5 because, in rare cases, children with MEN1 may develop tumors of the pituitary or parathyroid glands. The typical age of onset for MEN1 syndrome is in the teens or 20s, but the first tumors in someone with MEN1 may develop earlier or later. The symptoms and types of tumors can differ even among members of the same family.
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Genetic testing is most often performed on a blood sample. Some labs can also use saliva or a swab of the inside of the cheek to perform this testing.
\n \n
In up to 1 in 4 cases, the test may not find a mutation even though you may be showing signs of the disorder.2 In these cases, the cause could be an unknown MEN1 mutation or a mutation in another gene. If your test doesn\u2019t find a MEN1-related mutation, your doctor may order other tests to find out if your symptoms are due to another cause.
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How do doctors treat MEN1?
\n
Although MEN1 can\u2019t be cured, most people with the disorder lead long and productive lives. Your doctor will monitor your health and provide treatment as needed.
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Managing symptoms and monitoring tumors
\n
Your doctor will monitor your symptoms and screen for the signs of MEN1-related tumors on a regular basis. Commonly used screening tests include
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Blood tests. These tests will help your doctor monitor levels of hormones and other substances linked to MEN1-related tumors. Examples include calcium and parathyroid hormone, prolactin, gastrin, and markers for certain tumors.
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Imaging tests. Your doctor may order imaging tests to monitor the size and growth of existing tumors and to detect new ones, including tumors that don\u2019t release hormones or cause symptoms. These tests include magnetic resonance imaging (MRI), computed tomography (CT) scan, and ultrasound. Other tests that look for abnormal hormone receptors\u2014proteins that attach to certain hormones\u2014on the surface of tumors can help detect tumors that may not be visible on an MRI or CT scan.
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Based on your symptoms and test results, your doctor may prescribe different medicines to manage the progress of the disorder.
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Treating tumors
\n
If the tumors are small and not causing symptoms, no treatment may be needed. Doctors will follow these tumors with blood and imaging tests.
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Treatment varies depending on the location and type of tumor. For example
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Parathyroid tumors are most often treated with surgery to remove the affected glands. If surgery is not possible, your doctor may prescribe medicines to control calcium levels.
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Tumors of the pancreas and digestive tract are often treated with medicines to control symptoms such as too much stomach acid. Other treatment options include surgery to remove the tumor(s), freezing or burning tumors that have spread to the liver without removing them, and, more rarely, systemic chemotherapy\u2014treatment with anticancer drugs that travel through the blood to cells all over your body.
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Pituitary gland tumors are most often treated with medicines and/or surgery. Radiation therapy may also be used, but more rarely.
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Treating multiple tumors. People with MEN1 often develop many tumors at the same time. As a result, treatment is more complicated than among people who have a single tumor or very few tumors. Sometimes, MEN1-related tumors may be larger, more aggressive, and resistant to treatment than other tumors.2
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Surgery to remove tumors. Surgery is often successful in removing MEN1-related tumors and curing related symptoms. But in some cases, the tumors may grow back or spread to lymph nodes, the liver, or, more rarely, the bones. Your doctor may prescribe medicines to reduce the size of the tumor and treat related problems.
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Postsurgery treatment. If a surgery removes an entire endocrine gland\u2014or more than three parathyroid glands\u2014your doctor may prescribe medicines to replace the hormones that your body is no longer making. You may also need to take other medicines and supplements, such as calcium and vitamin D, to address these deficiencies.
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How can genetic counseling help?
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Genetic counseling is a source of information and support to families affected by or at risk for a genetic disorder. For example, genetic counselors can help you and your family
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understand how genetic testing is done
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weigh the medical, social, financial, and ethical decisions involved in getting tested
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discuss available options on how to manage the disease
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make informed decisions regarding whether to have children and discuss options for testing a child, a fetus, or an embryo for a known familial mutation in MEN1
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find out which members of the family are at risk and might benefit from genetic testing for a known familial MEN1 mutation
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Genetic counselors can also refer you to a range of support services, including education sources, advocacy and support groups, other health professionals, and local or state services.
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You can find genetic counselors near you using the Find a Genetic Counselor search tool from the National Society for Genetic Counselors. When using the tool, under \u201cTypes of Specialization,\u201d choose \u201cCancer.\u201d
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Clinical Trials for MEN1
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The NIDDK conducts and supports clinical trials in many diseases and conditions, including endocrine diseases. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.
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What are clinical trials for MEN1?
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Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about disease and improve health care for people in the future.
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Researchers are studying many aspects of MEN1, including new treatments for this condition.
What clinical studies for MEN1 are looking for participants?
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You can view a filtered list of clinical studies on MEN1 that are open and recruiting at www.ClinicalTrials.gov. You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the National Institutes of Health does not review these studies and cannot ensure they are safe. Always talk with your health care provider before you participate in a clinical study.
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References
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Roland W. Stein, M.D., Vanderbilt University
How did Creutzfeldt-Jakob disease (CJD) occur in people treated with pituitary human growth hormone (hGH)?
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Before scientists learned how to make synthetic hormones, many animal hormones, such as insulin, were used to treat human disorders. Growth hormone from animals did not work in humans. Human growth hormone (pituitary hGH) was therefore made from human pituitary glands by the National Hormone and Pituitary Program (NHPP), funded by the U.S. Department of Health and Human Services (HHS). From 1963 to 1985, the NHPP sent pituitary hGH to hundreds of doctors across the country. As a part of research studies, doctors used the hormone to treat nearly 7,700 children for failure to grow.
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In 1985, the HHS learned that three young men treated with pituitary hGH died of Creutzfeldt-Jakob disease (CJD), a rare and incurable brain disease. The HHS believed these illnesses were related to pituitary hGH. The HHS immediately stopped the distribution of the hormone and began a national study to learn more about how pituitary hGH treatment may have caused this problem. The HHS continues to monitor individuals who received pituitary hGH through the NHPP for CJD.
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How many people treated with NHPP-distributed hGH got CJD in the United States?
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The HHS has identified 36 cases of CJD among the nearly 7,700 people in the United States who received NHPP pituitary hGH. None of the 36 people who got CJD began treatment with pituitary hGH after 1977, the year that the NHPP began producing pituitary hGH in a laboratory (headed by Dr. Albert Parlow) using a new purification step. To date, data show that among the three countries that produced the most pituitary-derived hGH (France, United Kingdom, United States), the United States administered hGH to many more recipients but has had a much lower number of reported hGH-associated CJD cases. Scientists believe the new purification process substantially contributed to this lower overall risk of hGH-associated CJD. Today, the growth hormone used to treat patients is made biosynthetically and not from human pituitary glands. Biosynthetic growth hormone (bGH), also known as recombinant human growth hormone (rhGH), poses no threat of infection with CJD.
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Based on NHPP records, the HHS estimated 7,700 people were treated with pituitary hGH from the NHPP. Of these, the HHS got the names and addresses of 6,272 from their doctors and treatment centers so that their health could be monitored. Another 1,400 people are believed to have been treated with pituitary hGH; however, the HHS does not have their names and addresses. The HHS hoped to learn about CJD and other health problems in the unmonitored group of 1,400 and notified many doctors about the problem of CJD, asking them to report CJD among people treated with pituitary hGH. The HHS has learned that five of the 36 people with confirmed CJD were among the 1,400 people the HHS was not able to identify and study.
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Some U.S. laboratories that made pituitary hGH for the NHPP also made hGH for use in other countries. In addition to the 36 people treated in the U.S., the HHS learned that six people in New Zealand and two people in Brazil who received U.S.-made pituitary hGH may also have gotten CJD. Thus, a total of 44 people who were treated with pituitary hGH made in the United States may have gotten CJD.
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Before bGH was available, several pharmaceutical companies made pituitary hGH. Some children treated in the U.S. received hormone produced by these companies when NHPP hGH was not available to them. Some of the 36 people with confirmed CJD received hGH from both the NHPP and a pharmaceutical company. The HHS learned of an individual treated in the U.S. who developed CJD and received only commercial pituitary hGH. That person was not eligible for NHPP hGH and received pituitary hGH made by two pharmaceutical companies.
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How many people treated with pituitary hGH got CJD in other countries?
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People treated with pituitary hGH in other countries also got CJD. HHS doctors share information with doctors around the world about health issues such as CJD and read reports about CJD and other health problems related to pituitary hGH treatment.
**New Zealand has reported six people with CJD among 159 who received pituitary hGH. All six were among 49 people who received pituitary hGH made by the U.S. lab that supplied most NHPP pituitary hGH before 1977. We don\u2019t know why this rate \u2013 six out of 49 (12.2 percent)\u2014is so high in those in New Zealand who received American hormone. HHS scientists believe that this U.S.-made hormone did not undergo the same filtering process used in the United States when the hormone was put into vials. In addition, some hormone preparations sent to New Zealand were not distributed in the United States.
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New Zealand has little information on the hormone preparations used to treat the people who got CJD. Information provided to the HHS from medical authorities in New Zealand indicated the following dates of pituitary hGH treatment for the six New Zealand patients who developed CJD: 1964 to 1966, 1964 to 1970, 1965 to 1972, 1966 to 1972, 1967 to 1969, and 1970 to 1973. With no common period of treatment, it is unlikely that a single preparation exposed all six patients to CJD.
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There is some information on the hormone sent to New Zealand from the lab that also produced hormone for the NHPP before 1977. Some preparations and components of preparations were used in both countries and others were distributed only in the United States or in New Zealand.
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The time between the start of pituitary hGH treatment and the first sign of CJD symptoms was 14 to 51 years in the United States patients and 17 to 37 years in the New Zealand patients. The New Zealand patients who got CJD were treated with pituitary hGH for an average of 4.3 years. In the United States, average treatment time was 8.0 years in patients who got CJD.
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In France, 122 people with CJD were among the 1,700 treated with pituitary hGH. The pattern of exposure to CJD in France is very different from the pattern in the United States. In France, people who received pituitary hGH in 1984 and 1985 appear to be at highest risk for CJD. We have learned from animal studies that when scientists injected a greater amount of CJD infectious agent into an animal, it took less time for CJD to develop. Because of the larger number of people with CJD and shorter times between treatment and CJD onset in France, the level of infection in French hormone was probably higher than in the U.S. hormone. The purification procedure used in France differed from that begun in 1977 in the United States.
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The United Kingdom has reported 80 people with CJD among 1,849 who received pituitary hGH. Experts have also found CJD in two people in Holland, two people in Brazil, and one each in Austria, Qatar, and Ireland. France, the United Kingdom and Holland made their own hormone. The Brazilian patients got pituitary hGH from a U.S. lab that also made NHPP hormone before 1977. This was a different lab than the U.S. lab that made hormone for New Zealand. The Qatar patient received pituitary hGH made in France. The Austrian patient received pituitary hGH made by a pharmaceutical company. Four Australian women developed CJD after receiving other human pituitary hormones as fertility treatments.
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Are people treated with pituitary hGH at risk for other diseases or problems?
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Most people were treated with pituitary hGH because their pituitary glands did not make enough of their own GH. Some of these people also had problems making other pituitary hormones. One of these hormones tells the adrenal glands to make cortisol, a hormone needed for life. People lacking this hormone are at risk of death from adrenal crisis, but adrenal crisis can be prevented. More pituitary hGH recipients have died from adrenal crisis than from CJD. Pituitary hGH did not cause adrenal problems, but some people who received hGH have a pituitary problem that puts them at risk for adrenal crisis. Please read the health alert and discuss this information with your doctor.
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Besides CJD, no other serious or fatal health risks from pituitary hGH treatment have been found.
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\"Mad Cow\" Disease
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Starting in 1996, reports of a new form of CJD in young people who lived in the United Kingdom have raised concerns worldwide.
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Since at least 1985, some cattle in the United Kingdom have developed a disease called bovine spongiform encephalopathy (BSE), or \"mad cow\" disease. \"Mad cow\" disease is a sickness in cattle that is caused by an agent that is similar, but not identical, to the agents that cause the most common forms of CJD in people. Individuals who consume products made from cattle infected with the agent that causes \"mad cow\" disease can become infected with the agent themselves and develop the human form of \"mad cow\" disease, called variant CJD (vCJD). In humans, vCJD and the more common forms of CJD (those without the word \"variant\") are separate diseases. From the first report of vCJD in 1996 through November 2019, 232 cases of the infection have been confirmed worldwide, mostly in the United Kingdom. Researchers believe all but three of these 229 individuals got vCJD by eating beef from animals with \"mad cow\" disease. The exceptions were persons who are believed to have developed vCJD because they received infected blood or blood product from a donor who had acquired the agent by eating beef from animals with \"mad cow\" disease.
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In the United States, four cases of vCJD have been found. According to the Centers for Disease Control and Prevention (CDC), two people most likely acquired their infection in the United Kingdom, one person most likely acquired the infection in Saudi Arabia, and one person most likely acquired the infection in Kuwait or Russia. The specific oversees country where the latter person\u2019s infection occurred is less clear than that of the other three persons because, unlike the others, this person had no established link with a country where other known vCJD cases likely had been infected.
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People who received pituitary hGH are not at higher risk for vCJD.
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AIDS
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HIV, also known as the human immunodeficiency virus, causes AIDS. Pituitary hGH does not cause AIDS. HIV is destroyed by the methods used to make pituitary hGH. People who have been treated with pituitary hGH do not have a higher risk for AIDS.
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Low Levels of GH in Adults
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Some people who received pituitary hGH as children may have low levels of GH as adults and might therefore benefit from bGH as adults. People with low levels of growth hormone as adults may have symptoms or changes like these:
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more body fat
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less muscle
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less bone mass
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less strength
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less energy
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If you lacked GH as a child and have these problems as an adult, ask your doctor whether they might be due to low GH. Because these conditions are common in many people, they are not always due to low GH. Studies have shown that GH treatment in adults with low GH reduces fat and increases muscle mass. Effects on strength, energy, and bone fractures in GH-deficient adults receiving GH replacement are not as clear.
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Today, GH is completely synthetic. It is not made from human pituitaries. It poses no threat of contamination. The Human Growth Foundation (HGF) is one source of information about growth-related disorders. The Foundation can be reached at 1-800-451-6434.
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Cancer
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HHS studies of people treated with pituitary hGH supplied by the NHPP show no increased risk of cancer in those who did not have tumors before pituitary hGH treatment. Many people who received NHPP pituitary hGH had brain tumors that caused their lack of GH. People who have had one tumor have an increased risk for getting other tumors.
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In previous updates, we reported that in 1988, Japanese doctors reported an increased risk of leukemia in people treated with GH. Subsequent studies of individuals who were given pituitary hGH in the United States, Japan, and the United Kingdom found no higher rate of leukemia among those who did not have tumors and/or radiation before treatment with pituitary hGH.
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Emotional Problems
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No studies have shown that pituitary hGH causes changes in personality, emotional problems, or suicide.
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What are the symptoms of CJD?
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CJD does not cause the same symptoms in everyone. In most people who got CJD from pituitary hGH, the first signs they noticed were difficulty with walking and balance, dizziness, and/or clumsiness. Later, some began to slur words and have jerky movements. They also had trouble seeing, remembering, and/or thinking clearly.
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The disease becomes worse very quickly. When individuals have symptoms like these over a long period of time (such as a year) without getting much worse, they do not have CJD. Occasional forgetfulness, clumsiness, or headaches do not mean one has CJD. You should discuss concerns with your doctor if you are not sure.
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CJD is a rare disease. Most cases of CJD are not linked to pituitary hGH. When CJD is not linked to pituitary hGH, the first symptoms are usually mental changes such as confusion, problems thinking clearly, memory loss, behavior changes, and dementia. Though symptoms may differ, there are similar changes in the brain tissue of all patients with CJD.
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What is my risk for getting CJD from NHPP pituitary hGH?
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No one can say what an individual person\u2019s risk is. Of the approximately 7,700 people who received NHPP pituitary hGH, 36 people got CJD. The two things that seem to be connected with getting CJD after pituitary hGH treatment are
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1. How long a person was treated:
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In the United States, the average length of time for pituitary hGH treatment through the NHPP was about 3 years. For those individuals who developed CJD, the average length of treatment was about 8.0 years.
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Even though longer treatment time increased the risk for CJD in the United States, in other countries CJD has developed after shorter treatment periods.
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2. When a person was treated:
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All of the 36 individuals treated with NHPP hGH who got CJD in the United States started pituitary hGH before 1977. No CJD has been reported in Americans who began treatment with NHPP hormone after 1977, when production of NHPP hormone was moved to a laboratory (headed by Dr. Albert Parlow) that used a new method of purifying pituitary hGH. Research in animals showed the newer purification steps introduced in 1977 reduced the risk of CJD transmission. An analysis of NHPP hGH recipients was completed taking into account the differences in follow-up time and the duration of treatment of recipients starting treatment before or after 1977. That analysis found that the new purification steps greatly reduced and may have eliminated the risk for CJD infection.
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Two cases of CJD have been reported in individuals who received commercially prepared pituitary hGH. An Austrian person was treated with pituitary hGH (Crescormon, from Kabi Pharma) for 14 months and died from CJD 22 years later. An American who was too tall to be eligible for NHPP hormone was treated with pituitary hGH made by two pharmaceutical companies (Asellacrin, from Serono, and Crescormon, from Kabi Pharma). This individual was treated with commercial hGH for 23 months and died just over 26 years later. The methods used to produce these commercial hormone preparations were not identical to the method used in Dr. Parlow\u2019s laboratory but did include a version of the important new purification step that has been shown to reduce CJD infectivity.
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Overall, one out of about 214 people (36 out of about 7,700 people) who were treated with NHPP pituitary hGH got CJD.
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However, one in about 71 people who began treatment before 1977 got CJD.
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Who can tell me when I was treated and for how long?
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The best source for details on your treatment is the doctor or center that gave you pituitary hGH. To protect patient privacy, the HHS did not ask for the names of those treated with pituitary hGH until 1985, when the first CJD cases were reported. In 1985, the HHS asked doctors and treatment centers for the names and addresses of recipients to inform them of the risk of CJD. Specific treatment for most recipients was not included. If your doctor is not available, HHS staff can check its records for any information about your treatment. You can call 1-800-860-8747 or email healthinfo@niddk.nih.gov with your questions.
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We know which pituitary hGH preparations were sent to each treatment center and when they were sent. However, because individual doctors administered the pituitary hGH, we don\u2019t know which preparation each person might have gotten. We have tried to find this information in the medical records of patients who developed CJD, but many doctors did not note the specific preparation in their records. When records were incomplete, it was assumed that patients who got CJD might have been exposed to all preparations sent to their treatment center during the time they were treated. Since it is impossible to confidently identify high- risk or risk-free hormone, we do not think that details on the hormone preparations that individuals received will help to clarify individual level of risk.
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Did the hormone I took cause CJD?
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We have not found any particular preparation of pituitary hGH that is especially likely to carry CJD. We believe that CJD did not come from a single infected pituitary gland or preparation. Prior to 1977, in an effort to extract as much hormone as possible from the pituitary glands, the glands were often processed repeatedly. Hormone extracted from the same pituitaries was often included in many hormone preparations. Also, patients who got CJD were treated on average for 8.0 years and received many different hormone preparations. This makes it very difficult to identify any preparation associated with transmitting CJD.
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Doctors wanted to see if a specific preparation of pituitary hGH could transmit CJD. To try to find the pituitary hGH that could have caused CJD, HHS researchers did two things:
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1. They set up a test in animals, injecting samples of all available preparations of pituitary hGH directly into the brains of monkeys. CJD develops more rapidly if injected into the brain than under the skin, as hGH was used in people. The animals were watched for 10 years. The brains of all animals were examined for signs of CJD. If an animal got sick with CJD, it would help researchers to understand which vials of pituitary hGH were contaminated with the agent that causes CJD.
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2. They studied people treated with pituitary hGH to see who got CJD and which hormone preparation they might have received based on which preparations were sent to their doctor.
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Results:
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\n
The animal tests did not help find the pituitary hGH that might have caused CJD. One animal developed the disease 5\u00bd years after injection of pituitary hGH. Two other animals that received injections from different vials of the same pituitary hGH preparation did not develop CJD.
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None of the people who developed CJD are known to have received the hormone preparation that made the animal sick. At most, two patients (whose records are incomplete) may have received this pituitary hGH preparation. Because of this, we do not believe that the patients who received the hormone preparation that transmitted CJD to the animal have a greater risk of developing CJD than others treated with pituitary hGH. Because each preparation of pituitary hGH was used to fill multiple vials, it is not known if CJD contamination was spread evenly among all vials of pituitary hGH that came from a particular preparation. It\u2019s possible that one vial got more contamination and another got little or none from the same preparation of pituitary hGH. It is believed that multiple preparations of pituitary hGH probably had very low levels of the CJD infectious agent. With such low levels of contamination, some vials of a preparation might carry CJD while other vials would not. Further, most of the people who got CJD received pituitary hGH for long periods of time and received many different preparations.
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If I develop CJD, will my family get it? If I get pregnant, will my baby get it?
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Scientists do not believe that CJD is transmitted through casual day-to- day contact or through sexual contact.
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Therefore, spouses and children of individuals with CJD are not in danger. Except for rare genetic forms of CJD (which are unrelated to pituitary hGH), a pregnant woman does not pass CJD to her unborn baby. CJD from pituitary hGH does not affect the genes.
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Can a test tell if I will get CJD?
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Today, when a person has symptoms and findings on neurological examination that may be due to CJD, additional testing may be recommended to help in the diagnosis. Two commonly used tests are the electroencephalogram (EEG) and magnetic resonance imaging (MRI). While these brain tests are useful if they show characteristic features of CJD, such features may be absent, particularly early in the course of the disease. A third test that can help doctors diagnose CJD requires a sample of spinal fluid. To obtain the sample for testing, a doctor performs a lumbar puncture, or spinal tap. A lumbar puncture is considered an invasive test, as a needle is inserted into a person\u2019s spinal canal in the lower back.
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Scientists are working on tests to diagnose CJD that are more accurate, safer, and less invasive than the currently available tests. One such test is an easy-to-use nasal brush test that collects cells along the mucous membranes in a person\u2019s nasal cavity for analysis. Although more study is needed before this test can be used on people with neurologic problems, scientists believe the nasal brush test could make it possible to rapidly and accurately diagnose CJD.
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Can I donate blood or organs?
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People who received only recombinant hGH (that is, those who only received hGH after 1985) and family members of pituitary hGH recipients can donate blood, blood products, organs and tissue unless they are not eligible to donate for other reasons. Although the risk of transfusion transmission of the type of CJD that can occur in pituitary hGH recipients is believed to be very low, the possibility cannot be ruled out. Therefore, the FDA has recommended in an abundance of caution that people who report that they have received pituitary hGH should not donate blood or blood products. Organs and tissues may be donated, but the potential donor should disclose to the recipient organization, in advance, that they have received pituitary hGH and may be at increased risk for the development of CJD.
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Donation of Blood and Blood Products
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Even though pituitary hGH has been taken off the FDA blood donor prohibited medication list, as a precaution, the FDA continues to recommend that individuals who report receiving cadaveric pituitary hGH should not donate blood. The FDA has established recommendations on the donation of blood and blood components to reduce the possible transmission of CJD.
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Donation of Organs and Tissues
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Careful donor screening is required to prevent the spread of potentially transmissible diseases, including CJD, by donor organs and tissues. The FDA has established eligibility rules for the donation of human organs and tissues to reduce the spread of potentially transmissible diseases. Organs and tissues from pituitary hGH recipients may be considered for donation, but potential donors should disclose to the recipient organization, in advance, that they have received pituitary hGH and may be at increased risk for the development of CJD. Decisions about the donation and receipt of specific organs and tissues are made on a case-by-case basis, taking the shortages of organs and tissues and their possible life-saving benefits into account.
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Donation of Body for Research \n
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Pituitary hGH recipients who wish to donate their bodies to science should disclose to the recipient organization, in advance, that they have received pituitary hGH and may be at increased risk for the development of CJD.
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How is CJD diagnosed?
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CJD is usually diagnosed based on signs and symptoms of the illness, how severe they are, and how quickly they become worse. However, doctors must study brain tissue from a biopsy or autopsy in order to make a definite diagnosis of CJD.
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Other tests can strongly suggest CJD, the best of which was recently developed. The CSF-QuIC test is a test that helps doctors diagnose CJD in patients with symptoms. This test detects an abnormal protein in the spinal fluid. When this abnormal protein is detected in a patient, it is very likely that the person has CJD. It is much easier and safer to take a sample of spinal fluid than to do a brain biopsy. Unfortunately, this test has not yet been determined to identify CJD in patients who do not have symptoms. Researchers from many countries, including the United States, have reported success using MRI to diagnose CJD and vCJD in people with symptoms of the disease. MRI is a safe and painless tool that allows doctors to look at images of the brain and does not involve the collection of brain or spinal fluid samples.
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What does research tell us about CJD?
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Although CJD is a rare disorder, some of the world\u2019s leading researchers are working hard to learn more about this disease.
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About 10 percent of the people who get CJD have the inherited type. Some people have gotten CJD from medical procedures such as pituitary hGH injections, tissue grafts, or corneal transplants. Scientists don\u2019t fully understand what causes CJD. Evidence suggests that a unique infectious agent called a prion [PREE-on] may be the cause. A prion is an unusual infectious agent because it contains no genetic material.
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It is a protein that takes on different forms. In its normal, harmless form, the protein is curled into a spiral. In its infectious form, the protein folds into an abnormal shape. Somehow, these abnormal proteins change the shape of normal proteins. This change begins a serious chain reaction that results in brain problems.
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People with inherited CJD have an abnormal gene that leads to changes in their prion protein. This gene makes the protein likely to assume the abnormal shape. Exposure to the abnormal form of the protein can also occur through injection of contaminated pituitary hGH, tissue grafts, and corneal transplants and through exposures to infected brain tissue.
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If CJD results from a defect in protein folding, it may be possible to identify drugs that can help the prion protein assume its proper shape. Such drugs would slow or stop the progress of the disease. Treatments like these are being studied by researchers. Researchers in both Europe and the United States are also trying to develop a test that will identify CJD before symptoms appear.
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More information and medical journal articles about CJD and growth hormone therapy can be found on the National Institute of Diabetes and Digestive and Kidney Diseases Information Center web page Human Growth Hormone and Creutzfeldt-Jakob Disease Resource List.
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Why should people treated with pituitary hGH know about CJD?
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Some parents did not tell their children about receiving treatment with pituitary hGH and the possible risk of CJD.
\n
These children are now adults. Although the HHS no longer sends annual information about the problem of CJD in pituitary hGH recipients, the HHS does maintain a mailing list should any important new information become available. If parents are no longer available to receive HHS mailings, their adult children may not have access to important new information. Some pituitary hGH recipients have learned about the risk of CJD from newspaper stories. Others heard about it when they tried to give blood. Those who were not told by their parents are often angry when they hear about it outside the family. Any parent of an individual who received pituitary hGH who has not received any mailings from the HHS\u2014the last correspondence was sent in June 1999\u2014should contact the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) with the adult child\u2019s current address. Knowledgeable staff members are glad to answer any questions that parents or recipients may have.
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How can the U.S. Department of Health and Human Services (HHS) help me?
\n
If you have any questions, please call the phone numbers listed below. If you call the toll-free number, a recording will ask you to leave your name, phone number, and a good time to reach you. A staff member will call you back.
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You can also call, write, or have your doctor contact the National Institutes of Health (NIH) at
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National Institutes of Health NIDDK Office of Communications and Public Liaison Building 31 Room 9A06 31 Center Drive, MSC 2560 Bethesda, MD 20892-2560 Phone: 301-496-3583 Toll-free: 1-800-860-8747 Email: healthinfo@niddk.nih.gov
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This website is updated when we get new information, including new reports of CJD. We will mail updates in the future only when there is major new information. Some examples would be
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Development of a licensed diagnostic test for non-symptomatic CJD
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Development of preventive therapy or treatment for CJD
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How can I get support and information?
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The Creutzfeldt-Jakob Disease Foundation, Inc. (cjdfoundation.org) was created in 1993 by two families who lost relatives to CJD and the neurologist who treated their family members. This nonprofit corporation seeks to promote awareness of CJD through research and education and to reach out to people who have lost loved ones to this illness. For information on CJD from the NIH, see the National Institute of Neurological Disorders and Stroke (NINDS) Creutzfeldt-Jacob Disease Fact Sheet.
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The Human Growth Foundation (HGF) (www.hgfound.org) is a nonprofit organization concerned with children\u2019s growth disorders and adult GH deficiency. The HGF has information available online and through its toll-free number, 1-800-451-6434. The HGF also supports an Internet mailing list to help the exchange of information about adult GH deficiency and adult GH replacement therapy.
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How can I help with the follow-up study?
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Pituitary hGH recipients, their families, and their doctors can help by telling the HHS (NIDDK) of any deaths from any cause in someone who received pituitary hGH, especially if CJD is suspected or confirmed. Family members are asked to give HHS doctors permission to review medical records if a pituitary hGH recipient dies. Allowing the HHS to review these records adds to a growing knowledge base that may benefit thousands of people.
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Address changes for pituitary hGH recipients should be sent by recipients, their families, or their doctors to the NIDDK Office of Communications and Public Liaison at the NIH.
\n \n
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
Primary hyperparathyroidism is a disorder of the parathyroid glands, four pea-sized glands located on or near the thyroid gland in the neck. \u201cPrimary\u201d means this disorder begins in the parathyroid glands, rather than resulting from another health problem such as kidney failure. In primary hyperparathyroidism, one or more of the parathyroid glands is overactive. As a result, the gland makes too much parathyroid hormone (PTH).
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Too much PTH causes calcium levels in your blood to rise too high, which can lead to health problems such as bone thinning and kidney stones. Doctors usually catch primary hyperparathyroidism early through routine blood tests, before serious problems occur.
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View full-sized imageThe parathyroid glands are located on or near the thyroid gland in the neck.
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What do the parathyroid glands do?
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The parathyroid glands\u2019 only purpose is to make PTH, which helps maintain the right balance of calcium in your body. PTH raises blood calcium levels by
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causing bone, where most of your body\u2019s calcium is stored, to release calcium into the blood
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helping your intestines absorb calcium from food
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helping your kidneys hold on to calcium and return it to your blood instead of flushing it out in urine
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When the level of calcium in your blood falls too low, the parathyroid glands release just enough PTH to bring your blood calcium levels back to normal.
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You need calcium for good health. This mineral helps build bones and teeth and keep them strong. Calcium also helps your heart, muscles, and nerves work normally.
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Although their names are similar, the parathyroid glands and the thyroid gland are not related.
\n
How common is primary hyperparathyroidism?
\n
In the United States, about 100,000 people develop primary hyperparathyroidism each year.1 Primary hyperparathyroidism is one of the most common hormonal disorders.
\n
Who is more likely to develop primary hyperparathyroidism?
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Primary hyperparathyroidism most often affects people between age 50 and 60. Women are affected 3 to 4 times more often than men.1 The disorder was more common in African Americans, followed by Caucasians, in one large study performed in North America.1
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What are the complications of primary hyperparathyroidism?
\n
Primary hyperparathyroidism most often affects the bones and kidneys, although it also may play a part in other health problems.
\n
Weakened bones
\n
High PTH levels trigger the bones to release more calcium than normal into the blood. The loss of calcium from the bones may weaken them.
\n
Kidney stones
\n
The small intestine may absorb more calcium from food, adding to high levels of calcium in your blood. Extra calcium that isn\u2019t used by your bones and muscles goes to your kidneys and is flushed out in urine. Too much calcium in your urine can cause kidney stones.
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Other complications
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High blood calcium levels might play a part in other problems, such as heart disease, high blood pressure, and trouble concentrating. However, more research is needed to better understand how primary hyperparathyroidism affects the heart, blood vessels, and brain.
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What are the symptoms of primary hyperparathyroidism?
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Most people with primary hyperparathyroidism have no symptoms. When symptoms appear, they\u2019re often mild and similar to those of many other disorders. Symptoms include
In about 8 out of 10 people with primary hyperparathyroidism, a benign, or noncancerous, tumor called an adenoma has formed in one of the parathyroid glands.2 The tumor causes the gland to become overactive. In most other cases, extra PTH comes from two or more adenomas or from hyperplasia, a condition in which all four parathyroid glands are enlarged. People with rare inherited conditions that affect the parathyroid glands, such as multiple endocrine neoplasia type 1 or familial hypocalciuric hypercalcemia, are more likely to have more than one gland affected.
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Rarely, primary hyperparathyroidism is caused by cancer of a parathyroid gland.
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How do doctors diagnose primary hyperparathyroidism?
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Doctors diagnose primary hyperparathyroidism when a blood test shows high blood calcium and PTH levels. Sometimes PTH levels are in the upper portion of the normal range, when they should drop to low-normal or below normal in response to high calcium levels. Other conditions can cause high calcium, but elevated PTH is the only source in primary hyperparathyroidism.
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Routine blood tests can detect high blood calcium levels. High blood calcium may cause health care professionals to suspect hyperparathyroidism, even before symptoms appear.
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Sometimes PTH levels are high but calcium levels are not. Doctors don\u2019t routinely test for PTH but may do so if you have osteoporosis or another disorder that affects bone strength. In some cases, this may be the first phase of primary hyperparathyroidism, before calcium levels start to rise.
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Once doctors diagnose hyperparathyroidism, a 24-hour urine collection can help find the cause. This test measures certain chemicals, such as calcium and creatinine, a waste product that healthy kidneys remove. You will collect your urine over a 24-hour period and your health care professional will send it to a lab for analysis. Results of the test may help tell primary hyperparathyroidism from hyperparathyroidism caused by a kidney disorder. The test can also rule out familial hypocalciuric hypercalcemia, a rare genetic disorder, as a cause.
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What tests do doctors use to look for complications of primary hyperparathyroidism?
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Once doctors diagnose primary hyperparathyroidism, they may use other tests to look for bone weakness, kidney problems, and low levels of vitamin D.
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Bone mineral density test
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Dual energy x-ray absorptiometry, also called a DXA or DEXA scan, uses low-dose x-rays to measure bone density. During the test, you will lie on a padded table while a technician moves the scanner over your body. A bone expert or radiologist will read the scan.
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During a DXA scan, you will lie on a padded table while a technician moves the scanner over your body.
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Kidney imaging tests
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Doctors may use one of the following imaging tests to look for kidney stones.
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Ultrasound. Ultrasound uses a device called a transducer that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician does the procedure. A radiologist reads the images, which can show kidney stones.
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Abdominal x-ray. An abdominal x-ray is a picture of the abdomen that uses low levels of radiation and is recorded on film or on a computer. During an abdominal x-ray, you lie on a table or stand up. A technician positions the x-ray machine close to your abdomen and asks you to hold your breath so the picture won\u2019t be blurry. A radiologist reads the x-ray, which can show the location of kidney stones in the urinary tract. Not all stones are visible on an abdominal x-ray.
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Computed tomography (CT) scans. CT scans use a combination of x-rays and computer technology to create images of your urinary tract. CT scans sometimes use a contrast medium\u2014a dye or other substance that makes structures inside your body easier to see. Contrast medium isn\u2019t usually needed to see kidney stones. For the scan, you\u2019ll lie on a table that slides into a tunnel-shaped machine that takes the x-rays. A radiologist reads the images, which can show the size and location of a kidney stone.
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Vitamin D blood test
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Health care professionals test for vitamin D levels because low levels are common in people with primary hyperparathyroidism. In patients with primary hyperparathyroidism, the low vitamin D level can further stimulate the parathyroid glands to make even more parathyroid hormone. Also, a very low vitamin D level may cause a secondary form of hyperparathyroidism, which resolves when vitamin D levels are returned to normal.
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How do doctors treat primary hyperparathyroidism?
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Guidelines help doctors to decide whether or not parathyroid surgery should be recommended. You might be a candidate for surgery if you meet any of these guidelines
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Blood calcium > 1 mg/dL above normal
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Bone density by DXA < -2.5 at any site (lumbar spine, hip, or forearm)
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History of kidney stones or evidence of kidney stones or calcifications in the kidney by imaging (e.g., X-ray, ultrasound, CT scan). Evidence for stone risk by 24-hour urine with excessive calcium and other stone risk factors.
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A fracture resulting from relatively little force, such as a fall from a standing or sitting position (a fragility fracture)
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Age < 50
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Doctors most often recommend parathyroid surgery, particularly if the patient meets one or more of the guidelines noted above. It is also not inappropriate to recommend surgery in those who do not meet guidelines as long as there are no medical contraindications to surgery. In those who do not meet guidelines or do not choose surgery, the doctor will monitor the patient\u2019s condition. If there is evidence for progressive disease (e.g., higher calcium level, lower bone density, a fracture, kidney stone), surgery would be advised. For patients who are not going to have parathyroid surgery, even though guidelines are met, doctors can prescribe medicines to control the high blood calcium or improve the bone density.
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Surgery
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Surgery to remove the overactive parathyroid gland or glands is the only sure way to cure primary hyperparathyroidism. Doctors recommend surgery for people with clear symptoms or complications of the disease. In people without symptoms, doctors follow the above guidelines to identify who might benefit from parathyroid surgery.2 Surgery can lead to improved bone density and can lower the chance of forming kidney stones.
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When performed by experienced surgeons, surgery almost always cures primary hyperparathyroidism.
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Surgeons often use imaging tests before surgery to locate the overactive gland or glands to be removed. The tests used most often are sestamibi, ultrasound, and CT scans. In a sestamibi scan, you will get an injection, or shot, of a small amount of radioactive dye in your vein. The overactive parathyroid gland or glands then absorb the dye. The surgeon can see where the dye has been absorbed by using a special camera.
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Surgeons use two main types of operations to remove the overactive gland or glands.
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Minimally invasive parathyroidectomy. Also called focused parathyroidectomy, surgeons use this type of surgery when they think only one of the parathyroid glands is overactive. Guided by a tumor-imaging test, your surgeon will make a small incision, or cut, in your neck to remove the gland. The small incision means you will probably have less pain and a faster recovery than people who have more invasive surgery. You can go home the same day. Your doctor may use regional or general anesthesia during the surgery.
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Bilateral neck exploration. This type of surgery uses a larger incision that lets the surgeon find and look at all four parathyroid glands and remove the overactive ones. If you have bilateral neck exploration, you will probably have general anesthesia and may need to stay in the hospital overnight.
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When performed by experienced surgeons, surgery almost always cures primary hyperparathyroidism.
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Parathyroid surgery is safe. Rarely, problems can occur after surgery. In about 1 out of every 100 people, the nerves controlling the vocal cords are damaged during surgery, which most often results in hoarseness.3 This condition usually gets better on its own.
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Low calcium levels in the blood may occur after surgery but usually return to normal in a few days or weeks. On rare occasions, not enough parathyroid tissue is left to make PTH, which can result in hypoparathyroidism.
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Monitoring
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Some people who have mild primary hyperparathyroidism may not need surgery right away, or even any surgery, and can be safely monitored.
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You may want to talk with your doctor about long-term monitoring if you
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don\u2019t have symptoms
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have only slightly high blood calcium levels
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have normal kidneys and bone density
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Long-term monitoring should include regular doctor visits, a yearly blood test to measure calcium levels and check your kidney function, and a bone density test every 1 to 2 years.
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If you and your doctor choose long-term monitoring, you should
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drink plenty of water so you don\u2019t get dehydrated
Cinacalcet is a medicine that decreases the amount of PTH the parathyroid glands make and lowers calcium levels in the blood. Doctors may prescribe cinacalcet to treat very high calcium levels in people with primary hyperparathyroidism who can\u2019t have surgery.
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Cinacalcet does not improve bone density. If you have bone loss, your doctor may prescribe alendronate or other medications to help increase bone density.
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Should I change my diet if I have primary hyperparathyroidism?
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You don\u2019t need to change your diet or limit the amount of calcium you get from food and beverages. You will need to take a vitamin D supplement if your vitamin D levels are low. Talk with your health care professional about how much vitamin D you should take.
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If you lose all your healthy parathyroid tissue and develop lasting low-calcium levels, you\u2019ll need to take both calcium and vitamin D for life.
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References
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: John P. Bilezikian, M.D., Columbia University
A prolactinoma is a benign (noncancerous) tumor of the pituitary gland that produces a hormone called prolactin. Located at the base of the brain, the pituitary is a pea-sized gland that controls the production of many hormones.
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Prolactin signals a woman\u2019s breasts to produce milk during pregnancy and breastfeeding. Having too much prolactin in the blood, a condition called hyperprolactinemia, can cause infertility and other problems. In most cases, prolactinomas and related health problems can be successfully treated with medicines.
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\n The pituitary gland sits at the base of the brain. \n
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How common are prolactinomas?
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Small, benign pituitary tumors are fairly common in the general population. A prolactinoma is the most common type of pituitary tumor, making up about 40 percent of all pituitary tumors.1
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Who is more likely to develop a prolactinoma?
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Women are more likely than men to develop a prolactinoma. These tumors rarely occur in children and adolescents. In children, prolactinomas may prevent the start or block the progression of puberty.
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\n Prolactinomas occur more often in women than men. \n
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What are the complications of having a prolactinoma?
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Having a prolactinoma can lead to different symptoms and problems among women and men. Some of these are caused by having too much prolactin in the body, while others are linked to the size and location of the tumor.
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Excess prolactin, or hyperprolactinemia, can lower levels of sex hormones in both women and men. Related complications can include
Prolactinomas are usually small, less than 1 centimeter in diameter. These small tumors are called \u201cmicroprolactinomas.\u201d Less commonly, a tumor may grow to more than 1 centimeter in diameter. These larger tumors are called \u201cmacroprolactinomas.\u201d Macroprolactinomas may press against nearby parts of the pituitary gland and the brain. Complications can include
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vision problems, caused when the tumor presses on the optic nerves or optic chiasm, the part of the brain where the two optic nerves cross over each other
Women often report symptoms earlier than men because they may notice changes in their periods or milky discharge from their breasts when they are not pregnant or breastfeeding. But women who are taking sex hormones\u2014in birth control pills or hormone replacement therapy\u2014may not experience these changes.2 The same is true for women who have reached menopause and no longer have periods. Among these women, and among men, a lack of clear signs and symptoms may lead to a delayed diagnosis.
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What causes prolactinomas?
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Most pituitary tumors develop on their own. The cause of these tumors is unknown. In some cases, genetic factors may play a role. For example, the inherited disorder multiple endocrine neoplasia type 1 increases the risk for prolactinomas.
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What else can cause prolactin levels to rise?
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Prolactin levels normally rise during pregnancy and breastfeeding. They may also rise slightly at other times because of1
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physical stress, such as a painful blood draw
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exercise
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a meal
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sexual intercourse
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nipple stimulation
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injury to the chest area
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epileptic seizures
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These increases in prolactin are usually small and temporary. Other than a prolactinoma, the factors that most often lead to excess prolactin in the blood are medicines, illnesses, and other pituitary tumors.
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Medicines. The brain chemical dopamine helps curb the production of prolactin in the body. Any medicine that affects the production or use of dopamine can make prolactin levels rise.
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Medicines that can increase prolactin levels include some types of
Although the hormone estrogen stimulates the release of prolactin, estrogen-containing birth control pills and hormone replacement therapy have not been found to cause hyperprolactinemia.4
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If high prolactin levels are because of a medicine, these levels will usually return to normal 3 to 4 days after the drug is stopped.
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Other illnesses. Illnesses that may increase prolactin levels include
shingles\u2014particularly when lesions affect your chest
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Other pituitary tumors. Other large tumors located in or near the pituitary gland may also raise prolactin levels, usually by preventing dopamine from reaching the pituitary gland.
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Sometimes the cause of excess prolactin is unknown.
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How do doctors diagnose prolactinomas?
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Doctors diagnose prolactinomas based on the results of two tests
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Blood test. The prolactin blood test will measure the level of prolactin in your blood. If the level is too high, your doctor will order an imaging test to detect a possible tumor.
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Imaging tests. The preferred test is the magnetic resonance imaging (MRI) scan, which uses radio waves and magnets to create detailed images of your internal organs and soft tissues without x-rays. If an MRI is not a good option for you (for example, if you have a pacemaker or other implant that has metal), your doctor may order a computed tomography (CT) scan instead. The results of the imaging test usually will allow your doctor to confirm a diagnosis of prolactinoma and determine its size and location.
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\n A blood test is used to detect high levels of prolactin. \n
After confirming the prolactinoma diagnosis, your doctor may conduct other tests to find out if the tumor is affecting other hormones. Depending on the tumor\u2019s size, your doctor may also ask you to take a vision test.
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How do doctors treat prolactinomas?
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Doctors commonly treat prolactinomas with medicines. More rarely, surgery or radiation therapy may be used. The goals of treatment are to
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bring prolactin levels back to normal
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shrink the tumor
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make sure the pituitary gland is working properly
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correct any problems caused by the tumor, such as menstrual problems, milky discharge from the breasts, low testosterone levels, headaches, or vision problems
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Medicines
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Medicines called dopamine agonists control prolactin levels and shrink the tumor very effectively. These drugs mimic the effects of the brain chemical dopamine.
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Two dopamine agonists are most commonly used to treat prolactinomas
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bromocriptine, a drug that must be taken twice or three times daily
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cabergoline, a drug that can be taken once or twice per week
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Cabergoline is the preferred drug for treating prolactinomas, because it is more effective than bromocriptine and has fewer side effects.1
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Outcomes. For most small prolactinomas, dopamine agonists bring prolactin levels back to normal and shrink tumors in 4 out of 5 patients.5
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Side effects. Common side effects of the drugs include nausea, vomiting, and dizziness. Both medicines should always be taken with food. Starting treatment at a low dose and taking the medicine at bedtime can reduce side effects.
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Complications. Although dopamine agonists have been linked to heart valve damage, these problems were found mainly among people taking these medicines to treat Parkinson\u2019s disease. These patients typically take much higher doses (usually about 10 times higher) of these medicines than are used to treat prolactinomas. If you need to take a high dose of a dopamine agonist, your doctor may order an echocardiogram (echo) to check your heart valves and heart function. Rarely, psychiatric disorders related to impulse control, such as compulsive gambling, have been seen in people taking these medicines.6
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Duration of treatment. You may have to take these medicines for a long time to prevent the tumor from growing back, especially if the prolactinoma is large. After 2 years, the medicines may be slowly reduced and stopped if prolactin levels are normal and the tumor is no longer visible.1 But if your prolactin level goes back up again, you may need to go back on the medicine for as long as needed to bring your prolactin level under control.
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Surgery
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Although doctors most often treat prolactinomas with medicines, in some cases surgery may be an option. Examples include
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you can\u2019t tolerate the medicines
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the medicines aren\u2019t working for you
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you take antipsychotic medicines that interact with the medicines used to treat prolactinomas
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In some cases, when a prolactinoma is large, a woman may choose to have surgery to remove the tumor before trying to become pregnant.
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Two types of surgery may be used
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Transsphenoidal surgery is most commonly used to treat prolactinoma. The surgery is done through an incision, or cut, at the back of the nasal cavity or under the upper lip.
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Transcranial surgery is used more rarely if the tumor is large or has spread to other areas. The surgeon removes the tumor through an opening in the skull.
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Outcomes. The success of the surgery depends on many factors, including
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skill and experience of the surgeon
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size and location of the tumor
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When done by an experienced surgeon, the surgery corrects prolactin levels in about 90 percent of people with small tumors and 50 percent of those with large tumors.7 For people with larger prolactinomas that can only be partly removed, medicines often can return prolactin levels to a normal range after surgery.
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Side effects and complications. Side effects of the surgery can include
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low pituitary function, or hypopituitarism
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temporary diabetes insipidus, a condition that leads to frequent urination and excessive thirst
More rarely, if medicines and surgery fail to reduce prolactin levels, radiation therapy may be used. This type of treatment uses high-energy x-rays or particle waves to kill tumor cells. Depending on the size and location of the tumor, the total radiation dose is delivered in one session, or in lower doses over the course of 4 to 6 weeks.
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Outcomes. Prolactin levels return to normal in 1 out of 3 patients treated with radiation therapy.1 However, as radiation treatment lowers prolactin levels over time, it may take years to reach this outcome. Your doctor is likely to prescribe medicines while you wait to see results.
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Side effects and complications. The most common side effect is low levels of thyroid hormone. In up to half of patients, radiation therapy may also lead to a decrease in other pituitary hormones.8 Vision loss and brain injury are rare complications. Rarely, other types of tumors can develop many years later in areas that were in the path of the radiation beam.
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How do doctors treat prolactinomas during pregnancy?
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Before pregnancy. Having a prolactinoma may make it difficult for you to become pregnant, but treatment with dopamine agonists is very effective in restoring fertility.
\n Use of dopamine agonists is usually stopped once a pregnancy is confirmed. \n
When pregnancy is confirmed. Although studies suggest that both bromocriptine and cabergoline can be safely taken in the early stages of pregnancy, bromocriptine is typically preferred because of its longer safety record.1 As soon as your pregnancy is confirmed, your doctor will usually advise you to stop taking these medicines to prevent any possible effects on the fetus.
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During pregnancy. Prolactin levels normally increase during pregnancy, preparing your breasts to make milk after your baby is born. The pituitary gland often doubles in size during pregnancy. Your prolactinoma may also grow in size, especially if it is already large. If you begin to have symptoms such as headaches and changes in vision, your doctor may recommend that you start taking the medicine again.
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After delivery. After delivery, women with small prolactinomas can usually nurse their babies. If your prolactinoma is large, your doctor may suggest that you consult with an endocrinologist about breastfeeding.
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Doctors don\u2019t usually measure prolactin levels during pregnancy and breastfeeding. Your doctor will usually begin to do so again a couple of months after you stop nursing. In some cases, prolactin levels remain normal after delivery and nursing.9
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Clinical Trials for Prolactinoma
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The NIDDK conducts and supports clinical trials in many diseases and conditions, including endocrine diseases. The trials look to find new ways to prevent, detect, or treat disease and improve quality of life.
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What are clinical trials for prolactinoma?
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Clinical trials\u2014and other types of clinical studies\u2014are part of medical research and involve people like you. When you volunteer to take part in a clinical study, you help doctors and researchers learn more about disease and improve health care for people in the future.
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Researchers are studying many aspects of prolactinoma, including new treatments for this condition.
What clinical studies for prolactinoma are looking for participants?
\n
You can view a filtered list of clinical studies on prolactinoma that are open and recruiting at www.ClinicalTrials.gov. You can expand or narrow the list to include clinical studies from industry, universities, and individuals; however, the National Institutes of Health does not review these studies and cannot ensure they are safe. Always talk with your health care professional before you participate in a clinical study.
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References
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Andrew R. Hoffman, M.D., VA Palo Alto Health Care System and Stanford University School of Medicine
Thyroid disease is a group of disorders that affects the thyroid gland. The thyroid is a small, butterfly-shaped gland in the front of your neck that makes thyroid hormones. Thyroid hormones control how your body uses energy, so they affect the way nearly every organ in your body works\u2014even the way your heart beats.
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Sometimes the thyroid makes too much or too little of these hormones. Too much thyroid hormone is called hyperthyroidism and can cause many of your body\u2019s functions to speed up. \u201cHyper\u201d means the thyroid is overactive. Learn more about hyperthyroidism in pregnancy. Too little thyroid hormone is called hypothyroidism and can cause many of your body\u2019s functions to slow down. \u201cHypo\u201d means the thyroid is underactive. Learn more about hypothyroidism in pregnancy.
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If you have thyroid problems, you can still have a healthy pregnancy and protect your baby\u2019s health by having regular thyroid function tests and taking any medicines that your doctor prescribes.
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What role do thyroid hormones play in pregnancy?
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Thyroid hormones are crucial for normal development of your baby\u2019s brain and nervous system. During the first trimester\u2014the first 3 months of pregnancy\u2014your baby depends on your supply of thyroid hormone, which comes through the placenta. At around 12 weeks, your baby\u2019s thyroid starts to work on its own, but it doesn\u2019t make enough thyroid hormone until 18 to 20 weeks of pregnancy.
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Two pregnancy-related hormones\u2014human chorionic gonadotropin (hCG) and estrogen\u2014cause higher measured thyroid hormone levels in your blood. The thyroid enlarges slightly in healthy women during pregnancy, but usually not enough for a health care professional to feel during a physical exam.
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Thyroid problems can be hard to diagnose in pregnancy due to higher levels of thyroid hormones and other symptoms that occur in both pregnancy and thyroid disorders. Some symptoms of hyperthyroidism or hypothyroidism are easier to spot and may prompt your doctor to test you for these thyroid diseases.
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Another type of thyroid disease, postpartum thyroiditis, can occur after your baby is born.
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Hyperthyroidism in Pregnancy
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What are the symptoms of hyperthyroidism in pregnancy?
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Some signs and symptoms of hyperthyroidism often occur in normal pregnancies, including faster heart rate, trouble dealing with heat, and tiredness.
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Other signs and symptoms can suggest hyperthyroidism:
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fast and irregular heartbeat
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shaky hands
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unexplained weight loss or failure to have normal pregnancy weight gain
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What causes hyperthyroidism in pregnancy?
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Hyperthyroidism in pregnancy is usually caused by Graves\u2019 disease and occurs in 1 to 4 of every 1,000 pregnancies in the United States.1 Graves\u2019 disease is an autoimmune disorder. With this disease, your immune system makes antibodies that cause the thyroid to make too much thyroid hormone. This antibody is called thyroid stimulating immunoglobulin, or TSI.
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Graves\u2019 disease may first appear during pregnancy. However, if you already have Graves\u2019 disease, your symptoms could improve in your second and third trimesters. Some parts of your immune system are less active later in pregnancy so your immune system makes less TSI. This may be why symptoms improve. Graves\u2019 disease often gets worse again in the first few months after your baby is born, when TSI levels go up again. If you have Graves\u2019 disease, your doctor will most likely test your thyroid function monthly throughout your pregnancy and may need to treat your hyperthyroidism.1 Thyroid hormone levels that are too high can harm your health and your baby\u2019s.
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Rarely, hyperthyroidism in pregnancy is linked to hyperemesis gravidarum\u2014severe nausea and vomiting that can lead to weight loss and dehydration. Experts believe this severe nausea and vomiting is caused by high levels of hCG early in pregnancy. High hCG levels can cause the thyroid to make too much thyroid hormone. This type of hyperthyroidism usually goes away during the second half of pregnancy.
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Less often, one or more nodules, or lumps in your thyroid, make too much thyroid hormone.
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How can hyperthyroidism affect me and my baby?
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Untreated hyperthyroidism during pregnancy can lead to
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miscarriage
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premature birth
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low birthweight
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preeclampsia\u2014a dangerous rise in blood pressure in late pregnancy
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thyroid storm\u2014a sudden, severe worsening of symptoms
Rarely, Graves\u2019 disease may also affect a baby\u2019s thyroid, causing it to make too much thyroid hormone. Even if your hyperthyroidism was cured by radioactive iodine treatment to destroy thyroid cells or surgery to remove your thyroid, your body still makes the TSI antibody. When levels of this antibody are high, TSI may travel to your baby\u2019s bloodstream. Just as TSI caused your own thyroid to make too much thyroid hormone, it can also cause your baby\u2019s thyroid to make too much.
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Tell your doctor if you\u2019ve had surgery or radioactive iodine treatment for Graves\u2019 disease so he or she can check your TSI levels. If they are very high, your doctor will monitor your baby for thyroid-related problems later in your pregnancy.
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An overactive thyroid in a newborn can lead to
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a fast heart rate, which can lead to heart failure
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early closing of the soft spot in the baby\u2019s skull
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poor weight gain
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irritability
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Sometimes an enlarged thyroid can press against your baby\u2019s windpipe and make it hard for your baby to breathe. If you have Graves\u2019 disease, your health care team should closely monitor you and your newborn.
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How do doctors diagnose hyperthyroidism in pregnancy?
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Your doctor will review your symptoms and do some blood tests to measure your thyroid hormone levels. Your doctor may also look for antibodies in your blood to see if Graves\u2019 disease is causing your hyperthyroidism. Learn more about thyroid tests and what the results mean.
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How do doctors treat hyperthyroidism during pregnancy?
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If you have mild hyperthyroidism during pregnancy, you probably won\u2019t need treatment. If your hyperthyroidism is linked to hyperemesis gravidarum, you only need treatment for vomiting and dehydration.
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If your hyperthyroidism is more severe, your doctor may prescribe antithyroid medicines, which cause your thyroid to make less thyroid hormone. This treatment prevents too much of your thyroid hormone from getting into your baby\u2019s bloodstream. You may want to see a specialist, such as an endocrinologist or expert in maternal-fetal medicine, who can carefully monitor your baby to make sure you\u2019re getting the right dose.
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Doctors most often treat pregnant women with the antithyroid medicine propylthiouracil (PTU) during the first 3 months of pregnancy. Another type of antithyroid medicine, methimazole, is easier to take and has fewer side effects, but is slightly more likely to cause serious birth defects than PTU. Birth defects with either type of medicine are rare. Sometimes doctors switch to methimazole after the first trimester of pregnancy. Some women no longer need antithyroid medicine in the third trimester.
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Small amounts of antithyroid medicine move into the baby\u2019s bloodstream and lower the amount of thyroid hormone the baby makes. If you take antithyroid medicine, your doctor will prescribe the lowest possible dose to avoid hypothyroidism in your baby but enough to treat the high thyroid hormone levels that can also affect your baby.
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Antithyroid medicines can cause side effects in some people, including
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allergic reactions such as rashes and itching
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rarely, a decrease in the number of white blood cells in the body, which can make it harder for your body to fight infection
If you don\u2019t hear back from your doctor the same day, you should go to the nearest emergency room.
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You should also contact your doctor if any of these symptoms develop for the first time while you\u2019re taking antithyroid medicines:
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increased tiredness or weakness
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loss of appetite
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skin rash or itching
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easy bruising
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If you are allergic to or have severe side effects from antithyroid medicines, your doctor may consider surgery to remove part or most of your thyroid gland. The best time for thyroid surgery during pregnancy is in the second trimester.
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Radioactive iodine treatment is not an option for pregnant women because it can damage the baby\u2019s thyroid gland.
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Hypothyroidism in Pregnancy
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What are the symptoms of hypothyroidism in pregnancy?
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Symptoms of an underactive thyroid are often the same for pregnant women as for other people with hypothyroidism. Symptoms include
Most cases of hypothyroidism in pregnancy are mild and may not have symptoms.
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What causes hypothyroidism in pregnancy?
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Hypothyroidism in pregnancy is usually caused by Hashimoto\u2019s disease and occurs in 2 to 3 out of every 100 pregnancies.1 Hashimoto\u2019s disease is an autoimmune disorder. In Hashimoto\u2019s disease, the immune system makes antibodies that attack the thyroid, causing inflammation and damage that make it less able to make thyroid hormones.
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How can hypothyroidism affect me and my baby?
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Untreated hypothyroidism during pregnancy can lead to
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preeclampsia\u2014a dangerous rise in blood pressure in late pregnancy
These problems occur most often with severe hypothyroidism.
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Because thyroid hormones are so important to your baby\u2019s brain and nervous system development, untreated hypothyroidism\u2014especially during the first trimester\u2014can cause low IQ and problems with normal development.
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How do doctors diagnose hypothyroidism in pregnancy?
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Your doctor will review your symptoms and do some blood tests to measure your thyroid hormone levels. Your doctor may also look for certain antibodies in your blood to see if Hashimoto\u2019s disease is causing your hypothyroidism. Learn more about thyroid tests and what the results mean.
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How do doctors treat hypothyroidism during pregnancy?
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Treatment for hypothyroidism involves replacing the hormone that your own thyroid can no longer make. Your doctor will most likely prescribe levothyroxine, a thyroid hormone medicine that is the same as T4, one of the hormones the thyroid normally makes. Levothyroxine is safe for your baby and especially important until your baby can make his or her own thyroid hormone.
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Your thyroid makes a second type of hormone, T3. Early in pregnancy, T3 can\u2019t enter your baby\u2019s brain like T4 can. Instead, any T3 that your baby\u2019s brain needs is made from T4. T3 is included in a lot of thyroid medicines made with animal thyroid, such as Armour Thyroid, but is not useful for your baby\u2019s brain development. These medicines contain too much T3 and not enough T4, and should not be used during pregnancy. Experts recommend only using levothyroxine (T4) while you\u2019re pregnant.
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Some women with subclinical hypothyroidism\u2014a mild form of the disease with no clear symptoms\u2014may not need treatment.
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If you had hypothyroidism before you became pregnant and are taking levothyroxine, you will probably need to increase your dose. Most thyroid specialists recommend taking two extra doses of thyroid medicine per week, starting right away. Contact your doctor as soon as you know you\u2019re pregnant.
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Your doctor will most likely test your thyroid hormone levels every 4 to 6 weeks for the first half of your pregnancy, and at least once after 30 weeks.1 You may need to adjust your dose a few times.
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Postpartum Thyroiditis
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What is postpartum thyroiditis?
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Postpartum thyroiditis is an inflammation of the thyroid that affects about 1 in 20 women during the first year after giving birth1 and is more common in women with type 1 diabetes. The inflammation causes stored thyroid hormone to leak out of your thyroid gland. At first, the leakage raises the hormone levels in your blood, leading to hyperthyroidism. The hyperthyroidism may last up to 3 months. After that, some damage to your thyroid may cause it to become underactive. Your hypothyroidism may last up to a year after your baby is born. However, in some women, hypothyroidism doesn\u2019t go away.
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Not all women who have postpartum thyroiditis go through both phases. Some only go through the hyperthyroid phase, and some only the hypothyroid phase.
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What are the symptoms of postpartum thyroiditis?
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The hyperthyroid phase often has no symptoms\u2014or only mild ones. Symptoms may include irritability, trouble dealing with heat, tiredness, trouble sleeping, and fast heartbeat.
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Symptoms of the hypothyroid phase may be mistaken for the \u201cbaby blues\u201d\u2014the tiredness and moodiness that sometimes occur after the baby is born. Symptoms of hypothyroidism may also include trouble dealing with cold; dry skin; trouble concentrating; and tingling in your hands, arms, feet, or legs. If these symptoms occur in the first few months after your baby is born or you develop postpartum depression, talk with your doctor as soon as possible.
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What causes postpartum thyroiditis?
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Postpartum thyroiditis is an autoimmune condition similar to Hashimoto\u2019s disease. If you have postpartum thyroiditis, you may have already had a mild form of autoimmune thyroiditis that flares up after you give birth.
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How do doctors diagnose postpartum thyroiditis?
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If you have symptoms of postpartum thyroiditis, your doctor will order blood tests to check your thyroid hormone levels.
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How do doctors treat postpartum thyroiditis?
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The hyperthyroid stage of postpartum thyroiditis rarely needs treatment. If your symptoms are bothering you, your doctor may prescribe a beta-blocker, a medicine that slows your heart rate. Antithyroid medicines are not useful in postpartum thyroiditis, but if you have Grave\u2019s disease, it may worsen after your baby is born and you may need antithyroid medicines.
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You\u2019re more likely to have symptoms during the hypothyroid stage. Your doctor may prescribe thyroid hormone medicine to help with your symptoms. If your hypothyroidism doesn\u2019t go away, you will need to take thyroid hormone medicine for the rest of your life.
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Is it safe to breastfeed while I\u2019m taking beta-blockers, thyroid hormone, or antithyroid medicines?
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Certain beta-blockers are safe to use while you\u2019re breastfeeding because only a small amount shows up in breast milk. The lowest possible dose to relieve your symptoms is best. Only a small amount of thyroid hormone medicine reaches your baby through breast milk, so it\u2019s safe to take while you\u2019re breastfeeding. However, in the case of antithyroid drugs, your doctor will most likely limit your dose to no more than 20 milligrams (mg) of methimazole or, less commonly, 400 mg of PTU.
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Thyroid Disease and Eating During Pregnancy
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What should I eat during pregnancy to help keep my thyroid and my baby\u2019s thyroid working well?
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Because the thyroid uses iodine to make thyroid hormone, iodine is an important mineral for you while you\u2019re pregnant. During pregnancy, your baby gets iodine from your diet. You\u2019ll need more iodine when you\u2019re pregnant\u2014about 250 micrograms a day.1 Good sources of iodine are dairy foods, seafood, eggs, meat, poultry, and iodized salt\u2014salt with added iodine. Experts recommend taking a prenatal vitamin with 150 micrograms of iodine to make sure you\u2019re getting enough, especially if you don\u2019t use iodized salt.1 You also need more iodine while you\u2019re breastfeeding since your baby gets iodine from breast milk. However, too much iodine from supplements such as seaweed can cause thyroid problems. Talk with your doctor about an eating plan that\u2019s right for you and what supplements you should take. Learn more about a healthy diet and nutrition during pregnancy.
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Clinical Trials
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The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other components of the National Institutes of Health (NIH) conduct and support research into many diseases and conditions.
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What are clinical trials, and are they right for you?
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Clinical trials are part of clinical research and at the heart of all medical advances. Clinical trials look at new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. Find out if clinical trials are right for you.
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What clinical trials are open?
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Clinical trials that are currently open and are recruiting can be viewed at www.ClinicalTrials.gov.
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References
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This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. NIDDK translates and disseminates research findings to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by NIDDK is carefully reviewed by NIDDK scientists and other experts.
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The NIDDK would like to thank: Linda Barbour, M.D., M.S.P.H., FACP, University of Colorado School of Medicine
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