hypothyroidism

Definition

Hypothyroidism, or underactive thyroid, develops when the thyroid gland fails to produce or secrete as much thyroxine (T₄) as the body needs. Because T₄ regulates such essential functions as heart rate, digestion, physical growth, and mental development, an insufficient supply of this hormone can slow life-sustaining processes, damage organs and tissues in every part of the body, and lead to life-threatening complications.

Description

Hypothyroidism is one of the most common chronic diseases in the United States. Symptoms may not appear until years after the thyroid has stopped functioning and they are often mistaken for signs of other illnesses, menopause, or aging. Although this condition is believed to affect as many as 11 million adults and children, as many as two of every three people with hypothyroidism may not know they have the disease.

Nicknamed "Gland Central" because it influences almost every organ, tissue, and cell in the body, the thyroid is shaped like a butterfly and located just below the Adam's apple. The thyroid stores iodine the body gets from food and uses this mineral to create T₄. Low T₄ levels can alter weight, appetite, sleep patterns, body temperature, sex drive, and a variety of other physical, mental, and emotional characteristics.

There are three types of hypothyroidism. The most common is primary hypothyroidism, in which the thyroid doesn't produce an adequate amount of T₄. Secondary hypothyroidism develops when the pituitary gland does not release enough of the thyroid-stimulating hormone (TSH) that prompts the thyroid to manufacture T₄. Tertiary hypothyroidism results from a malfunction of the hypothalamus, the part of the brain that controls the endocrine system. Drug-induced hypothyroidism, an adverse reaction to medication, occurs in two of every 10,000 people, but rarely causes severe hypothyroidism.

Hypothyroidism is at least twice as common in women as it is in men. Although hypothyroidism is most common in women who are middle-aged or older, the disease can occur at any age. Newborn infants are tested for congenital thyroid deficiency (cretinism) using a test that measures the levels of thyroxine in the infant's blood. Treatment within the first few months of life can prevent mental retardation and physical abnormalities. Older children who develop hypothyroidism suddenly stop growing.

Factors that increase a person's risk of developing hypothyroidism include age, weight, and medical history. Women are more likely to develop the disease after age 50; men, after age 60. Obesity also increases risk. A family history of thyroid problems or a personal history of high cholesterol levels or such autoimmune diseases as lupus, rheumatoid arthritis, or diabetes can make an individual more susceptible to hypothyroidism.

— Maureen Haggerty

1. Insufficient production of thyroid hormones.
2. A pathological condition resulting from severe thyroid insufficiency, which may lead to cretinism or myxedema.

Hypothyroidism is due to underactivity of the thyroid gland, and results from its failure to secrete sufficient thyroid hormones into the bloodstream.

For normal function, the thyroid gland relies upon stimulation by a hormone from the pituitary gland known appropriately as thyroid stimulating hormone (TSH). Primary hypothyroidism is due to failure of the thyroid itself, whilst secondary hypothyroidism occurs when the pituitary secretes inadequate TSH. Primary hypothyroidism is the usual reason for thyroid underactivity.

There are several potential causes of primary hypothyroidism. It may for example be due to insufficient intake of iodine in the diet, since iodine is an essential constituent of thyroid hormones. This is a major health problem in many regions of the underdeveloped world and ranks first as a global cause of thyroid deficiency. In contrast, congenital hypothyroidism is due to a rare failure of the thyroid gland to develop during fetal life. Another infrequent cause of hypothyroidism is a failure in the complex biosynthetic pathway which leads to the secretion of its hormones by the thyroid gland (thyroid dyshormonogenesis). But if there is sufficient dietary iodine, the most common cause of hypothyroidism is autoimmune destruction of the cells which make up the basic functional unit of the thyroid gland — namely, the thyroid follicle. The thyroid gland is particularly prone to autoimmune disorders. Thus in Hashimoto's thyroiditis, which in the UK afflicts about 1 in 10 women, but only 1 in 100 men, there is progressive hypothyroidism with declining secretion of thyroid hormones. The thyroid is gradually infiltrated by lymphocytes and the follicular architecture of the gland breaks down. At the same time, the overall mass of the gland can increase, and if untreated a large multinodular goitre sometimes develops. Hashimoto's thyroiditis is named after the Japanese surgeon who gave the first clear description of the condition in 1912. In 1956 it was demonstrated by Doniach, Roitt, and Campbell in London that Hashimoto's thyroiditis is further characterized by the presence in the circulating blood of thyroid autoantibodies (anti-thyroglobulin and anti-thyroid peroxidase).

Most of the symptoms of hypothyroidism in adults are the result of lowered cellular metabolism, due to the inadequate output of thyroid hormones. Typically, the patient feels cold, lethargic, and depressed. There is often weight gain, a puffy appearance (myxoedema), dry hair, and maybe a goitre. The pulse tends to be slow, cardiac output is reduced, and in women (the majority of sufferers) there may be menstrual irregularities. In children, since thyroid hormones are required for growth, there is stunted growth along with lethargy and obesity. One of the particular problems of this condition is that because hypothyroidism develops slowly these symptoms are insidious; they can go unnoticed or be wrongly attributed, for example, to the menopause or to natural ageing.

Inadequacy of thyroid hormones is particularly serious for the fetus, because they are required for the development of the nervous system in utero. In iodine-deficient regions of the world, this leads to the birth of neurological cretins, who have suffered major and irreversible damage to their central nervous system. It is estimated that, even in these days, 100 000 such cretins are born each year. In contrast, the incidence of neonatal hypothyroidism in iodine-replete Western society — a condition often referred to as ‘sporadic cretinism’ — is about 1 in 4000 live births; this is due to failure of the fetal thyroid to develop. This congenital hypothyroidism, unlike the neurological cretin, is amenable to treatment with thyroid hormones.

Hypothyroidism can readily be treated by oral thyroxine, which is one of the two hormones synthesized by the thyroid gland. This was first demonstrated by George Murray, a physician in Hartlepool. In 1891 he reported to the Newcastle Medical Research Society the beneficial effects of administering extracts of sheep thyroids to his profoundly hypothyroid patients. This was the first example of hormone replacement therapy.

— N. J. Marshall

See also goitre; hormones; thyroid.

Underactivity of the thyroid gland, leading to reduced secretion of thyroid hormones and a reduction in basal metabolic rate. Commonly associated with goitre due to iodine deficiency. In hypothyroid adults there is a characteristic moon-faced appearance, lethargy, and mental apathy. In infants, hypothyroidism can lead to severe mental retardation, cretinism. See also thyrotoxicosis.

Diminished activity of the thyroid gland with decreased secretion of thyroxin, resulting in lowered basal metabolic rate, lethargy, sleepiness, dysmenorrhea in females, and a tendency toward obesity. Occasionally there is accompanying gingival hyperplasia. The condition is called cretinism in children and myxedema in adults.

Definition

Hypothyroidism, or a condition of insufficient thyroid hormone in the body, develops when the thyroid gland fails to produce or secrete as much thyroxine (T₄) and triiodothyronine (T₃) as the body needs. Because T₄ regulates such essential functions as heart rate, digestion, physical growth, and mental development, an insufficiency of this hormone can slow life-sustaining processes, damage organs and tissues in every part of the body, and lead to life-threatening complications.

Description

Hypothyroidism is one of the most common chronic diseases in the United States. Symptoms may not appear until years after the thyroid has stopped functioning, and they are often mistaken for signs of other illnesses, menopause, or aging. Although this condition is believed to affect as many as 11 million adults and children, as many as two of every three people with hypothyroidism may not know they have the disease.

The thyroid gland influences almost every organ, tissue, and cell in the body. It is shaped like a butterfly and located just below the Adam's apple. The thyroid stores iodine the body gets from food and uses this mineral to create T₄ and T₃. Low T₄ levels can alter weight, appetite, sleep patterns, body temperature, sex drive, and a variety of other physical, mental, and emotional characteristics.

There are three types of hypothyroidism. The most common is primary hypothyroidism, in which the thyroid doesn't produce an adequate amount of T₄. Secondary hypothyroidism develops when the pituitary gland does not release enough of the thyroid-stimulating hormone (TSH) that prompts the thyroid to manufacture T₄. Tertiary hypothyroidism results from a malfunction of the hypothalamus, the part of the brain that controls the endocrine system. Drug-induced hypothyroidism, an adverse reaction to medication, occurs in two of every 10,000 people, but rarely causes severe hypothyroidism.

Hypothyroidism is at least twice as common in women as it is in men. Although hypothyroidism is most common in women who are middle-aged or older, the disease can occur at any age. Newborn infants are tested for congenital (acquired in utero (Latin)) thyroid deficiency (cretinism) using a test that measures the levels of thyroxine and TSH in the infant's blood. Treatment within the first few months of life can prevent mental retardation and physical abnormalities. Older children who develop hypothyroidism suddenly stop growing.

Factors that increase a person's risk of developing hypothyroidism include age, weight, and medical history. Women are more likely to develop the disease after age 50; men, after age 60. Obesity (excessively fat condition) also increases the risk. A family history of thyroid problems or a personal history of high cholesterol levels or such autoimmune diseases as lupus, rheumatoid arthritis, or diabetes can make an individual more susceptible to hypothyroidism.

Causes & Symptoms

Hypothyroidism is most often the result of Hashimoto's disease, also known as chronic thyroiditis (inflammation of the thyroid gland). In this disease, the immune system fails to recognize that the thyroid gland is part of the body's own tissue and attacks it as if it were a foreign body. The attack by the immune system impairs thyroid function and sometimes destroys the gland. Other causes of hypothyroidism include:

• Radiation (the process whereby an element like radium emits rays). Radioactive (the quality some atoms have of producing energy) iodine used to treat hyperthyroidism (overactive thyroid) or radiation treatments for head or neck cancers can destroy the thyroid gland.
• Surgery. Removal of the thyroid gland because of cancer or other thyroid disorders can result in hypothyroidism.
• Viruses (very small organisms that cause disease) and bacteria (very small one-cell organisms that divide and can cause disease). Infections that depress thyroid hormone production usually cause permanent hypothyroidism.
• Human immunodeficiency virus (HIV). Among viruses, HIV, the virus that causes acquired immunodeficiency syndrome, or AIDS, may cause overt hypothyroidism. A 2004 report said that hypothyroidism occurs more often in HIV-infected patients taking highly active antiretroviral therapy (HAART).

• Medications. Nitroprusside, lithium, or iodides can induce hypothyroidism. Because patients who use these medications are closely monitored by their doctors, this side effect is very rare.
• Pituitary gland malfunction. This is a rare condition in which the pituitary gland fails to produce enough TSH to activate the thyroid's production of T_4.
• Congenital defect. One of every 4,000 babies is born without a properly functioning thyroid gland.
• Diet. Because the thyroid makes T₄ from iodine drawn from food, an iodine-deficient diet can cause hypothyroidism. Adding iodine to table salt and other common foods has eliminated iodine deficiency in the United States. Certain foods (cabbage, rutabagas, peanuts, peaches, soybeans, spinach) can interfere with thyroid hormone production.
• Environmental contaminants. Certain industrial chemicals, such as PCBs, found in the local environment at high levels may also cause hypothyroidism.

Hypothyroidism sometimes is referred to as a "silent" disease because early symptoms may be so mild that no one realizes anything is wrong. Untreated symptoms become more noticeable and severe, and can lead to confusion and mental disorders, breathing difficulties, heart problems, fluctuations in body temperature, and death.

Someone who has hypothyroidism will probably have more than one of the following symptoms:

• Fatigue
• decreased heart rate
• progressive hearing loss
• weight gain
• problems with memory and concentration
• depression
• goiter (enlarged thyroid gland)
• muscle pain or weakness
• loss of interest in sex; decreased libido
• numb, tingling hands
• dry skin
• swollen eyelids
• dryness, loss, or premature graying of hair
• extreme sensitivity to cold
• constipation
• irregular menstrual periods
• hoarse voice

Hypothyroidism usually develops gradually. When the disease results from surgery or other treatment for hyperthyroidism, symptoms may appear suddenly and include severe muscle cramps in the arms, legs, neck, shoulders, and back. It's important to see a doctor if any of these symptoms appear unexpectedly. When hypothyroidism remains undiagnosed and untreated, a person may eventually develop myxedema. Symptoms of this rare but potentially deadly complication include enlarged tongue, swollen facial features, hoarseness, and physical and mental sluggishness.

Myxedema coma is characterized by unresponsiveness, irregular and shallow breathing, and a drop in blood pressure and body temperature. The onset of this medical emergency can be sudden in people who are elderly or have been ill, injured, or exposed to very cold temperatures; who have recently had surgery; or who use sedatives or antidepressants. Without immediate medical attention, myxedema coma can be fatal.

Diagnosis

The diagnosis of hypothyroidism is based on the patient's observations, medical history, physical examination, and thyroid function tests. Doctors who specialize in treating thyroid disorders (endocrinologists) are most apt to recognize subtle symptoms and physical indications of hypothyroidism. A blood test known as a thyroid-stimulating hormone (TSH) assay, tests of T₄ and T₃ levels, a thyroid nuclear medicine scan, and thyroid ultrasound are used to confirm the diagnosis. A woman being tested for hypothyroidism should let her doctor know if she is pregnant or breastfeeding. All patients should be sure their doctors are aware of any recent procedures involving radioactive materials or contrast media.

The TSH assay is extremely accurate, but some doctors doubt the test's ability to detect mild hypothyroidism. They advise patients to monitor their basal (resting) body temperature for below-normal readings that could indicate the presence of hypothyroidism. These readings should be taken for five consecutive days, starting on the second day of the menstrual cycle for female patients. The normal temperature reading is 97.5°F (36.4°C).

Treatment

Alternative treatments are aimed primarily at strengthening the thyroid gland and will not eliminate the need for thyroid hormone medications. They include nutritional therapy, herbal therapy, and exercise.

Nutritional Therapy

If a person is experiencing symptoms resembling those of hypothyroidism, it is best to talk to a family physician immediately for appropriate diagnosis and treatments. Nutritional therapy should only be complementary and not used to replace conventional treatment for this disorder. In 2004, a study found that feeding soy formula to infants with congenital hypothyroidism led to prolonged increases in TSH levels. The study authors recommended close follow-up and frequent TSH measures if infants are put on soy-based formulas.

A naturopath or a nutritionist may recommend the following dietary changes to improve mild hypothyroidism:

• Avoiding eating the following raw foods: cabbage, mustard, spinach, cassava roots, peanuts, soybeans, and peaches. They may interfere with thyroid hormone production if not cooked.
• Eating foods with high iodine content such as fish, shellfish, and seaweed.
• Taking multivitamin and mineral supplements daily. Vitamins A, B_2, B_3, B_6, E, and zinc are needed for normal thyroid hormone production.
• Strengthening thyroid function with thyroid preparations sold at local food stores. They are used to treat mild hypothyroidism only. Available products include thyroid extracts, iodine, zinc, or tyrosine. Most Americans may not need iodine supplements, as the daily requirement can easily be met by eating iodine-rich foods or using iodized salt. Consuming more than 600 mcg of iodine per day may result in toxicity.

Herbal Therapies

Herbal remedies to improve thyroid function and relieve thyroid symptoms include Siberian ginseng (for treatment of fatigue), Panax ginseng, and bladder wrack (Fucus vesiculosus,) which can be taken in capsule form or as a tea.

Homeopathic Remedies

Homeopathic treatments (tiny doses of diluted, safe remedies to promote healing) may gradually reduce the need for supplemental thyroid hormone in some patients. Homeopathic remedies for hypothyroidism include homeopathic thyroid as well as others based on the patient's individualized symptoms.

Exercise

Exercise improves thyroid function by stimulating production of thyroid hormone and making body tissues more responsive to the effects of thyroid hormone. It also increases the metabolic (chemical changes in cells providing energy to the body) rate and helps hypothyroid patients lose weight.

Allopathic Treatment

In allopathic treatment—medical practice that combats disease with remedies that produce effects different from those produced by the disease—natural or synthetic thyroid hormones are used to restore normal (euthyroid) thyroid hormone levels. Synthroid, or synthetic T₄, is easy to take and works for about 80% of patients. In addition, some patients need additional T₃. However, physicians have not agreed for many years on adding this therapy. In 2004, a study showed there were no benefits to adding T₃ to traditional T₄ therapy. Synthetic hormones are more effective than natural substances, but it may take several months to determine the correct dosage. Patients start to feel better within 48 hours, but symptoms will return if they stop taking the medication.

Most doctors prescribe levothyroxine sodium tablets, and most people with hypothyroidism will take the medication for the rest of their lives. Aging, other medications, and changes in weight and general health can affect how much replacement hormone a patient needs, and regular TSH tests are used to monitor hormone levels. Patients should not switch from one brand of thyroid hormone to another without a doctor's permission.

Possible side effects of too much T₄ or T₃ include osteoporosis (after long-term use), occasional anxiety, heart palpitations (very fast, strong heartbeat), insomnia, and occasional episodes of mania (acting crazed).

Regular exercise and a high-fiber diet can help maintain thyroid function and prevent constipation.

Expected Results

Thyroid hormone replacement therapy generally maintains normal thyroid hormone levels unless treatment is interrupted or discontinued. In 2004, a study showed that treating hypothyroidism reduces risk of cardiac disease, particularly from atherosclerosis, or hardened arteries from plaque buildup.

Prevention

Primary hypothyroidism can't be prevented, but routine screening of adults can detect the disease in its early stages and prevent complications.

Resources

Books

The Editors of Time-Life Books. The Medical Advisor: The Complete Guide to Alternative and Conventional Treatments. Alexandria, VA: Time-Life Books, 1996.

Langer, Stephen and James F. Scheer. Hypothyroidism: The Unsuspected Illness. New Canaan, CT: Keats Publishing, 1995.

Murray, Michael, and Joseph Pizzorno. Encyclopedia of Natural Medicine. Rocklin, CA: Prima Health, 1998.

Walker, Lynne Paige and Ellen Hodgson Brown. The Alternative Pharmacy. Paramus, NJ: Prentice Hall Press, 1998.

Wood, Lawrence C., David S. Cooper, and E. Chester Ridgway. Your Thyroid: A Home Reference. New York: Ballantine Books, 1996.

Periodicals

Conrad, S.C., H. Chiu, and B. L. Silverman. "Soy Formula Complicates Management of Congenital Hypothyroidism." Archives of Disease in Childhood (January 2004):37–41.

Elliott, William T. "T₄ Alone is OK for Hyperthyroidism Therapy." Critical Care Alert (February 2004):S2–S3.

Sadovsky, Richard. "Treating Hypothyroidism Reduces Atherosclerosis Risk." American Family Physician (February 1, 2004):656.

Zepf, Bill. "Hypothyroidism Common in Patients Infected With HIV." American Family Physician (March 15, 2004):1508.

Organizations

American Thyroid Association. Montefiore Medical Center. 111 E. 210th St., Bronx, NY 10467.

Endocrine Society. 4350 East West Highway, Suite 500, Bethesda, MD 20814-4410. (301) 941-0200.

Thyroid Foundation of America, Inc. Ruth Sleeper Hall, RSL 350, Boston, MA 02114-2968. (800) 832-8321 or (617) 726-8500.

Thyroid Society for Education and Research. 7515 S. Main St., Suite 545. Houston, TX 77030. (800) THYROID or (713) 799-9909.

[Article by: Mai Tran; Teresa G. Odle]

Definition

Hypothyroidism, or underactive thyroid, develops when the thyroid gland fails to produce or secrete as much thyroxine (T₄) and triiodothyonine (T₃) as the body needs. Because these thyroid hormones regulate such essential functions as heart rate, digestion, physical growth, and mental development, an insufficient supply of this hormone can slow metabolic processes, damage organs and tissues in every part of the body, and lead to life-threatening complications.

Description

Hypothyroidism is one of the most common chronic diseases in the United States. Symptoms may not appear until years after the thyroid has stopped functioning and often are mistaken for signs of other illnesses. Although this condition is believed to affect up to 11 million adults and children, as many as two out of every three people with hypothyroidism may not know they have the disease.

Nicknamed "Gland Central" because it influences almost every organ, tissue, and cell in the body, the thyroid is shaped like a butterfly and located just below the larynx, or Adam's apple, and in front of the trachea, or windpipe. The thyroid stores iodine that the body obtains from food, and uses this mineral to create the thyroid hormones. Low thyroid hormone levels can alter weight, appetite, sleep patterns, body temperature, and a variety of other physical, mental, and emotional characteristics.

Although hypothyroidism is most common in women who are middle-aged or older, the disease can occur at any age. In addition, an infant can be born with congenital hypothyroidism, i.e., without a functioning thyroid. In older children, the development of hypothyroidism may progress slowly and it may be several years before the disease is diagnosed.

Demographics

The most common cause of hypothyroidism in mid-to late-childhood and adolescence is Hashimoto's thyroiditis, which occurs in up to 1.2 percent of the school age population. Congenital hypothyroidism is less common. One out of every 4,000–5,000 infants is born without a properly functioning thyroid gland. Congenital hypothyroidism is twice as common in girls as in boys and about five times more common in whites than in blacks.

Causes and Symptoms

Congenital hypothyroidism is a disorder that affects infants from birth, resulting from the loss of thyroid function due to the failure of the thyroid gland to develop correctly. Sometimes the thyroid gland is absent or is ectopic, i.e., in an abnormal location. This congenital defect means that the infant does not produce sufficient thyroid hormones, resulting in abnormal growth and development as well as slower mental function.

Hypothyroidism may also be caused by an abnormality of the immune system that results in damage and destruction of the thyroid gland (Hashimoto's thyroiditis). This process can result in either loss of thyroid tissue or enlargement of the thyroid. In most cases, there is no pain or tenderness associated with this disease, although sometimes persons affected complain of difficulty in swallowing, as if they had a lump in the throat.

Less often, hypothyroidism develops when the pituitary gland fails and does not release enough thyroid-stimulating hormone (TSH), which stimulates the thyroid to produce and secrete normal amounts of T₄ and T₃. TSH may be deficient for several reasons:

• disease of the pituitary gland (occurs rarely)
• disease of the hypothalamus (located about the pituitary), which stimulates the pituitary gland
• tumor, cyst, or other abnormal structure between the hypothalamus and pituitary gland that prevents the pituitary from receiving the stimulus to secrete TSH

Other causes of hypothyroidism include:

• Radiation. Radioactive iodine used to treat hyperthyroidism (overactive thyroid) or radiation treatments for head or neck cancers can destroy the thyroid gland.
• Surgery. Removal of the thyroid gland because of cancer or other thyroid disorders can result in hypothyroidism.
• Viruses and bacteria. Infections that depress thyroid hormone production usually cause permanent hypothyroidism.
• Medication. Nitroprusside, lithium, or iodides can induce hypothyroidism. Because patients who use these medications are closely monitored by their doctors, this side effect is very rare.
• Environmental contaminants. Certain man-made chemicals such as PCBs, found in the local environment at high levels, may also cause hypothyroidism.

Often babies with congenital hypothyroidism will appear normal at birth, which is why screening is vital. However, some infants may have one of more of the following symptoms:

• large size (despite poor feeding habits) and increased birth weight
• puffy face and swollen tongue
• hoarse cry
• low muscle tone
• cold extremities
• persistent constipation, with distended abdomen
• lack of energy, sleeping most of the time and appearing tired when awake
• little or no growth

Children born with symptoms have a greater risk of developmental delay than children born without symptoms. The longer a child with hypothyroidism remains untreated, the greater is the loss of intellectual capacity, as measured by the standard intelligence testing (IQ). The ultimate IQ has been shown to be significantly higher in children whose hypothyroidism was detected and treated prior to six weeks of age, compared to those children whose hypothyroidism went untreated for six to 12 weeks.

Hypothyroidism that develops after birth is sometimes referred to as a silent disease because early symptoms may be so mild that no one realizes anything is wrong. Untreated symptoms become more noticeable and severe, and can lead to confusion and mental disorders, breathing difficulties, heart problems, fluctuations in body temperature, and death.

A child or adolescent who has hypothyroidism may have one or more of the following symptoms:

• fatigue
• decreased heart rate
• progressive hearing loss
• weight gain
• problems with memory and concentration
• depression
• goiter (enlarged thyroid gland)
• muscle pain or weakness
• numb, tingling hands
• dry skin
• swollen eyelids
• dryness or loss of hair
• extreme sensitivity to cold
• constipation
• delayed (common) or early (rare) onset of sexual development at adolescence
• irregular menstrual periods
• elevated cholesterol levels in the blood
• hoarse voice

Although hypothyroidism usually develops gradually, when the disease results from surgery or other treatment for hyperthyroidism, symptoms may appear suddenly and include severe muscle cramps in the arms, legs, neck, shoulders, and back.

People whose hypothyroidism remains undiagnosed and untreated may eventually develop myxedema. Symptoms of this rare, but potentially deadly, complication include enlarged tongue, swollen facial features, hoarseness, and physical and mental sluggishness. Myxedema coma can cause unresponsiveness; irregular, shallow breathing; low blood sugar; and drops in blood pressure and body temperature. The onset of this medical emergency can be sudden in children with undiagnosed hypothyroidism; it can be brought on by illness, injury, surgery, use of sedatives or anti-depressants, or exposure to very cold temperatures. Without immediate medical attention, myxedema coma can be fatal.

When to Call the Doctor

The doctor should be called if signs of hypothyroidism or myxedema are present. Every child who has a decrease in rate of growth in height during childhood and adolescence should be tested to determine if the growth problem is caused by hypothyroidism.

Diagnosis

In the United States, newborn infants between 24 and 72 hours old are tested for congenital thyroid deficiency (cretinism) using a test that measures the levels of thyroxine in the infant's blood. If the levels are low, the physician will likely repeat the blood test to confirm the diagnosis. The physician may take an x ray of the infant's legs. In an infant with hypothyroidism, the ends of the bones have an immature appearance. Treatment within the first few months of life can prevent mental retardation and physical abnormalities.

Older children who develop hypothyroidism may suddenly stop growing. If the child was above average height before the disease occurred, he or she may now be short compared to other children of the same age. Therefore, the most important feature of hypothyroidism in a child is a decrease in the rate of growth in height. If the disease is recognized early and adequately treated, the child will grow at an accelerated rate until reaching the same growth percentile where the child measured before the onset of hypothyroidism. Diagnosis of hypothyroidism is based on the patient's observations, medical history, physical examination, and thyroid function tests. Doctors who specialize in treating thyroid disorders (endocrinologists) are most likely to recognize subtle symptoms and physical indications of hypothyroidism. A diagnostic evaluation may include a blood test known as a thyroid-stimulating hormone (TSH) assay, thyroid nuclear medicine scan, thyroid ultrasound, or needle aspiration biopsy (which is also used to provide information on thyroid masses). All patients should be sure their doctors are aware of any recent procedures involving radioactive materials or contrast media.

The blood test is extremely accurate, but some doctors doubt its ability to detect mild hypothyroidism. They advise patients to monitor their basal (resting) body temperature for below-normal readings that could indicate the presence of hypothyroidism.

Alternative Treatment

Alternative treatments are primarily aimed at strengthening the thyroid but will not eliminate the need for thyroid hormone medications. Herbal remedies to improve thyroid function and relieve symptoms of hypothyroidism include bladder wrack (Fucus vesiculosus), which can be taken in capsule form or as a tea. The shoulder stand yoga position (done at least once daily for 20 minutes) is believed to improve thyroid function.

Nutritional Concerns

Because the thyroid makes T₄ from iodine in food, an iodine-deficient diet can cause hypothyroidism. Adding iodine to table salt and other common foods has eliminated iodine deficiency in the United States. Some foods, including cabbage, rutabagas, radishes, peanuts, peaches, soybeans, and spinach, can interfere with thyroid hormone production. Anyone with hypothyroidism may want to avoid these foods. A high-fiber diet along with regular exercise is recommended to help maintain thyroid function and prevent constipation.

Prognosis

Thyroid hormone replacement therapy generally maintains normal thyroid hormone levels unless treatment is interrupted or discontinued.

Prevention

Hypothyroidism usually cannot be prevented, but the symptoms and effects of the disease can be controlled by prompt diagnosis and treatment.

Parental Concerns

Parents must ensure that medication is taken on a routine basis by making the process a part of the family's lifestyle. Taking the medication as prescribed helps assure the child's optimal growth and development.

Resources

Books

Gomez, Joan. Thyroid Problems in Women and Children: Self-Help and Treatment. Alameda, CA: Hunter House, 2003.

Langer, Stephen, and James F. Scheer. Hypothyroidism: The Unsuspected Illness. New Canaan, CT: Keats Publishing, 1995.

Pratt, Maureen. The First Year—Hypothyroidism: An Essential Guide for the Newly Diagnosed. New York: Marlowe and Company, 2003.

Rosenthal, M. Sara. The Hypothyroid Sourcebook: Everything You Need to Know. New York: McGraw Hill, 2002.

Shomon, Mary J. Living Well with Hypothyroidism: What Your Doctor Doesn't Tell You...That You Need to Know. New York: Harper Resource, 2000.

Wood, Lawrence C., et al. Your Thyroid: A Home Reference. New York: Ballantine Books, 1996.

Organizations

American Thyroid Association. Montefiore Medical Center, 111 E. 210th St., Bronx, NY 10467. Web site: www.thyroid.org.

Endocrine Society. 4350 East West Highway, Suite 500, Bethesda, MD 20814-4410. (301) 941-0200. Web site: www.endosociety.org.

Thyroid Foundation of America, Inc. Ruth Sleeper Hall, RSL 350, Boston, MA 02114-2968. (800) 832-8321 or (617) 726-8500. Web site: www.tsh.org.

Thyroid Society for Education and Research. 7515 S. Main St., Suite 545, Houston, TX 77030. (800) THYROID or (713) 799-9909. Web site: www.the-thyroid-society.org.

Web Sites

Thyroid Diseases. National Institutes of Health. Available online at: www.nlm.nih.gov/medlineplus/thyroiddiseases.html.

[Article by: Judith Sims, M.S. Maureen Haggerty]

Hypothyroidism is the condition that reflects decreased concentrations of thyroid hormones, due to any cause. The resulting hypometabolic state causes decreased heat production and generally slows many of the bodies' processes. Its prevalence is 1 to 3 percent of young to middle-aged adults, mainly women, and its incidence rises with age. Severe hypothyroidism occurs in 2 to 4 percent of women older than seventy years of age, and milder forms of disease in 8 to 15 percent. Outside of North America, iodine deficiency is a major cause of hypothyroidism. In the United States, causes include Hashimoto's disease and treatment of hyperthyroidism—either by surgery or radioactive iodine (I-131). Treatment for hypothyroidism consists of hormone supplementation, generally synthetic l-thyroxine, taken once per day.

(SEE ALSO: Goiter; Hyperthyroidism; Iodine; Thyroid Disorders; Thyroid Function Tests)

Bibliography

Shapiro, L. (1999). "Hypothyroidism." In Atlas of Clinical Endocrinology, Vol. 1: Thyroid Diseases, ed. M. I. Surks. Philadelphia, PA: Current Medicine.

— MARTIN I. SURKS

Deficiency of thyroid gland activity, with underproduction of thyroxine, or the condition resulting from it. Common in adult dogs, particularly certain breeds, as a result of an idiopathic atrophy of the thyroid or a lymphocytic thyroiditis. Alopecia, weight gain, mental dullness, fatigue, cold intolerance, infertility and neurological deficits are seen. In food animals the syndrome is classical neonatal colloid goiter. See also goiter.

• autoimmune h. — see lymphocytic thyroiditis.
• congenital h. — results from congenital thyroid dysgenesis, defective hormone synthesis or severe iodine deficiency. There is dwarfism, macroglossia and mental dullness.
• iatrogenic h. — may follow treatment for hyperparathyroidism in cats.
• juvenile h. — congenital hypothyroidism (above).
• primary h. — that resulting from disease of the thyroid glands.
• secondary h. — caused by a deficiency of thyroid-stimulating hormone, usually as a result of a lesion in the pituitary gland.
• tertiary h. — caused by a lack of synthesis or release of thyrotropin releasing hormone.

Hypothyroidism
Classification and external resources
Thyroxine (T4) normally produced in 20:1 ratio to triiodothyronine (T3)
ICD-10	E03.9
ICD-9	244.9
DiseasesDB	6558
eMedicine	med/1145
MeSH	D007037

Hypothyroidism is the disease state in humans and in animals caused by insufficient production of thyroid hormone by the thyroid gland. Cretinism is a form of hypothyroidism found in infants.

Contents 1 Causes 1.1 General psychological associations 2 Symptoms 2.1 Early symptoms 2.2 Late symptoms 2.3 Less common symptoms 3 Diagnostic testing 4 Treatment 4.1 Treatment controversy 4.2 Subclinical hypothyroidism 5 See also 6 References 7 Further reading 8 External links

Causes

About three percent of the general population is hypothyroidic.^[1] Factors such as iodine deficiency or exposure to Iodine-131 (I-131) can increase that risk. There are a number of causes for hypothyroidism. Historically, and still in many developing countries, iodine deficiency is the most common cause of hypothyroidism worldwide. In iodine-replete individuals, hypothyroidism is mostly caused by Hashimoto's thyroiditis, or by a lack of the thyroid gland or a deficiency of hormones from either the hypothalamus or the pituitary.

Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring life-long treatment.

Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.

Hypothyroidism is also a relatively common disease in domestic dogs, with some specific breeds having a definite predisposition.^[2]

Temporary hypothyroidism can be due to the Wolff-Chaikoff effect. A very high intake of iodine can be used to temporarily treat hyperthyroidism, especially in an emergency situation. Although iodine is substrate for thyroid hormones, high levels prompt the thyroid gland to take in less of the iodine that is eaten, reducing hormone production.

Hypothyroidism is often classified by the organ of origin:^[3][4]

Type	Origin	Description
Primary	thyroid gland	The most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodine therapy for hyperthyroidism.
Secondary	pituitary gland	Occurs if the pituitary gland does not create enough thyroid stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine. Although not every case of secondary hypothyroidism has a clear-cut cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery.[5]
Tertiary	hypothalamus	Results when the hypothalamus fails to produce sufficient thyrotropin-releasing hormone (TRH). TRH prompts the pituitary gland to produce thyrotropin (TSH). Hence may also be termed hypothalamic-pituitary-axis hypothyroidism.

General psychological associations

Hypothyroidism can be caused by lithium-based mood stabilizers, usually used to treat bipolar disorder (previously known as manic depression).

In addition, patients with hypothyroidism and psychiatric symptoms may be diagnosed with:^[6]

• Atypical depression (which may present as dysthymia)
• Bipolar spectrum syndrome (including bipolar I or bipolar II disorder, cyclothymia, or premenstrual syndrome)
• Inattentive ADHD or sluggish cognitive tempo

Symptoms

In adults, hypothyroidism is associated with the following symptoms:^[5][7][8]

Early symptoms

• Poor muscle tone (muscle hypotonia)
• Fatigue
• Cold intolerance, increased sensitivity to cold
• Depression
• Muscle cramps and joint pain
• Carpal Tunnel Syndrome
• Goiter
• Thin, brittle fingernails
• Thin, brittle hair
• Paleness
• Decreased sweating
• Dry, itchy skin
• Weight gain and water retention^[9][10][11]
• Bradycardia (low heart rate – less than sixty beats per minute)
• Constipation

Late symptoms

• Slow speech and a hoarse, breaking voice – deepening of the voice can also be noticed
• Dry puffy skin, especially on the face
• Thinning of the outer third of the eyebrows (sign of Hertoghe)
• Abnormal menstrual cycles
• Low basal body temperature

Less common symptoms

• Impaired memory^[12]
• Impaired cognitive function (brain fog) and inattentiveness
• A slow heart rate with ECG changes including low voltage signals. Diminished cardiac output and decreased contractility.
• Reactive (or post-prandial) hypoglycemia^[13]
• Sluggish reflexes
• Hair loss
• Anemia caused by impaired haemoglobin synthesis (decreased EPO levels), impaired intestinal iron and folate absorption or B12 deficiency^[14] from pernicious anemia
• Difficulty swallowing
• Shortness of breath with a shallow and slow respiratory pattern.
• Increased need for sleep
• Irritability and mood instability
• Yellowing of the skin due to impaired conversion of beta-carotene^[15] to vitamin A
• Impaired renal function with decreased GFR.
• Elevated serum cholesterol
• Acute psychosis (myxedema madness) is a rare presentation of hypothyroidism
• Decreased libido^[16] due to impairment of testicular testosterone synthesis.
• Decreased sense of taste and smell (anosmia)
• Puffy face, hands and feet (late, less common symptoms)
• Gynecomastia

Diagnostic testing

To diagnose primary hypothyroidism, many doctors simply measure the amount of thyroid-stimulating hormone (TSH) being produced by the pituitary gland. High levels of TSH indicate that the thyroid is not producing sufficient levels of thyroid hormone (mainly as thyroxine (T₄) and smaller amounts of triiodothyronine (T₃)). However, measuring just TSH fails to diagnose secondary and tertiary hypothyroidism, thus leading to the following suggested blood testing if the TSH is normal and hypothyroidism is still suspected:

• Free triiodothyronine (fT₃)
• Free levothyroxine (fT₄)
• Total T₃
• Total T₄

Additionally, the following measurements may be needed:

• 24 hour urine free T₃^[17]
• Antithyroid antibodies — for evidence of autoimmune diseases that may be damaging the thyroid gland
• Serum cholesterol — which may be elevated in hypothyroidism
• Prolactin — as a widely available test of pituitary function
• Testing for anemia, including ferritin
• Basal body temperature

Treatment

Main article: Medical use of thyroid hormones

Hypothyroidism is treated with the levorotatory forms of thyroxine (L-T₄) and triiodothyronine (L-T₃). Both synthetic and animal-derived thyroid tablets are available and can be prescribed for patients in need of additional thyroid hormone. Thyroid hormone is taken daily, and doctors can monitor blood levels to help assure proper dosing. There are several different treatment protocols in thyroid replacement therapy:

T₄ Only

This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is currently the standard treatment in mainstream medicine.^[18]

T₄ and T₃ in Combination

This treatment protocol involves administering both synthetic L-T₄ and L-T₃ simultaneously in combination.^[19]

Desiccated Thyroid Extract

Desiccated thyroid extract is an animal based thyroid extract, most commonly from a porcine source. It is also a combination therapy, containing natural forms of L-T₄ and L-T₃.^[20]

Treatment controversy

The current standard treatment in thyroid therapy is levothyroxine only, and the American Association of Clinical Endocrinologists (AACE) states that desiccated thyroid hormone, combinations of thyroid hormone, or triiodothyronine should not generally be used for replacement therapy.^[18] Nevertheless, there exists some controversy about whether this treatment protocol is optimal, and recent studies have given conflicting results.

Two recent studies comparing synthetic T4 versus synthetic T4 + T3 have shown "clear improvements in both cognition and mood" from combination therapy.^{[19] [21]} Another study comparing synthetic T4 and desiccated thyroid extract showed marked improvements in virtually all symptom categories when certain patients were switched from synthetic T4 to desiccated thyroid extract.^[20]

However, other studies have shown no improvement in mood or mental abilities for those on combination therapy, and possibly impaired well-being from subclinical hyperthyroidism.^[22] Also, a 2007 metaanalysis of the nine controlled studies so far published found no significant difference in the effect on psychiatric symptoms.^[23]

There is also concern among some practitioners about the use of T3 due to its short half life. T3 when used on its own as a treatment results in wide fluctuations across the course of a day in the thyroid hormone levels, and with combined T3/T4 therapy there continues to be wide variation throughout each day.^[24]

Subclinical hypothyroidism

Subclinical hypothyroidism occurs when thyrotropin (TSH) levels are elevated but thyroxine (T₄) and triiodothyronine (T₃) levels are normal.^[1] Prevalence estimates range 3–8%, increasing with age; incidence is more common in women than in men.^[25] In primary hypothyroidism, TSH levels are high and T₄ and T₃ levels are low. Endocrinologists are puzzled because TSH usually increases when T₄ and T₃ levels drop. TSH prompts the thyroid gland to make more hormone. Endocrinologists are unsure how subclinical hypothyroidism affects cellular metabolic rates (and ultimately the body's organs) because the levels of the active hormones are adequate. Some have proposed treating subclinical hypothyroidism with levothyroxine, the typical treatment for overt hypothyroidism, but the benefits and the risks are unclear. Reference ranges have been debated as well. The American Association of Clinical Endocrinologists (ACEE) considers 0.45–4.5 mIU/L, with the ranges down to 0.1 and up to 10 mIU/L requiring monitoring but not necessarily treatment.^[26] There is always the risk of overtreatment and hyperthyroidism. Some studies have suggested that subclinical hypothyroidism does not need to be treated. A meta-analysis by the Cochrane Collaboration found no benefit of thyroid hormone replacement except "some parameters of lipid profiles and left ventricular function."^[27] A more recent metanalysis looking into whether subclinical hypothyroidism may increase the risk of cardiovascular disease, as has been previously suggested,^[28] found a possible modest increase and suggested further studies be undertaken with coronary heart disease as an end point "before current recommendations are updated."^[29]

See also

• Subacute lymphocytic thyroiditis

References

1. ^ ^{a b} Jack DeRuiter (2002) (PDF). Thyroid Pathology. pp. 30. http://www.auburn.edu/~deruija/endp_thyroidpathol.pdf. 
2. ^ Brooks W (01/06/2008). "Hypothyroidism in Dogs". The Pet Health Library. VetinaryPartner.com. http://www.veterinarypartner.com/Content.plx?P=A&A=461. Retrieved 2008-02-28. 
3. ^ Simon H (2006-04-19). "Hypothyroidism". University of Maryland Medical Center. http://www.umm.edu/patiented/articles/what_causes_hypothyroidism_000038_2.htm. Retrieved 2008-02-28. 
4. ^ Department of Pathology (June 13, 2005). "Pituitary Gland -- Diseases/Syndromes". Virginia Commonwealth University (VCU). http://www.pathology.vcu.edu/education/endocrine/endocrine/pituitary/diseases.html. Retrieved 2008-02-28. 
5. ^ ^{a b} American Thyroid Association (ATA) (2003) (PDF). Hypothyroidism Booklet. pp. 6. http://www.thyroid.org/patients/brochures/Hypothyroidism%20_web_booklet.pdf#search=%22hypothyroidism%22. 
6. ^ Heinrich TW, Grahm G (2003). "Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited". Primary care companion to the Journal of clinical psychiatry 5 (6): 260–266. PMID 15213796. 
7. ^ MedlinePlus Encyclopedia Hypothyroidism — primary — see list of Symptoms
8. ^ "Hypothyroidism — In-Depth Report." The New York Times. Copyright 2008
9. ^ "Hypothyroidism" (PDF). American Association of Clinical Endocrinologists. http://www.aace.com/pub/thyroidbrochures/pdfs/Hypothyroidism.pdf. 
10. ^ Yeum CH, Kim SW, Kim NH, Choi KC, Lee J (July 2002). "Increased expression of aquaporin water channels in hypothyroid rat kidney". Pharmacol. Res. 46 (1): 85–8. doi:10.1016/S1043-6618(02)00036-1. PMID 12208125. 
11. ^ Thyroid and Weight. The American Thyroid Association
12. ^ Cognitive function in untreated hypothyroidism and hyperthyroidism
13. ^ Hofeldt FD, Dippe S, Forsham PH (1972). "Diagnosis and classification of reactive hypoglycemia based on hormonal changes in response to oral and intravenous glucose administration" (PDF). Am. J. Clin. Nutr. 25 (11): 1193–201. PMID 5086042. http://www.ajcn.org/cgi/reprint/25/11/1193.pdf. 
14. ^ Vitamin B12 deficiency common in primary hypothyroidism.
15. ^ Cracking the Metabolic Code (Volume 1 of 2) by James B. Lavalle R.Ph. C.C.N. N.D, ISBN 1442950390, page 100
16. ^ Effects of thyroid status on pituitary gonadotropin and testicular reserve in men.
17. ^ Baisier W. Hertoghe J. Eeckhaut W. Thyroid insufficiency. Is TSH the only diagnostic tool? J Nutr Environ ed. 2000;10:105–113. "Thyroid insufficiency. Is TSH the only diagnostic tool?"
18. ^ ^{a b} American Association of Clinical Endocrinologists (November/December 2002). "Medical Guidelines For Clinical Practice For The Evaluation And Treatment Of Hyperthyroidism And Hypothyroidism" (PDF). Endocrine Practice 8 (6): 457–469. PMID 15260011. http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf. 
19. ^ ^{a b} Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ (February 1999). "Effects of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism". N. Engl. J. Med. 340 (6): 424–9. doi:10.1056/NEJM199902113400603. PMID 9971866. http://content.nejm.org/cgi/content/full/340/6/424. 
20. ^ ^{a b} Baisier, W.V.; Hertoghe, J.; Eeckhaut, W. (September 2001). "Thyroid Insufficiency. Is Thyroxine the Only Valuable Drug?". Journal of Nutritional and Environmental Medicine 11 (3): 159–66. doi:10.1080/13590840120083376.  — Abstract
21. ^ Robertas Bunevicius, Arthur J. Prange Jr. (June 2000). "Mental improvement after replacement therapy with thyroxine plus triiodothyronine: relationship to cause of hypothyroidism". The International Journal of Neuropsychopharmacology 3 (2): 167–174. doi:10.1017/S1461145700001826. PMID 11343593. http://journals.cambridge.org/action/displayAbstract?aid=52289. 
22. ^ Siegmund W, Spieker K, Weike AI, et al. (June 2004). "Replacement therapy with levothyroxine plus triiodothyronine (bioavailable molar ratio 14 : 1) is not superior to thyroxine alone to improve well-being and cognitive performance in hypothyroidism". Clin. Endocrinol. (Oxf) 60 (6): 750–7. doi:10.1111/j.1365-2265.2004.02050.x. PMID 15163340. 
23. ^ Joffe RT, Brimacombe M, Levitt AJ, Stagnaro-Green A (2007). "Treatment of clinical hypothyroidism with thyroxine and triiodothyronine: a literature review and metaanalysis". Psychosomatics 48 (5): 379–84. doi:10.1176/appi.psy.48.5.379. PMID 17878495. 
24. ^ Saravanan P, Siddique H, Simmons DJ, Greenwood R, Dayan CM (April 2007). "Twenty-four hour hormone profiles of TSH, Free T3 and free T4 in hypothyroid patients on combined T3/T4 therapy". Exp. Clin. Endocrinol. Diabetes 115 (4): 261–7. doi:10.1055/s-2007-973071. PMID 17479444. 
25. ^ Fatourechi V (2009). "Subclinical hypothyroidism: an update for primary care physicians". Mayo Clinic Proceedings. Mayo Clinic 84 (1): 65–71. PMID 19121255. 
26. ^ "Subclinical Thyroid Disease". Guidelines & Position Statements. The American Association of Clinical Endocrinologists. July 11, 2007. http://www.aace.com/pub/positionstatements/subclinical.php. Retrieved 2008-06-08. 
27. ^ Villar H, Saconato H, Valente O, Atallah A (2007). "Thyroid hormone replacement for subclinical hypothyroidism". Cochrane database of systematic reviews (Online) (3): CD003419. doi:10.1002/14651858.CD003419.pub2. PMID 17636722. 
28. ^ Biondi B, Palmieri EA, Lombardi G, Fazio S (December 2002). "Effects of subclinical thyroid dysfunction on the heart". Ann. Intern. Med. 137 (11): 904–14. PMID 12458990. 
29. ^ Ochs N, Auer R, Bauer DC, et al. (June 2008). "Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality". Ann. Intern. Med. 148 (11): 832–45. PMID 18490668. http://www.annals.org/cgi/content/full/148/11/832. 

Further reading

• Tchong L; Veloski C; Siraj ES, "Hypothyroidism: management across the continuum", Journal of Clinical Outcomes Management, 2009 May;16(5):231-235 (full article)

External links

• Hypothyroidism symptoms, causes, various classifications, and additional details
• Hypothyroidism Booklet - American Thyroid Association

v • d • e Endocrine pathology: endocrine diseases (E00-35, 240-259) Pancreas/ glucose metabolism Hypofunction Diabetes mellitus types: (type 1, type 2, MODY 1 2 3 4 5 6) · complications (coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy, cardiomyopathy) insulin receptor (Rabson-Mendenhall syndrome) · Insulin resistance Hyperfunction Hypoglycemia · beta cell (Hyperinsulinism) · G cell (Zollinger-Ellison syndrome) Hypothalamic/ pituitary axes Hypothalamus gonadotropin (Kallmann syndrome, Adiposogenital dystrophy) · CRH (Tertiary adrenal insufficiency) · vasopressin (Neurogenic diabetes insipidus) · general (Hypothalamic hamartoma) Pituitary Hyperpituitarism anterior (Acromegaly, Hyperprolactinaemia, Pituitary ACTH hypersecretion) · posterior (SIADH) · general (Nelson's syndrome) Hypopituitarism anterior (Kallmann syndrome, Growth hormone deficiency, ACTH deficiency/Secondary adrenal insufficiency) · posterior (Neurogenic diabetes insipidus) · general (Empty sella syndrome, Pituitary apoplexy, Sheehan's syndrome, Lymphocytic hypophysitis) Thyroid Hypothyroidism Iodine deficiency · Cretinism (Congenital hypothyroidism) · Myxedema · Euthyroid sick syndrome Hyperthyroidism Hyperthyroxinemia (Thyroid hormone resistance, Familial dysalbuminemic hyperthyroxinemia) · Hashitoxicosis · Thyrotoxicosis factitia · Graves' disease Thyroiditis Acute infectious · Subacute (De Quervain's, Subacute lymphocytic) · Autoimmune/chronic (Hashimoto's, Postpartum, Riedel's) Goitre Endemic goitre · Toxic nodular goitre · Toxic multinodular goitre Thyroid nodule Parathyroid Hypoparathyroidism Pseudohypoparathyroidism Hyperparathyroidism Primary · Secondary · Tertiary · Osteitis fibrosa cystica Adrenal Hyperfunction aldosterone: Hyperaldosteronism/Primary aldosteronism (Conn syndrome, Bartter syndrome, Glucocorticoid remediable aldosteronism) · AME · Liddle's syndrome · 17α CAH cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome) sex hormones: 21α CAH · 11β CAH Hypofunction/ Adrenal insufficiency (Addison's, WF) aldosterone: Hypoaldosteronism (21α CAH, 11β CAH) cortisol: CAH (Lipoid, 3β, 11β, 17α, 21α) sex hormones: 17α CAH Gonads ovarian: Polycystic ovary syndrome · Premature ovarian failure testicular: enzymatic (5-alpha-reductase deficiency, 17-beta-hydroxysteroid dehydrogenase deficiency) · Androgen receptor (Androgen insensitivity syndrome) general: Hypogonadism (Delayed puberty) · Hypergonadism (Precocious puberty) Height Gigantism · Dwarfism/Short stature (Laron syndrome, Psychogenic dwarfism) Multiple Autoimmune polyendocrine syndrome (APS1, APS2) · Carcinoid syndrome · Multiple endocrine neoplasia (1, 2A, 2B) · Progeria · Woodhouse-Sakati syndrome endocrine navs: anat/physio/dev/hormones, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc

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