hyperthyroidism

Definition

Hyperthyroidism is the overproduction of thyroid hormones by an overactive thyroid.

Description

Located in the front of the neck, the thyroid gland produces the hormones thyroxine (T₄) and triiodothyro-nine (T₃) that regulate the body's metabolic rate by helping to form protein ribonucleic acid (RNA) and increasing oxygen absorption in every cell. In turn, the production of these hormones are controlled by thyroid-stimulating hormone (TSH) that is produced by the pituitary gland. When production of the thyroid hormones increases despite the level of TSH being produced, hyperthyroidism occurs. The excessive amount of thyroid hormones in the blood increases the body's metabolism, creating both mental and physical symptoms.

The term hyperthyroidism covers any disease which results in overabundance of thyroid hormone. Other names for hyperthyroidism, or specific diseases within the category, include Graves' disease, diffuse toxic goiter, Basedow's disease, Parry's disease, and thyrotoxicosis. The disease is 10 times more common in women than in men, and the annual incidence of hyperthyroidism in the United States is about one per 1,000 women. Although it occurs at all ages, hyperthyroidism is most likely to occur after the age of 15. There is a form of hyperthyroidism called Neonatal Grave's disease, which occurs in infants born of mothers with Graves' disease. Occult hyperthyroidism may occur in patients over 65 and is characterized by a distinct lack of typical symptoms. Diffuse toxic goiter occurs in as many as 80% of patients with hyperthyroidism.

— Teresa Norris

1. Pathologically excessive production of thyroid hormones.
2. The condition resulting from excessive activity of the thyroid gland, characterized by increased basal metabolism.

The classic picture of excessive thyroid activity is that of a patient with Graves' disease — a form of thyrotoxicosis. Robert Graves was a renowned Dublin physician, whose bicentenary was celebrated in 1996. In addition to promoting a radical innovation in medical education — ward rounds with bedside teaching — he wrote in 1835 the first clear description of this disease. In a short paper titled ‘Palpitation of the heart with enlargement of the thyroid gland’, he recognized the defining significance of a ‘triad’ of symptoms: goitre, protruding eyes, and palpitations.

In the UK about 2% of women will suffer from thyroid overactivity (hyperthyroidism). It is ten times less likely among men. The hyperthyroidism of at least 50% of the patients is due to Graves' disease — now known to be an autoimmune condition.

Normally, thyroid activity is subject to positive regulation by thyroid stimulating hormone (TSH), which is secreted from the pituitary and stimulates thyroid growth and function. Very rarely, thyrotoxicosis is caused by excessive production of TSH. Hyperthyroidism of non-autoimmune origin is usually due to either a toxic nodular goitre (‘Plummer's disease’, after a physician at the Mayo Clinic in the 1920s) or a toxic adenoma — a benign tumour in which the cells retain the follicular arrangement characteristic of the thyroid gland. In complete contrast, the overactivity encountered in Graves' disease is due to the aberrant production of autoantibodies, known as thyroid stimulating antibodies. These mimic TSH and persistently stimulate the thyroid follicular cells. These antibodies are unique in having a stimulating as opposed to a blocking action. They were first described in a classic series of studies conducted in the 1950-60s by Adams and Purves in the University of Otago.

Thyroid overactivity results in the secretion of excessive amounts of thyroid hormones into the bloodstream. As a consequence, the clinical symptoms are the exaggerated effects of thyroid hormones on peripheral tissues. The basal metabolic rate increases and the effects of some other hormones — notably adrenaline — are potentiated. The symptoms include persistent weight loss despite a healthy appetite, sweating, hand tremor, and often a goitre. The patient is agitated, fatigues easily, and is intolerant of heat. Adrenaline potentiation is most seriously manifested by atrial fibrillation (a fast, irregular heartbeat). Some symptoms are additionally indicative of an autoimmune origin of the hyperthyroidism — Graves' disease. These include eye signs, which range from protruding eyes (exophthalmos) to — in very rare cases — optic nerve compression with loss of vision. There can also be a characteristic thickening of the skin over the lower legs and on the tops of the feet or big toes. If there is a goitre, it is a diffuse enlargement and an isotope scan shows that the entire gland is uniformly overactive.

A hyperthyroid patient may be rendered euthyroid (hormone levels within normal limits) with antithyroid drugs, for example carbimazole, which inhibit the biosynthesis of thyroid hormones. After treatment for 12-18 months, spontaneous remissions occur in about half the patients with Graves' disease, so that if the antithyroid drugs are withdrawn the symptoms do not recur. This is typical of the ‘waxing and waning’ of some autoimmune conditions, and remissions were described without specific treatment in the early nineteenth-century reports. By contrast, spontaneous remission will not occur in patients suffering from hyperthyroidism of non-autoimmune origin. If remission is not achieved, long-term treatment usually requires partial or total elimination of the thyroid. This is achieved either by the use of radioiodine or by surgical removal (thyroidectomy).

— N. J. Marshall

See also goitre; hormones; hypothyroidism; thyroid.

(Parry’s dis H ease), abnormalities of calorigenic mechanisms, body tissues, blood, and body fluids and of the circulatory, muscular, and nervous systems resulting from an excessive elaboration of thyroid hormone. Manifestations include increased sweating, increased appetite, intolerance to heat, weight loss, increased protein-bound iodine (PBI), early shedding of primary teeth and early eruption of permanent teeth, tachycardia, palpitation, tremors, nervousness, muscular weakness, diarrhea, increased excretion of calcium and phosphorus, hypocholester-olemia, creatinuria, and osteoporosis. May occur as the result of primary hyperplasia, hyperfunctioning nodular goiters, functional benign tumor, or adenoma of the thyroid gland. See also goiter, exophthalmic.

Definition

Hyperthyroidism is the overproduction of thyroid hormones by an overactive thyroid gland.

Description

Located in the front of the neck, the thyroid gland produces the hormones thyroxine (T₄) and triiodothyro-nine (T₃) that regulate the body's metabolic rate by helping to form protein ribonucleic acid (RNA) and increasing oxygen absorption in every cell. In turn, the production of these hormones is controlled by a thyroid-stimulating hormone (TSH) that is produced by the pituitary gland. When production of the thyroid hormones increases despite the level of TSH being produced, hyperthyroidism occurs. The excessive amount of thyroid hormones in the blood increases the body's metabolism, creating both mental and physical symptoms.

The term hyperthyroidism covers any disease that results in an overabundance of thyroid hormone. Other names for hyperthyroidism, or specific diseases within the category, include Graves' disease, diffuse toxic goiter, Basedow's disease, Parry's disease, and thyrotoxicosis. Hyperthyroidism affects 2.5 million people in the United States, but could affect up to 4.5 million people because more than half of the people with thyroid disease don't know they have it. Although it occurs at all ages, hyperthyroidism is most likely to occur after the age of 15. There is a form of hyperthyroidism called neonatal Graves' disease, which occurs in infants born of mothers with Graves' disease. Occult hyperthyroidism may occur in patients over age 65 and is characterized by a distinct lack of typical symptoms. Diffuse toxic goiter occurs in as many as 80% of patients with hyperthyroidism.

Causes & Symptoms

Hyperthyroidism is often associated with the body's production of auto-antibodies in the blood that cause the thyroid to grow and secrete excess thyroid hormone. This condition, as well as other forms of hyperthyroidism, may be inherited. Regardless of the cause, hyperthyroidism produces the same symptoms, including weight loss with increased appetite, shortness of breath and fatigue, intolerance to heat, heart palpitations (strong, very fast heartbeats), increased frequency of bowel movements, weak muscles, tremors, anxiety, and difficulty sleeping. Women also may notice decreased menstrual flow and irregular menstrual cycles.

Patients with Graves' disease often have a goiter (visible enlargement of the thyroid gland), although as many as ten percent do not. These patients also may have bulging eyes. Thyroid storm, a serious form of hyperthyroidism, may show up as sudden and acute symptoms, some of which mimic typical hyperthyroidism but with the addition of fever, substantial weakness, extreme restlessness, confusion, emotional swings or psychosis, and perhaps even coma.

Diagnosis

Physicians will look for physical signs and symptoms indicated by patient history. On inspection, the physician may note symptoms such as a goiter or eye-bulging. Other symptoms or family history may be clues to a diagnosis of hyperthyroidism. An elevated basal (lowest range of normal) body temperature above 98.6 degrees Fahrenheit (37 degrees centigrade) may be an indication of a heightened basal metabolic rate (which measures the energy used to maintain vitality) and hyperthyroidism. A simple blood test can be performed to determine the amount of thyroid hormone in the patient's blood. The diagnosis usually is straightforward with this combination of clinical history, physical examination, and routine blood hormone tests. Radioimmunoassay, or a test to show concentrations of thyroid hormones with the use of a radioisotope (a chemical element capable of radioactive or atomic transformations) mixed with fluid samples, helps confirm the diagnosis. A thyroid scan is a nuclear medicine procedure involving injection of a radioisotope dye that will tag the thyroid and help produce a clear image of inflammation or involvement of the entire thyroid.

Other tests can determine thyroid function and thyroid-stimulating hormone levels. Ultrasonography (a test whereby high-frequency sound waves (ultrasound) are bounced off tissues and echoes are converted to pictures (sonograms), computed tomography or (CT) scan (an x-ray computer procedure that produces a detailed picture of a cross-section of the body), and magnetic resonance imaging (MRI) (an x-ray technique that produces a detailed image of the inner body using a powerful magnet, radio waves, and a computer) may provide visual confirmation of a diagnosis or help to determine the extent of involvement.

Treatment

Alternative treatments for hyperthyroidism include nutritional therapy, herbal therapy, and homeopathy, the use of tiny doses of diluted and harmless remedies to catalyze healing.

Nutritional Therapy

Consumption of such foods as broccoli, Brussels sprouts, cabbage, cauliflower, kale, rutabagas, spinach, turnips, peaches, and pears can help naturally suppress thyroid hormone production. Dairy products and any stimulants such as tea, coffee, soda, and other caffeinated drinks should be avoided. Under the supervision of a trained physician, high dosages of certain vitamin/mineral combinations can help alleviate hyperthyroidism.

Homeopathy

An experienced homeopath may give patients specific remedies tailored to their overall personality profile as well as their specific symptoms. Symptomatic treatments may include Iodium or Natrum muriaticum.

Other Therapies

Other alternative treatments that may help relieve hyperthyroidism symptoms include traditional Chinese medicine and Western herbal medicine. Stress reduction techniques such as meditation also may prove beneficial. Patients should contact experienced herbalists for specific preparations and treatment.

Allopathic Treatment

Allopathy is the theory or system of medical practice that combats disease by use of remedies that produce

effects different from those produced by the disease. Treatment will depend on the specific disease and individual circumstances such as age, severity of disease, and other conditions affecting a patient's health.

Antithyroid Drugs

Antithyroid drugs often are administered to help the patient's body cease overproduction of thyroid hormones. In 2004, some drugs used to interfere with the thyroid gland's uptake of iodine were propylthiouracil (PTU) and methimazole (Tapazole®). Medication may work for young adults, pregnant women, and others. Women who are pregnant should be treated with the lowest dose required to maintain thyroid function in order to minimize the risk of hypothyroidism (underactive thyroid gland function) in the infant.

Radioactive Iodine

Radioactive iodine often is prescribed to damage cells that make thyroid hormone. The cells need iodine to make the hormone, so they will absorb any iodine found in the body. The patient may take an iodine capsule daily for several weeks, resulting in the eventual shrinkage of the thyroid, reduced hormone production, and a return to normal blood levels. A single large oral dose of radioactive iodine simplifies treatment but should only be given to patients who are not of reproductive age or are not planning to have children, since a large amount can concentrate in the reproductive organs (gonads).

Surgery

Patients treated with thyroidectomy, or surgery involving of partial or total removal of the thyroid, most often suffer from large goiter and have suffered relapses, even after repeated attempts to address the disease through drug therapy with iodine. Following thyroidectomy or iodine therapy, patients must be carefully monitored for years to watch for signs of hypothyroidism, or insufficient production of thyroid hormones. Hypothyroidism can occur as a complication of thyroid production suppression.

Expected Results

Hyperthyroidism generally is treatable and carries a good prognosis. Most patients lead normal lives with proper treatment. The majority of patients who receive radioactive iodine report feeling better within about three to six weeks of treatment. Thyroid storm, however, can be life-threatening and can lead to heart, liver, or kidney failure. Some patients who undergo radioactive iodine treatment or surgery become hypothyroid.

Prevention

There are no known prevention methods for hyperthyroidism, since its causes are either inherited or not completely understood. The best prevention tactic is knowledge of family history and close attention to symptoms and signs of the disease. Careful attention to prescribed therapy can prevent complications of the disease.

Resources

Books

The Burton Goldberg Group. Alternative Medicine. Puyallup, WA: Future Medicine Publishing Inc., 1994.

Zand, Janet, Allan N. Spreen, and James B. LaValle. "Hyperthyroidism." Smart Medicine for Healthier Living. Garden City Park, NY: Avery Publishing Group, 1999.

Periodicals

Lazarus, John H. "Hyperthyroidism." The Lancet 340 (February 1, 1997): 339–342.

"Thyroid Disorders; Facts to Know." NWHRC Health Center—Thyroid Disorders (March 2, 2004).

"Thyroid Disorders; Treatment." NWHRC Health Center—Thyroid Disorders (March 2, 2004).

Organizations

The Thyroid Foundation of America. 350 Ruth Sleeper Hall RSL 350, Parkman Street, Boston, MA 02114. (800) 832–8321. .

Other

"Endocrine disorder and endocrine surgery." Endocrine Web. .

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

Definition

Hyperthyroidism is the overproduction of thyroid hormones by an overactive thyroid.

Description

The term hyperthyroidism covers any disease which results in overabundance of thyroid hormone. Other names for hyperthyroidism, or specific diseases within the category, include Graves' disease, diffuse toxic goiter, Basedow's disease, Parry's disease, and thyrotoxicosis.

Located in the front of the neck, the thyroid gland produces the hormones thyroxin (T4) and triiodothyronine (T3), which regulate the body's metabolic rate by helping to form protein ribonucleic acid (RNA) and increasing oxygen absorption in every cell. In turn, the production of these hormones is controlled by thyroid-stimulating hormone (TSH) that is produced by the pituitary gland. When production of the thyroid hormones increases despite the level of TSH being produced, hyperthyroidism occurs. The excessive amount of thyroid hormones in the blood increases the body's metabolism, creating both mental and physical symptoms.

Demographics

Only about 5 percent of all individuals with hyperthyroidism are younger than 15 years of age. About five times as many girls as boys develop hyperthyroidism. Almost all cases of pediatric hyperthyroidism are the form called Graves' disease. There is a form of hyperthyroidism called neonatal Graves' disease, which occurs in infants born of mothers with Graves' disease. Children with other conditions, such as trisomy 21, Addison's disease, diabetes, systemic lupus erythematosus, rheumatoid arthritis, myasthenia gravis, vitiligo, pernicious anemia, and immune thrombocytopenic purpura are more likely to develop Graves' disease.

Causes and Symptoms

Hyperthyroidism is often associated with the body's production of autoantibodies in the blood which causes the thyroid to grow and secrete excess thyroid hormone. This condition, as well as other forms of hyperthyroidism, may be inherited. Regardless of the cause, hyperthyroidism produces the same symptoms, including weight loss with increased appetite, shortness of breath and fatigue, intolerance to heat, heart palpitations, increased frequency of bowel movements, weak muscles, tremors, anxiety, and difficulty sleeping. Adolescent girls may also notice decreased menstrual flow and irregular menstrual cycles.

Patients with Graves' disease often have a goiter (visible enlargement of the thyroid gland), although as many as 10 percent do not. These patients may also have bulging eyes. Thyroid storm, a serious form of hyperthyroidism, may show up as sudden and acute symptoms, some of which mimic typical hyperthyroidism, as well as the addition of fever, substantial weakness, extreme restlessness, confusion, emotional swings or psychosis, or coma. Fortunately, such a fulminant course of Graves' disease is rare in children and adolescents.

Babies with neonatal Graves' disease may suffer from prematurity, airway obstruction, and heart failure. Death occurs in as many as 16 percent of these babies, and other complications from which survivors may suffer include craniosynostosis (early closure of the sutures of the skull, which can result in compression of the growing brain), and developmental delay.

When to Call the Doctor

Parents should contact a child's pediatrician if the child shows the following symptoms: rapid weight loss, shortness of breath, intolerance to heat, heart palpitations, increased frequency of bowel movements, weak muscles, tremors, anxiety, and difficulty sleeping. An enlarged thyroid gland, seen as a bulge in the neck, should be examined by a doctor.

Diagnosis

Physicians will look for physical signs and symptoms indicated by patient history. On inspection, the physician may note symptoms such as a goiter or eye bulging. Other symptoms or family history may be clues to a diagnosis of hyperthyroidism. An elevated body temperature (basal body temperature) above 98.6°F (37°C) may be an indication of a heightened metabolic rate (basal metabolic rate) and hyperthyroidism. A simple blood test can be performed to determine the amount of thyroid hormone in the patient's blood. The diagnosis is usually straightforward with this combination of clinical history, physical examination, and routine blood hormone tests. Radioimmunoassay (a test to show concentrations of thyroid hormones with the use of a radioisotope mixed with fluid samples) helps confirm the diagnosis. A thyroid scan is a nuclear medicine procedure involving injection of a radioisotope dye, which tags the thyroid and helps produce a clear image of inflammation or involvement of the entire thyroid. Other tests can determine thyroid function and thyroid-stimulating hormone levels. Ultrasonography, computed tomography scans (CT scan), and magnetic resonance imaging (MRI) may provide visual confirmation of a diagnosis or help to determine the extent of involvement.

Treatment

Treatment depends on the specific disease and individual circumstances such as age, severity of disease, and other conditions affecting a patient's health.

Antithyroid Drugs

Antithyroid drugs are often administered to help the patient's body cease overproduction of thyroid hormones. This medication may work for young adults, pregnant women, and others. Women who are pregnant should be treated with the lowest dose required to maintain thyroid function in order to minimize the risk of hypothyroidism in the infant.

Radioactive Iodine

Radioactive iodine is often prescribed to damage cells that make thyroid hormone. The cells need iodine to make the hormone, so they absorb any iodine found in the body. The patient may take an iodine capsule daily for several weeks, resulting in the eventual shrinkage of the thyroid, reduced hormone production, and a return to normal blood levels. Some patients may receive a single larger oral dose of radioactive iodine to treat the disease more quickly. This should only be done for patients who are not of reproductive age or are not planning to have children, since a large amount can concentrate in the reproductive organs (gonads).

Surgery

Some patients may undergo surgery to treat hyperthyroidism. Most commonly, patients treated with thyroidectomy, in the form of partial or total removal of the thyroid, suffer from large goiter and have suffered relapses, even after repeated attempts to address the disease through drug therapy. Some patients may be candidates for surgery because they were not good candidates for iodine therapy or refused iodine administration. Patients receiving thyroidectomy or iodine therapy must be carefully monitored for years to watch for signs of hypothyroidism (insufficient production of thyroid hormones), which can occur as a complication of thyroid production suppression.

Prognosis

Hyperthyroidism is generally treatable and carries a good prognosis. Most patients lead normal lives with proper treatment. Thyroid storm, however, can be life-threatening and can lead to heart, liver, or kidney failure. Luckily, this form of fulminant hyperthyroidism is rare in children and adolescents.

Prevention

As of 2004 there are no known prevention methods for hyperthyroidism; its causes are either inherited or not completely understood. The best prevention tactic is knowledge of family history and close attention to symptoms and signs of the disease. Careful attention to prescribed therapy can prevent complications of the disease.

Parental Concerns

Parents should be aware that hyperthyroidism is very rare in young children. However, once diagnosed, the condition needs short- and long-term treatment, with regular follow-up visits to the doctor.

Resources

Books

"Hyperthyroidism." In Nelson Textbook of Pediatrics. Edited by Richard E. Behrman et al. Philadelphia: Saunders, 2004.

Periodicals

Hanna, C. E. "Adolescent Thyroid Disorders." Adolescent Medicine 13 (February 2002): 13–35.

Organizations

Thyroid Foundation of America. 350 Ruth Sleeper Hall, RSL 350, Parkman St., Boston, MA 02114. Web site: www.clark.net/pub/tfa.

[Article by: Teresa Norris, RN Rosalyn Carson-DeWitt, MD]

Hyperthyroidism is the condition that reflects excessive concentrations of thyroid hormones, due to any cause. The resulting hypermetabolic state causes increased heat production and accelerates many of the bodies' processes. Common causes are Graves' disease, hyperfunctioning benign thyroid tumors, and thyroid inflammations. Untreated, patients may have severe and progressive disability that includes weight loss, muscle weakness, loss of mineral from their bones, and increased risk for dangerous heart arrhythmias. Available treatments include one of several "antithyroid drugs," such as methimazole and propylthiouracil, that prevent overproduction of thyroid hormones, and radioctive iodine (I-131) treatment or surgery, which either destroy or remove the thyroid tissue.

(SEE ALSO: Goiter; Hypothyroidism; Thyroid Disorders; Thyroid Function Tests)

Bibliography

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

— MARTIN I. SURKS

Excessive functional activity of the thyroid gland. Rare in animals except in aged dogs and cats where it is associated with functional thyroid neoplasms.
Affected animals show increased thirst, weight loss despite an increased appetite, restlessness and cardiac arrhythmias.

• apathetic h. — a small percentage of hyperthyroidic cats show lethargy, depression and anorexia; may be due to associated dysfunction.

Hyperthyroidism
Classification and external resources
Triiodothyronine (T3, pictured) and thyroxine (T4) are both forms of thyroid hormone.
ICD-10	E05.
ICD-9	242.9
DiseasesDB	6348
MedlinePlus	000356
eMedicine	med/1109
MeSH	D006980

Hyperthyroidism is the term for overactive tissue within the thyroid gland, resulting in overproduction and thus an excess of circulating free thyroid hormones: thyroxine (T₄), triiodothyronine (T₃), or both. Thyroid hormone is important at a cellular level, affecting nearly every type of tissue in the body.

Thyroid hormone functions as a stimulus to metabolism and is critical to normal function of the cell. In excess, it both overstimulates metabolism and exacerbates the effect of the sympathetic nervous system, causing "speeding up" of various body systems and symptoms resembling an overdose of epinephrine (adrenaline). These include fast heart beat and symptoms of palpitations, nervous system tremor and anxiety symptoms, digestive system hypermotility (diarrhea), and weight loss.

On the other hand, a lack of functioning thyroid tissue results in a symptomatic lack of thyroid hormone, termed hypothyroidism.

Contents 1 Signs and symptoms 2 Causes 3 Diagnosis 4 Treatment 4.1 Temporary medical therapy 4.1.1 Thyrostatics 4.1.2 Beta-blockers 4.2 Permanent treatments 4.2.1 Surgery 4.2.2 Radioiodine 4.3 Thyroid storm 5 Veterinary medicine 5.1 Cats 5.2 Dogs 6 See also 7 References 8 Further reading 9 Additional images 10 External links

Signs and symptoms

Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, tremor, pretibial myxedema, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. Long term untreated hyperthyroidism can lead to osteoporosis. In the elderly, these classical symptoms may not be present.

Neurological manifestations can include tremors, chorea, myopathy, and in some susceptible individuals (particularly of Asian descent) periodic paralysis. An association between thyroid disease and myasthenia gravis has been recognized. The thyroid disease, in this condition, is autoimmune in nature and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and the relationship between the two entities is not well understood. Some very rare neurological manifestations that are dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.

Minor ocular (eye) signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare"), extra-ocular muscle weakness, and lid-lag. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). Extra-ocular muscle weakness may present with double vision. In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism.

Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball) which occurs specifically and uniquely in hyperthyroidism caused by Graves' disease (Note that not all exopthalmos is caused by Graves' disease, but when present with hyperthyroidism is diagnostic of Graves disease). This forward protrusion of the eyes is due to immune mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare.^[1]

Thyrotoxic crisis (or thyroid storm) is a rare but severe complication of hyperthyroidism, which may occur when a thyrotoxic patient becomes very sick or physically stressed. Its symptoms can include: an increase in body temperature to over 40 degrees Celsius (104 degrees Fahrenheit), tachycardia, arrhythmia, vomiting, diarrhea, dehydration, coma and death.

Causes

Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions.

The major causes in humans are:

• Graves' disease (the most common etiology with 70-80%)
• Toxic thyroid adenoma
• Toxic multinodular goitre

High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons:

• Inflammation of the thyroid is called thyroiditis. There are a number of different kinds of thyroiditis including Hashimoto's thyroiditis (immune mediated), and subacute thyroiditis (DeQuervain's). These may be initially associated with secretion of excess thyroid hormone, but usually progress to gland dysfunction and thus, to hormone deficiency and hypothyroidism.
• Oral consumption of excess thyroid hormone tablets is possible, as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed "hamburger hyperthyroidism").
• Amiodarone, an anti-arrhythmic drug is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.
• Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.

Diagnosis

A diagnosis may be suspected on history and physical examination, and is confirmed with blood tests.

Measuring the level of thyroid-stimulating hormone (TSH) in the blood is usually all that is required. A low TSH indicates that the pituitary gland is being inhibited by increased levels of T₄ and/or T₃ in the blood, and is therefore a reliable marker of hyperthyroidism. Rarely, a low TSH indicates primary failure of the pituitary, or temporary inhibition of the pituitary due to another illness (euthyroid sick syndrome) and so checking the T₄ and T₃ is still clinically useful.

Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, or anti-thyroid-peroxidase in Hashimoto's thyroiditis—a common cause of HYPOthyroidism—may also contribute to the diagnosis.

Thyroid scintigraphy is a useful test to distinguish between causes of hyperthyroidism, and this entity from thyroiditis.

In addition to testing the TSH levels, many doctors test for T3, Free T3, T4 and/or Free T4 for more detailed results.

The diagnosis of hyperthyroidism is confirmed by blood tests that show a decreased thyroid stimulating hormone (TSH) level and elevated T4 and T3 levels. TSH is a hormone made by the pituitary gland in the brain that tells the thyroid gland how much hormone to make. When there is too much thyroid hormone, the TSH will be low. A radioactive iodine scan (a test that uses injected radioactive iodine to examine the activity of the thyroid gland) will show an enlarged thyroid gland that is over-functioning.

Treatment

The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation.

Temporary medical therapy

Thyrostatics

Thyrostatics are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in UK) and methimazole (used in US), and propylthiouracil. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase, and thus, the formation of tetra-iodothyronine (T₄). Propylthiouracil also works outside the thyroid gland, preventing conversion of (mostly inactive) T₄ to the active form T₃. Because thyroid tissue usually contains a substantial reserve of thyroid hormone, thyrostatics can take weeks to become effective, and the dose often needs to be carefully titrated over a period of months.

A very high dose is often needed early in treatment, but if too high a dose is used persistently, patients can develop symptoms of hypothyroidism.

Beta-blockers

Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety are mediated by increases in beta adrenergic receptors on cell surfaces. Beta blockers are a class of drug which offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety. This doesn't help the underlying problem of excess thyroid hormone, but makes the symptoms much more manageable, particularly as definitive treatment with thryostatic drugs can take a number of months to work. Propranolol in the US, and Metoprolol in the UK, are most frequently used to augment treatment for hyperthyroid patients.^[2]

Permanent treatments

Surgery as an option predates the use of the less invasive radioisotope therapy, but is still required in cases where the thyroid gland is enlarged and causing compression to the neck structures, or the underlying cause of the hyperthyroidism may be cancerous in origin.

Surgery

Surgery (to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult. However, some Graves' disease patients who cannot tolerate medicines for one reason or another, patients who are allergic to iodine, or patients who refuse radioiodine opt for surgical intervention. Also, some surgeons believe that radioiodine treatment is unsafe in patients with unusually large gland, or those whose eyes have begun to bulge from their sockets, claiming that the massive dose of iodine needed will only exacerbate the patient's symptoms.

Radioiodine

In iodine-131 (Radioiodine) radioisotope therapy, radioactive iodine-131 is given orally (either by pill or liquid) on a one-time basis to destroy the function of a hyperactive gland. Patients who do not respond to the first dose are sometimes given an additional radioactive iodine treatment in a larger dose. The iodine given for ablative treatment is different from the iodine used in a scan. Radioactive iodine is given after a routine iodine scan, and uptake of the iodine is determined to confirm hyperthyroidism. The radioactive iodine is picked up by the active cells in the thyroid and destroys them. Since iodine is only picked up by thyroid cells (and picked up more readily by over-active thyroid cells), the destruction is local, and there are no widespread side effects with this therapy. Radioactive iodine ablation has been safely used for over 50 years, and the only major reasons for not using it are pregnancy and breast-feeding.

A common outcome following radioiodine is a swing to the easily treatable hypothyroidism, and this occurs in 78% of those treated for Graves' thyrotoxicosis and in 40% of those with toxic multinodular goiter or solitary toxic adenoma.^[3] Use of higher doses of radioiodine reduces the incidence of treatment failure, with the higher response to treatment consisting mostly of higher rates of hypothyroidism.^[4] There is increased sensitivity to radioiodine therapy in thyroids appearing on ultrasound scans as more uniform (hypoechogenic), due to densely packed large cells, with 81% later becoming hypothyroid, compared to just 37% in those with more normal scan appearances (normoechogenic).^[5]

Thyroid storm

Thyroid storm presents with extreme symptoms of hyperthyroidism. It is treated aggressively with resuscitation measure along with a combination of the above modalities including: an intravenous beta blockers such as propanolol, followed by a thionamide such as methimazole, a iodinated radiocontrast agents or an iodine solution if the radiocontrast agent is not available, and an intravenous steroid such as hydrocortisone.^[6]

Veterinary medicine

Cats

In veterinary medicine, hyperthyroidism is one of the most common endocrine conditions affecting older domesticated cats. Some veterinarians estimate that it occurs in up to 2% of cats over the age of 10.^[7] The disease has become significantly more common since the first reports of feline hyperthyroidism in the 1970s. In cats, one cause of hyperthyroidism tends to be benign tumors, but the reason those cats develop such tumors continues to be researched.

However, recent research published in Environmental Science & Technology, a publication of the American Chemical Society, suggests that many cases of feline hyperthyroidism are associated with exposure to environmental contaminants called polybrominated diphenyl ethers (PBDEs), which are present in flame retardants in many household products, particularly furniture and some electronic products.

The study from which the report was based, was conducted jointly by researchers at the EPA's National Health and Environmental Effects Laboratory and Indiana University. In the study, which involved 23 pet cats with feline hyperthyroidism, PDBE blood levels were three times as high as those in younger, non-hyperthyroid cats. Ideally, PBDE and related endocrine disruptors that seriously damage health would not be present in the blood of any animals or humans.

Most recently, mutations of the thyroid stimulating hormone receptor have been discovered which cause a constitutive activation of the thyroid gland cells. Many other factors may play a role in the pathogenesis of the disease such as goitrogens (isoflavones such as genistein, daidzein and quercertin) and iodine and selenium content in the diet.

The most common presenting symptoms are: rapid weight loss, tachycardia (rapid heart rate), vomiting, diarrhea, increased consumption of fluids (polydipsia) and food, and increased urine production (polyuria). Other symptoms include hyperactivity, possible aggression, heart murmurs, a gallop rhythm, an unkempt appearance, and large, thick nails. About 70% of afflicted cats also have enlarged thyroid glands (goiter).

The same three treatments used with humans are also options in treating feline hyperthyroidism (surgery, radioiodine treatment, and anti-thyroid drugs). Drugs must be given to cats for the remainder of their lives, but may be the least expensive option, especially for very old cats. Radioiodine treatment and surgery often cure hyperthyroidism. Some veterinarians prefer radioiodine treatment over surgery because it does not carry the risks associated with anesthesia. Radioiodine treatment, however, is not available in all areas for cats. The reason is that this treatment requires nuclear radiological expertise and facilities, since the animal's urine, sweat, saliva and stool are radioactive for several days after the treatment, requiring special inpatient handling and facilities usually for a total of 3 weeks (first week in total isolation and the next two weeks in close confinement).^[8] The guidelines for radiation levels vary from state to state; some states such as Massachusetts allow hospitalization for as little as two days before the animal is sent home with care instructions. Surgery tends to be done only when just one of the thyroid glands is affected (unilateral disease); however following surgery, the remaining gland may become over-active. As in people, one of the most common complications of the surgery is hypothyroidism.

Dogs

Hyperthyroidism is very rare in dogs (occurring in less than 1 or 2% of dogs), who instead tend to have the opposite problem: hypothyroidism. When hyperthyroidism does appear in dogs, it tends to be due to over-supplementation of the thyroid hormone during treatment for hypothyroidism. Symptoms usually disappear when the dose is adjusted.

Occasionally dogs will have functional carcinoma in the thyroid; more often (about 90% of the time) this is a very aggressive tumor that is invasive and easily metastasizes or spreads to other tissues (esp. the lungs), making prognosis very poor. While surgery is possible, it is often very difficult due to the invasiveness of the mass in surrounding tissue including the arteries, the esophagus, and windpipe. It may only be possible to reduce the size of the mass, thus relieving symptoms and also allowing time for other treatments to work.

If a dog does have a benign functional carcinoma (appears in 10% of the cases), treatment and prognosis is no different from that of the cat. The only real difference is that dogs tend to appear to be asymptotic, with the exception of having an enlarged thyroid gland appearing as a lump on the neck.

See also

• Carbimazole
• Hypothyroidism
• Goitrogen
• Graves' ophthalmopathy
• Graves' disease
• Subacute lymphocytic thyroiditis

References

1. ^ Faculty of Medicine & Dentistry (2006). "Course-Based Physical Examination - Endocrinology -- Endocrinology Objectives (Thyroid Exam)". Undergraduate Medical Education. University of Alberta. http://www.med.ualberta.ca/education/ugme/clinicaled12/clinskills_endocrinology.cfm?yr=1. Retrieved 2007-01-28. 
2. ^ Geffner DL, Hershman JM (July 1992). "β-Adrenergic blockade for the treatment of hyperthyroidism". The American Journal of Medicine 93 (1): 61–8. doi:10.1016/0002-9343(92)90681-Z. PMID 1352658. 
3. ^ Berglund J, Christensen SB, Dymling JF, Hallengren B (May 1991). "The incidence of recurrence and hypothyroidism following treatment with antithyroid drugs, surgery or radioiodine in all patients with thyrotoxicosis in Malmö during the period 1970-1974". Journal of Internal Medicine 229 (5): 435–42. doi:10.1111/j.1365-2796.1991.tb00371.x. PMID 1710255. 
4. ^ Esfahani AF, Kakhki VR, Fallahi B, et al. (2005). "Comparative evaluation of two fixed doses of 185 and 370 MBq 131I, for the treatment of Graves' disease resistant to antithyroid drugs". Hellenic Journal of Nuclear Medicine 8 (3): 158–61. PMID 16390021. 
5. ^ Markovic V, Eterovic D (September 2007). "Thyroid echogenicity predicts outcome of radioiodine therapy in patients with Graves' disease". The Journal of Clinical Endocrinology and Metabolism 92 (9): 3547–52. doi:10.1210/jc.2007-0879. PMID 17609305. 
6. ^ Tintinalli, Judith (2004). Emergency Medicine: A Comprehensive Study Guide, Sixth edition. McGraw-Hill Professional. p. 1312. ISBN 0071388753. 
7. ^ Shomon, Mary (2004). "Feline Hyperthyroidism: Frequently Asked Questions, Information About Overactive Thyroid Conditions in Cats". http://www.thyroid-info.com/articles/cat-hyper.htm. Retrieved June 24, 2009. ^{[self-published source?]}
8. ^ Little, Susan (2006). "Feline Hyperthyroidism" (PDF). Winn Feline Foundation. http://www.winnfelinehealth.org/Pages/Feline_Hyperthyroidism_Web.pdf. Retrieved June 24, 2009. 

Further reading

• Siraj, Elias S. (June 2008). "Update on the Diagnosis and Treatment of Hyperthyroidism". Journal of Clinical Outcomes Management 15 (6): 298–307. http://www.turner-white.com/memberfile.php?PubCode=jcom_jun08_hyperthyroidism.pdf. Retrieved June 24, 2009. 

Additional images

External links

For Humans

• Patient information: Hyperthyroidism Article at UpToDate
• Merck Manual article about hyperthyroidism

For Felines

• Gina Spadafori (1997-01-20). "Hyperthyroidism: A Common Ailment in Older Cats". The Pet Connection. Veterinary Information Network. http://www.veterinarypartner.com/Content.plx?P=A&S=0&C=0&A=138. Retrieved 2007-01-28. 

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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