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Hyperthyroidism

Last Updated: Mar 1, 2019

Overview

Hyperthyroidism occurs when the thyroid gland malfunctions and produces too much thyroid hormone. This condition is also known as overactive thyroid or thyrotoxicosis. An abnormal enlargement of the thyroid (goiter) develops in certain forms of hyperthyroidism.

thyroid gland

The thyroid gland is located in the anterior area of the neck and uses iodine atoms to produce two hormones, triiodothyronine (T3) and thyroxine (T4). T4 is produced and then converted to T3, the more active form of thyroid hormone. When these hormones are released in the blood, they affect numerous body functions, including metabolism, body temperature, body weight, heart rate, breathing, nervous system function, and muscle function. When a disorder makes the thyroid produce too much hormone, the body’s metabolism becomes abnormally accelerated.

Hyperthyroidism occurs in approximately 1% of the United States population. Most patients respond well to proper treatment although some experience potentially serious complications.

Causes and Risk Factors

Normally, an area of the brain called the hypothalamus signals the pituitary gland to produce thyroid-stimulating hormone (TSH) - a substance that regulates and maintains normal levels of thyroid hormones. When thyroid hormone levels are low, the pituitary releases TSH, which stimulates the thyroid to produce more T4. Conversely, when thyroid hormone levels are high, the pituitary decreases TSH and less T4 is produced. Certain diseases disrupt this system and cause the thyroid to produce excessive levels of T4 on its own. The most common causes of hyperthyroidism are Graves’ disease, toxic adenoma, toxic multinodular goiter, and thyroiditis.

  • Graves’ disease. Graves’s disease (or toxic diffuse goiter) is the most common cause of hyperthyroidism. This disease is an autoimmune disorder in which the immune system produces antibodies that target thyroid cells resulting in excess T4 production. A normal immune system only attacks foreign substances, like germs; however, in Graves’ disease, the immune system erroneously attacks the thyroid. Sometimes the attack includes the area behind the eyes (Graves ophthalmopathy) or the skin on the lower legs (Graves’ dermopathy). Graves’ disease is more common in women than men and it runs in families. The underlying cause of Graves’ disease is unknown.
  • Overactive thyroid nodules. Thyroid nodules (adenomas) are growths or lumps (usually noncancerous) that occur in 3-7% of the U.S. population. For unknown reasons, some thyroid nodules become overactive and release excess T4. Toxic adenoma is a single noncancerous overactive thyroid nodule. Toxic multinodular goiter refers to multiple overactive nodules.
  • Thyroiditis. Inflammation of the thyroid is called thyroiditis. The etiology of thyroiditis is often unknown. Autoimmune, viral, or drug-induced factors may be involved. Subacute thyroiditis is a particularly painful form of this disorder. Sometimes women develop thyroiditis after pregnancy (postpartum thyroiditis).
  • Iodine. Because the thyroid uses iodine to synthesize thyroid hormones, people who consume excess iodine (found in certain medications, dietary supplements, and foods) may develop hyperthyroidism.
  • Pituitary adenoma. A noncancerous growth (adenoma) of the pituitary may secrete excess TSH resulting in hyperthyroidism.
  • Thyroid medication. Excessive use of thyroid medication, used to treat low thyroid function, elevates the blood level of thyroid hormone above normal.

Symptoms

hypothalamus and pituitary gland in brain cross section

The most common symptoms of hyperthyroidism include:

  • Rapid heart rate (tachycardia)
  • Weight loss
  • Shortness of breath
  • Sweating
  • Increased sensitivity to heat
  • Nervousness and irritability
  • Fatigue
  • Muscle weakness
  • Enlargement of the thyroid
  • Changes in menstrual patterns
  • Increased bowel movement frequency
  • Skin thinning
  • Hair brittleness
  • Sleep difficulty.

Complications

Complications that may arise as a consequence of hyperthyroidism include:

  • Rapid, irregular heart rhythms
  • Congestive heart failure (when the heart inadequately pumps blood to the rest of the body)
  • Osteoporosis (weak, brittle bones) resulting from excess thyroid hormone’s interference with the bones’ absorption of calcium
  • Graves’ ophthalmopathy (eye protrusion, redness, swelling, tearing, sensitivity to light, and dryness)
  • Graves dermopathy (redness and swelling of the skin on the lower legs)
  • Thyrotoxic crisis, also called thyroid storm (a severe, life-threatening form of hyperthyroidism associated with fever, sweating, severe tachycardia, hypertension, heart failure, delirium, abdominal pain, and coma).

Diagnosis

The symptoms of hyperthyroidism may resemble other disorders, making the disease difficult to diagnose on the basis of symptoms alone. Additionally, symptoms are often diminished or absent in elderly patients.

Patients with hyperthyroidism may display a tremor, overactive reflexes, eye changes, and warm, sweaty skin. An enlarged thyroid is not always present.

Blood tests detect high levels of thyroid hormones T3 and T4 and a low level of TSH. Other blood tests detect the specific anti-thyroid antibody present in patients with Graves’ disease. You can even order a home thyroid test online, which allows you to collect and mail a small sample of your blood for quick lab results (but remember to share these with your healthcare provider afterward).

An ultrasound creates images of the thyroid to check for abnormal growths. A thyroid radioiodine uptake test is a type of scan that helps determine the underlying cause of the disease.

Treatment

  • Radioactive iodine therapy destroys the thyroid gland over several months. After treatment, the thyroid becomes underactive (hypothyroidism), so patients are then prescribed thyroid hormone replacement medication, such as levothyroxine.
  • Anti-thyroid medications (such as propylthiouracil or methimazole) suppress the thyroid’s production of hormones. The course of treatment works gradually and patients often need to continue the medication for a year or more. Following treatment, patients usually need thyroid hormone replacement. Liver damage is a potentially serious adverse effect of anti-thyroid medications.
  • Beta blockers are medications that slow the heart rate and lower blood pressure. Adverse effects include dizziness and fatigue.
  • Thyroidectomy, surgery to remove the thyroid gland, is rarely used to treat hyperthyroidism. Thyroidectomy is reserved for those patients who are not candidates for radioactive iodine or anti-thyroid medication.
  • Graves’ ophthalmopathy may be treated with steroid medications that reduce swelling behind the eyes, or surgery to remove a piece of orbital bone and relieve pressure on the eyes. Sometimes, eye muscle surgery is performed to realign the eyeballs and correct double vision.

There are no known methods to prevent naturally occurring forms of hyperthyroidism. However, patients who use thyroid medication should have their thyroid hormone levels checked at least once a year to avoid hyperthyroidism caused by taking too much medication.

Sources

  • Mandel SL, Larsen PR, Davies TF. Chapter 12. Thyrotoxicosis. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. Williams Textbook of Endocrinology, 12e. Philadelphia, PA: Elsevier Saunders; 2011.
  • Hyperthyroidism. National Endocrine and Metabolic Diseases Information Service (NEMDIS) website. http://endocrine.niddk.nih.gov/pubs/hyperthyroidism/index.aspx. Accessed May 13, 2014.
  • Hyperthyroidism (overactive thyroid). Mayo Clinic website. http://www.mayoclinic.org/diseases-conditions/hyperthyroidism/basics/definition/con-20020986. Accessed May 13, 2014.

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Tina Shahian, PhD

Tina is a writer for Innerbody Research, where she has written a large body of informative guides about health conditions.

PROFESSIONAL & EDUCATIONAL BACKGROUND

A communication specialist in life science and biotech subjects, Tina’s successful career is rooted in her ability to convey complex scientific topics to diverse audiences. Tina earned her PhD in Biochemistry from the University of California, San Francisco and her BS degree in Cell Biology from U.C. Davis. Tina Shahian’s Linkedin profile.

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