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Causes

By Mayo Clinic staff

Your thyroid gland produces two main hormones — thyroxine and triiodothyronine (T-3). These hormones circulate in your bloodstream and help regulate your metabolism. They maintain the rate at which your body uses fats and carbohydrates, help control your body temperature, influence your heart rate, and help regulate the production of proteins. Your thyroid gland also produces calcitonin — a hormone that helps regulate the amount of calcium in your blood.

Your pituitary gland and hypothalamus control the rate at which these hormones are produced and released. The process begins when the hypothalamus — an area at the base of your brain that acts as a thermostat for your whole system — signals your pituitary gland to make a hormone known as thyroid-stimulating hormone (TSH). Your pituitary gland — also located at the base of your brain — releases a certain amount of TSH, depending on how much thyroxine and T-3 are in your blood. Your thyroid gland, in turn, regulates its production of hormones based on the amount of TSH it receives from the pituitary gland.

Having a goiter doesn't necessarily mean that your thyroid gland isn't working normally. Even when it's enlarged, your thyroid may produce normal amounts of hormones. It might also, however, produce too much or too little thyroxine and T-3.

A number of factors can cause your thyroid gland to enlarge. Among the most common are:

  • Iodine deficiency. Iodine, which is essential for the production of thyroid hormones, is found primarily in seawater and in the soil in coastal areas. In the developing world, people who live inland or at high elevations are often iodine-deficient and can develop goiter when the thyroid enlarges in an effort to obtain more iodine. The initial iodine deficiency may be made even worse by a diet high in hormone-inhibiting foods, such as cabbage, broccoli and cauliflower. Although a lack of dietary iodine is the main cause of goiter in many parts of the world, this is not the case in countries where iodine is routinely added to table salt and other foods.
  • Graves' disease. Goiter can sometimes occur when your thyroid gland produces too much thyroid hormone (hyperthyroidism). In Graves' disease, antibodies produced by your immune system mistakenly attack your thyroid gland, causing it to produce excess thyroxine. This overstimulation causes the thyroid to swell.
  • Hashimoto's disease. Goiter can also result from an underactive thyroid (hypothyroidism). Like Graves' disease, Hashimoto's disease is an autoimmune disorder. But instead of causing your thyroid to produce too much hormone, Hashimoto's damages your thyroid so that it produces too little. Sensing a low hormone level, your pituitary gland produces more TSH to stimulate the thyroid, which then causes the gland to enlarge.
  • Multinodular goiter. In this condition, several solid or fluid-filled lumps called nodules develop in both sides of your thyroid, resulting in overall enlargement of the gland.
  • Solitary thyroid nodules. In this case, a single nodule develops in one part of your thyroid gland. Most nodules are noncancerous (benign) and don't lead to cancer.
  • Thyroid cancer. Thyroid cancer is far less common than benign thyroid nodules. Cancer of the thyroid often appears as an enlargement on one side of the thyroid.
  • Pregnancy. A hormone produced during pregnancy, human chorionic gonadotropin (HCG), may cause your thyroid gland to enlarge slightly.
  • Inflammation. Thyroiditis is an inflammatory condition that can cause pain and swelling in the thyroid.
References
  1. Thyroid disorders overview. The Hormone Foundation. http://www.hormone.org/Thyroid/overview.cfm. Accessed Nov. 3, 2010.
  2. Goiter. American Thyroid Association. http://www.thyroid.org/patients/patient_brochures/goiter.html. Accessed Nov. 3, 2010.
  3. Ross DS. Clinical manifestations and evaluation of obstructive or substernal goiter. http://www.uptodate.com/home/index.html. Accessed Nov. 3, 2010.
  4. Jameson JL, et al. Disorders of the thyroid gland. In: Fauci AS, et al. Harrison's Principles of Internal Medicine. 17th ed. New York, N.Y.: The McGraw-Hill Companies: 2008. http://www.accessmedicine.com/content.aspx?aID=2877579&searchStr=goiter. Accessed Nov. 3, 2010.
  5. Lal G, et al. Thyroid, parathyroid and adrenal. In: Brunicardi FC, et al. Schwartz's Principles of Surgery. 9th ed. New York, N.Y.: The McGraw-Hill Companies; 2010. http://www.accessmedicine.com/content.aspx?aID=5027231&searchStr=goiter#5027231. Accessed Nov. 3, 2010.
  6. Simple nontoxic goiter. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merck.com/mmpe/sec12/ch152/ch152i.html?qt=goiter&alt=sh. Accessed Nov. 3, 2010.
  7. Iodine deficiency. American Thyroid Association. http://www.thyroid.org/patients/patient_brochures/iodine_deficiency.html. Accessed Nov. 5, 2010.
  8. Hyperthyroidism. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merck.com/mmpe/sec12/ch152/ch152e.html. Accessed Nov. 5, 2010.
  9. Approach to the patient with a thyroid nodule. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merck.com/mmpe/sec12/ch152/ch152b.html. Accessed Nov. 5, 2010.
  10. Hypothyroidism. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merck.com/mmpe/sec12/ch152/ch152f.html. Accessed Nov. 5, 2010.
  11. Thyroid diseases. Lab Tests Online. http://www.labtestsonline.org/understanding/conditions/thyroid.html. Accessed Nov. 3, 2010.
  12. Ross DS. Treatment of obstructive or substernal goiter. http://www.uptodate.com/home/index.html. Accessed Nov. 3, 2010.
DS00217 Jan. 8, 2011

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