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February 2001
Vol. 4, No. 2, p. 72,
disease and disorders
BY FELICIA WILLIS
A Graves defect
Figure 1. Schematic representation of Caco-2 permeablility assay.
The gland scheme. The pituitary (anterior lobe) produces thyroid stimulating hormone (TSH). In Graves’ disease, autoantibodies are produced to TSH receptors on the thyroid cells. The antibodies stimulate the thyroid gland to overproduce thyroid hormone.
Robert Graves, Irish physician and leader of the Dublin School of Diagnosis, was one of the first physicians to fully describe what was originally referred to as exophthalmic goiter, now called Graves’ disease. The leading cause of hyperthyroidism, Graves’ disease occurs when there is a defect in the immune system that causes the production of autoantibodies to the TSH (thyroid stimulating hormone) receptor located on the surface of thyroid cells. These antibodies stimulate the thyroid, causing enlargement of the gland and overproduction of thyroid hormone. The precise trigger of the disease is unknown, but studies indicate that it may be either a genetic or immune system factor. The Graves’ gene in DNA has not yet been identified.

Symptoms of Graves’ disease include protruding eyes, weight loss, increased appetite, nervousness, restlessness, heat intolerance, sweating, fatigue, muscle cramps, tremor, frequent bowel movements, menstrual irregularities, goiter, rapid heartbeat, changes in sex drive, enlarged thyroid gland, heart palpitations, and blurred or double vision.

There are several elements contributing to the development (but not the cause) of Graves’ disease. There is a genetic predisposition to autoimmune disorders. Infections and stress play a part as well. Graves’ disease may have its onset after an external stressor and has also been known to follow a viral infection or pregnancy. Although Graves’ disease is not curable, it is a completely treatable disease.

The primary treatment for Graves’disease is to control the overactive thyroid gland. There are three standard ways of treating Graves’ disease but choice of treatment varies from country to country and physician to physician. Treatment usually depends on factors such as age, degree of illness, and patient preference. The first choice of treatment is with antithyroid drugs such as propylthiouracil and methimazole, which make it difficult for the thyroid to use iodine and thus hinder production of active thyroid hormone. The second treatment option is radioactive iodine (I-131), which actually destroys part or all of the thyroid, rendering the gland incapable of overproducing the hormone. The last treatment option is subtotal thyroidectomy, in which most of the thyroid gland is surgically removed and thus made also incapable of overproducing the hormone. Thyroid surgery can result in hypothyroidism, requiring long-term treatment with l-thyroxine. Beta-blockers are used to treat symptoms including rapid heart rate, sweating, and anxiety until hyperthyroidism is controlled. Prednisone is often prescribed to relieve severe inflammation. The eye problems of Graves’ disease usually resolve with treatment of the underlying disorder.

The prognosis for Graves’ disease patients is extremely favorable. Most patients respond well to treatment, but lifelong observation by a healthcare professional is important because possibly serious complications are associated with the disease. Antithyroid medications may also cause side effects. The more serious complications of prolonged, untreated, or improperly treated Graves’ disease include a weakened heart muscle, which can lead to heart failure, osteoporosis, or possible severe emotional disorders.

For further information
The American Thyroid Association: www.thyroid.org.
The Thyroid Foundation of America: www.tsh.org.

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