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Graves' disease

Graves-Basedow disease is a form of thyroiditis, an autoimmune disorder that stimulates the thyroid gland, being the most common cause of hyperthyroidism (overactivity of the thyroid). Also known in the English-speaking world simply as Graves' disease, it occurs most frequently in women (8:1 compared to men) of middle age. Symptoms include fatigue, weight loss and rapid heart beat. Because similar antibodies to those stimulating the thyroid also affect the eye, eye symptoms are also commonly reported. Treatment is with medication that reduces the production of thyroid hormone (thyroxin), surgery thyroidectomy or with radioactive iodine if refractory. more...

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Christina Rossetti famously suffered from this disease in later life.

Signs and symptoms

Graves-Basedow disease is a disorder characterized by a triad of hyperthyroidism, goitre, and exophthalmos (bulging eyeballs).

Due to the many physiological actions of thyroid hormone, many symptoms and signs are linked to Graves' disease:

  • Cardiac: cardiac arrhythmias (especially atrial fibrillation), tachycardia (increased heart rate), collapsing pulse and widened pulse pressure (difference between systolic and diastolic BP) and congestive cardiac failure with peripheral edema, ascites, anasarca.
  • Endocrine: weight loss in the presence of increased appetite, intolerance to heat, elevated basal metabolic rate
  • Dermatological: profuse sweating, thyroid acropachy (clubbing) of the fingernails, onycholysis (fingernail destruction), palmar erythema, pretibial myxedema (3 to 5% of Graves' patients, not to be confused with the myxedema of hypothyroidism)
  • Neurological: tremor (especially noticeable on extending the arms), apprehension, weakness, headache, proximal myopathy (difficulty rising from a chair or squatting position) and hyperactive deep tendon reflexes
  • Gastrointestinal: diarrhea (common), vomiting (rare)
  • Ophthalmological: thyroid eye disease (TED) characteristic of Graves disease include lid retraction (Dalrymple sign) above the superior corneoscleral limbus, lid lag (von Graefe's sign), proptosis or forward displacement of the globes, periorbital swelling and chemosis.

Extremely manifested disease that can sometimes be life-threatening is called the thyroid storm.


On the basis of the signs and symptoms, thyroid hormone (thyroxine or T4, triiodothyronine or T3) and thyroid-stimulating hormone (TSH) are determined in the medical laboratory. Free T4 and Free T3 is markedly elevated, while TSH is suppressed due to negative feedback. An elevated protein-bound iodine level may be detected. A large goiter is sometimes seen on X-rays.

Thyroid-stimulating antibodies may be detected serologically.


Most features are due to the production of autoantibodies that bind to the TSH receptor, which is present on the follicular cells of the thyroid (the cells that produce thryoid hormone). These antibodies activate the cells in the same fashion as TSH itself, leading to an elevated production of thyroid hormone.

The infiltrative opthalmopathy (thyroid eye disease) that is frequently encountered has been explained by the expression of the TSH receptor on retroorbital tissue.

The exact cause of antibody production is not known. Viral infection may trigger antibodies against its epitopes, which cross-react with the human TSH receptor. There appears to be a genetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.


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Administration of thyroxine in treated Graves' disease - Tips from Other Journals
From American Family Physician, 9/1/91

Hyperthyroidism in patients with Graves' disease is believed to result from the production of autoantibodies that bind and overstimulate thyroid-stimulating hormone (TSH) receptors. While antithyroid medication, surgery and radioactive iodine are all effective in the treatment of hyperthyroidism caused by Graves' disease, each method has significant limitations or possible side effects. Antithyroid drugs, such as propylthiouracil or methimazole, induce remission, but recurrence is common after discontinuation of therapy. Radioactive-iodine therapy or thyroidectomy usually causes hypothyroidism, which requires lifelong hormonal replacement therapy.

Researches examining other treatment strategies are focusing on suppressing TSH secretion by reducing the levels of autoantibodies to the TSH receptors. Somewhat paradoxically, this strategy may involve adding thyroxine to the treatment regimen of hyperthyroid patients. Hashizume and colleagues conducted a study to determine if administration of thyroxine could decrease the levels of antibodies to TSH receptors in patients with Graves' disease after they become euthyroid during treatment with methimazole.

The three-year study included 109 patients with hyperthyroidism caused by Graves' disease. The patients ranged in age from 17 to 58 years (mean age: 39 years). The patients first received 30 mg of methimazole daily for six months. All of the patients were euthyroid after six months. Sixty patients were then given 100 [mu]g of thyroxine and 10 mg of methimazole daily, and 49 were given placebo and 10 mg of methimazole daily. Levels of antibodies to TSH receptors were measured during treatment.

After 18 months, methimazole was discontinued. At that time, the TSH receptor antibody levels were more than eight times lower in the patients who had received thyroxine. Within three years after discontinuation of methimazole, 2 percent of the patients receiving thyroxine and 35 percent of the patients receiving placebo had recurrences of hyperthyroidism. The study findings indicate that the administration of thyroxine during antithyroid treatment significantly decreases the levels of antibodies to TSH receptors in patients with Graves' disease, therefore contributing to a delay in the recurrence of hyperthyroidism.

In an accompanying editorial, Ladenson points out that the study by Hashizume provides new evidence supporting the idea of combining antithyroid drug therapy and thyroid hormone therapy to maintain stable thyroid status and to prevent hypothyroidism that may result from the administration of an antithyroid drug in patients with Graves' disease. (New England Journal of Medicine, April 4, 1991, vol. 324, pp. 947, 989.)

COPYRIGHT 1991 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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