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
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