Carbimazole and the Autoimmune Response in Graves' Disease

Microsomal antibodies and antibodies directed toward the receptor for thyroid-stimulating hormone (TSH) decreased in parallel while patients with Graves' disease were taking carbimazole, whereas no significant changes were observed during treatment with placebo or propranolol. The changes in autoantibody levels during carbimazole treatment were independent of changes in serum thyroxine and could have been due to a direct effect of the drug on autoantibody synthesis. Evidence for this suggestion was provided when low doses of methimazole (the active metabolite of carbimazole) were found to inhibit thyroid-autoantibody production in cultured lymphocytes. Since thyroid lymphocytes are probably a major site of thyroid-antibody synthesis in Graves' disease and methimazole is concentrated in the thyroid during treatment, a local action of the drug on antibody production seems likely. This possibility could be important in the use of carbimazole to control hyperthyroidism. (N Engl J Med. 1980; 303:302–7.) METHIMAZOLE, the active metabolite of carbimazole, 1 is known to be concentrated in the thyroid 2 and to inhibit synthesis of thyroid hormone by impairing the conversion of iodine to organic compounds. 3 Previous studies have shown a reduction in the extent of lymphocytic infiltration of the thyroid in patients in whom Graves' disease is treated with carbimazole before operation. 4 Since thyroid lymphocytes are probably a major site of thyroid-autoantibody synthesis in Graves' disease, 5 , 6 this reduction in lymphocytic infiltration may be the result of a local action of the drug. Such an effect could be important in treatment since autoantibodies directed toward the . . .