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Journal of Clinical Endocrinology & Metabolism Vol. 62, No. 4 773-777
doi:10.1210/jcem-62-4-773
Copyright © 1986 by the Endocrine Society.
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Methimazole, but not Betamethasone, Prevents131I Treatment-Induced Rises in Thyrotropin Receptor Autoantibodies in Hyperthyroid Graves' Disease*

ANDERS GAMSTEDT, BENGT WADMAN and ANDERS KARLSSON

Departments of Internal Medicine, Regional Hospital Orebro University Hospital Uppsala, Sweden

Address all correspondence and requests for reprints to: Anders Gamstedt, M.D., Department of Internal Medicine, Regional Hospital,S–701 85 Orebro, Sweden.

The effects of methimazole or betamethasone therapy on the TSH receptor antibody response to radioiodine therapy were compared in a prospective randomized study of 60 patients with hyperthyroidism due to Graves' disease. The patients were followed for 1 yr after treatment with 131I. Twentythree patients received 131I alone, 17 were treated with methimazole for 2 months before and 3 months after 131I therapy, and 20 patientswere treated with betamethasone for 3 weeks before and 4 weeks after 131I therapy. 131I induced a transient rise in the meanserum level of TSH receptor autoantibodies, measured as TSH; binding inhibitory immunoglobulin (TBII), but in patients receiving methimazole treatment, no such rise occurred. In the betamethasone-treated patients, TBII increased similarly to that in patients treated with 131Ialone. In addition, in patients given betamethasone, there was an early decrease in total serum immunoglobulin G, which persisted throughout the follow-up period. In the other 2 groups, no changes in total immunoglobulin G were found.

The results demonstrate that in hyperthyroid Graves' disease, TBII, production is influenced by therapy. Methimazole abolished the 131I-induced increase in TBII, whereas betamethasone did not have such an inhibitory effect.

* This work was supported by the Swedish Medical Research Council(Grant 4996); Glaxa Lakenedel AB, Sweden; and the Orebro County Research Fund.

Received August 8, 1985.




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Copyright © 1986 by The Endocrine Society