This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by GAMSTEDT, A. Articles by KARLSSON, A. Search for Related Content PubMed PubMed Citation Articles by GAMSTEDT, A. Articles by KARLSSON, A.

Methimazole, but not Betamethasone, Prevents¹³¹I Treatment-Induced Rises in Thyrotropin Receptor Autoantibodies in Hyperthyroid Graves' Disease^*

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.

This article has been cited by other articles:

				F. Traisk, L. Tallstedt, M. Abraham-Nordling, T. Andersson, G. Berg, J. Calissendorff, B. Hallengren, P. Hedner, M. Lantz, E. Nystrom, et al. Thyroid-Associated Ophthalmopathy after Treatment for Graves' Hyperthyroidism with Antithyroid Drugs or Iodine-131 J. Clin. Endocrinol. Metab., October 1, 2009; 94(10): 3700 - 3707. [Abstract] [Full Text] [PDF]

				P. Laurberg, G. Wallin, L. Tallstedt, M. Abraham-Nordling, G. Lundell, and O. Torring TSH-receptor autoimmunity in Graves' disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study Eur. J. Endocrinol., January 1, 2008; 158(1): 69 - 75. [Abstract] [Full Text] [PDF]

				D. S. Cooper Antithyroid Drugs in the Management of Patients with Graves' Disease: An Evidence-Based Approach to Therapeutic Controversies J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3474 - 3481. [Full Text] [PDF]