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Thyroid Response, Especially to Thyrotropin-Binding Inhibitory Immunoglobulins, in Euthyroid Relatives of Patients with Graves' Disease: A Clinical Follow-Up

Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University Fukuoka
Kuma Hospital (K.K.), Kobe; the Department of Nuclear Medicine, Kyoto University, School of Medicine (K.K., A.H., J.K.) Kyoto
the First Department of Internal Medicine, Faculty of Medicine, Nagasaki University (S.N.) Nagasaki, Japan
the Department of Internal Medicine School of Medicine, University of California-Davis (L.F.K.) Sacramento, California 95817

Address requests for reprints to: Dr. Hajime Tamai, Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University 60, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812, Japan.

Three hundred and fifty-three euthyroid relatives of Graves' disease patients were tested for TSH binding inhibitory immunoglobulins (TBII). Eighteen had elevated levels of TBII, and 232 who had negative TBII levels also agreed to be followed for a period of 6–30 months. TBII was chosen as the critical screening measurement for this study, rather than thyroid-stimulating antibodies (TSAb) and thyroid-stimulating blocking antibodies (TSBAb), because of the availability and ease of use of TBII RIA kits. Eleven of the 18 subjects with elevated TBII were T₃ nonsuppressible (group I), and 10 of the 11 were TRH unresponsive. Nine of these 10 subjects showed TSH levels below 0.05 mU/L. The remaining 7 subjects were T₃ suppressible and TRH responsive (group II). Alterations in thyroid status occurred in 8 of the 11 subjects in group I during follow-up. One developed hypothyroidism, and 7 became hyperthyroid. The hypothyroid subject had initial titers of TBII, TSAb, and TSBAb that were markedly elevated, and TSAb disappeared when she became hypothyroid. Six of the 7 subjects who developed hyperthyroidism had elevated TSAb and negative TSBAb titers while they were euthyroid. All 7 subjects in group I I remained euthyroid during the follow-up period. Only 2 of the 232 relatives who initially had negative TBII titers became hyperthyroid during the follow-up period. The results indicate that euthyroid relatives with a family history of Graves' disease who have elevated TBII levels and suppressed basal serum TSH concentrations have a much higher potential to develop hyper-thyroidism than those who have normal or negative TBII levels.

Received October 3, 1989.