[Thyroid hormone autoantibodies in Hashimoto's disease and Graves' disease].

We previously reported the presence of thyroid hormone autoantibodies (THAA) in the sera from three (2 Hashimoto's thyroiditis, 1 Hashimoto's thyroiditis suspected) out of four sisters in a family and one patient with Graves' disease during treatment with methimazole (MMI). According to the investigations of the binding of labelled thyroid hormones, endogenous and/or therapeutic thyroid hormones interfered with their binding with THAA. This interference, however, was excluded when the sera were acidified with a 0.05M glycine-HCl buffer (pH 2.1) and all the liberated thyroid hormones were absorbed into dextrancoated charcoal. In this study, the specific binding of the tracer thyroid hormone to gamma-globulin was examined in hormone-stripped sera from patients with Hashimoto's disease (pretreatment n = 29; L-T4 treatment n = 9) and Graves' disease (pretreatment n = 21; MMI or propyl-thiouracil (PTU) treatment n = 22; MMI or PTU treatment after 131I therapy n = 8) under conditions in which the difference of the concentration of gamma-globulin in each case did not influence the binding. None of the patients examined had increased binding of 125I-T3 with their gamma-globulin. Elevated binding of 125I-T4 was found in sera obtained from 3 patients (2 pretreatment, 1 L-T4 treatment) with Hashimoto's disease and 7 patients (1 pretreatment, 4 MMI or PTU treatment, 2 MMI or PTU treatment after 131I therapy) with Graves disease. Seven (2 Hashimoto's disease, 5 Graves disease) out of these 10 patients with anti-T4 autoantibodies had antibodies against thyroglobulin (Tg) as measured by the hemagglutination method. Titers of anti-T4 autoantibodies and anti-Tg antibodies did not correlate. In Graves disease, anti-T4 autoantibodies were detected during the treatments in sera from 5 (3 MMI or PTU treatment, 2 MMI or PTU treatment after 131I therapy) out of 16 patients (10 MMI or PTU treatment, 6 MMI or PTU treatment after 131I therapy) who had anti-Tg antibodies. On the other hand, anti-T4 autoantibodies prior to the medication could not be found in sera from 5 patients with positive anti-Tg antibodies. From these results, it is suggested that antithyroid drugs and/or 131I therapy might induce the production of THAA in patients with Graves disease through the deterioration of immunological tolerance and/or through the modification of the Tg molecule.