[Studies on the radioreceptor assay of TSH: the properties of TSH-binding inhibitor immunoglobulins (TBII) in patients with Hashimoto's thyroiditis (author's transl)]

Abstract

TSH-binding inhibitor immunoglobulins (TBII) have been detected not only in patients with Graves' disease but also in those with Hashimoto's thyroiditis by using the radioreceptor assay of TSH. In the present study, the properties of TBII in patients with Hashimoto's thyroiditis are discussed. Two (7%) of 29 patients with Hashimoto's thyroiditis had detectable levels of TBII in their gamma-globulin fractions. Both patients were untreated and clinically hypothyroid. One of them had no goiter, and her thyroidal 99mTc uptake was 0% (normal range: 0.4 approximately 3.0%). Despite having potent TSH-binding inhibitor activity in the TSH radioreceptor assay, her serum or its IgG fraction (H-IgG) did not contain any significant anti-TSH antibody, LATS, LATS-protector or human thyroid adenylate cyclase (AC) stimulating activity. This H-IgG inhibited both human thyroid AC stimulation and c-AMP increase in mice thyroid glands induced by TSH or LATS. Furthermore, her serum caused significant inhibition of 131I-release by LATS in a McKenzie mouse bioassay. The present study demonstrates that the serum of one patient with Hashimoto's thyroiditis contained antibodies which 1) blocked the binding of lablled TSH to the receptor, 2) had no thyroid-stimulating activity by themselves, and 3) inhibited AC stimulation by TSH. Such antibodies may cause unresponsiveness to TSH stimulation, hypothyroidism, and, if this state persists for a long time, eventually may result in atrophy of the thyroid tissue. Further, these data indicate that TBII detected by the TSH radioreceptor assay did not always show thyroid stimulating activities.