Three patients with
Graves' disease and one patients with primary
myxedema had serum TSH-binding
immunoglobulins of high affinity detected by the TSH binding inhibition
immunoglobulin (TBII) assay. These IgGs bound 61%, 33%, 60% and 53% of radiolabeled TSH, respectively, higher than the maximal specific binding (25%) in the TBII assay. Such binding was detected even in the absence of
TSH receptor with only small differences in the precipitable radioactivity (61%, 28%, 61%, 54%, respectively, in comparison with the assay non-specific binding 11.3%). The 125I-bTSH binding of IgGs was competitively inhibited by the addition of bTSH, but not inhibited by hTSH. Moreover
IgG binding to bTSH was not inhibited by the addition of serial dilutions of TBII positive pooled Graves'
IgG (0.1-10 mg/ml) from different untreated patients. The titers of these TSH binding
antibodies were not changed during the treatment of
Graves' disease. Following guinea pig fat cell membrane receptor purification, the
IgG of one patient with
Graves' disease revealed TBII activity of 43.7% inhibition of 125I-bTSH binding to the
TSH receptor without binding activity of 125I-bTSH in the absence of the
TSH receptor. These studies suggest that anti-TSH
antibodies and
TSH receptor antibodies are present independent of one another in sera of some patients with autoimmune
thyroid diseases and anti-TSH
antibodies result in false TBII assay results.