Identification of separate determinants on the thyrotropin receptor reactive with Graves' thyroid-stimulating antibodies and with thyroid- stimulating blocking antibodies in idiopathic myxedema: these determinants have no homologous sequence on gonadotropin receptors

1992 ◽  
Vol 6 (2) ◽  
pp. 168-180 ◽  
Author(s):  
S. Kosugi
Keyword(s):  
Homologous Sequence ◽  
Thyrotropin Receptor ◽  
Gonadotropin Receptors ◽  
Thyroid Stimulating Antibodies ◽  
Idiopathic Myxedema ◽  
Blocking Antibodies

scholarly journals A Case of Subacute Thyroiditis Accompanied by Thyroid Stimulating Antibodies and Thyroid Stimulation-Blocking Antibodies

1997 ◽  
Vol 73 (1) ◽  
pp. 49-54
Author(s):  
Takashi NAGAI ◽  
Youko NAGAI ◽  
Takashi TOMIZAWA ◽  
Tetsuo NEGISHI ◽  
Masami MURAKAMI ◽  
...  
Keyword(s):  
Subacute Thyroiditis ◽  
Thyroid Stimulating Antibodies ◽  
Blocking Antibodies

scholarly journals Comparison of a Bridge Immunoassay with Two Bioassays for Thyrotropin Receptor Antibody Detection and Differentiation

2019 ◽  
Vol 51 (06) ◽  
pp. 341-346 ◽  
Author(s):  
Stephanie Allelein ◽  
Tanja Diana ◽  
Margret Ehlers ◽  
Michael Kanitz ◽  
Derik Hermsen ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Nodular Goiter ◽  
Antibody Detection ◽  
Luciferase Expression ◽  
Thyrotropin Receptor ◽  
Thyrotropin Receptor Antibody ◽  
Highly Sensitive ◽  
Chemiluminescent Immunoassay ◽  
Bridge Technology ◽  
Blocking Antibodies

AbstractA rapid and fully automated chemiluminescent immunoassay for the detection of thyrotropin receptor autoantibodies (TSHR-Ab) based on a bridge technology was compared with two bioassays that measure either stimulating (TSAb) or blocking (TBAb) antibodies for the detection and differentiation of TSHR-Ab. A total of 229 patients with various thyroid disorders [151 with Graves’ disease (GD), 35 with Hashimoto’s thyroiditis (HT), 32 with nodular goiter, and 11 with thyroid cancer] were included. The bridge immunoassay was performed according to the manufacturer’s instructions (cut-off>0.55 IU/l). TSAb and TBAb were measured with reporter bioassays. Blocking activity was defined as percent inhibition of luciferase expression relative to induction with bovine TSH alone (cut-off>34% inhibition). TSAb was reported as percentage of specimen-to-reference ratio (> 140 SRR%). The 3 TSHR-Ab assays were negative in all patients with benign euthyroid nodular goiter and differentiated thyroid cancer. In contrast, in all patients with GD, irrespective of the disease duration, TSHR-Ab positivity was present in 127 of 151 (84%) and 140 (93%) for the bridge assay and TSAb bioassay, respectively (p<0.001). Fifteen of 151 (10%) GD samples were positive in the TSAb bioassay but negative in the bridge assay. The bridge assay and the TSAb bioassay correlated positively (r=0.39, p<0.0001) in patients with GD. Both assays detected TSHR-Ab in all ten untreated hyperthyroid patients with GD. In GD patients with a duration of less than six months, 27/29 (93%) and 28 (97%) were TSHR-Ab positive with the bridge and TSAb bioassay, respectively. In comparison, TSHR-Ab were present in two of 35 (6%) and five (14%) HT patients with the bridge and TSAb bio-assay, respectively. TSHR blocking antibodies were present in one (3%) patient with HT and in two (1%) patients with GD; these two GD patients were also bridge assay positive but TSAb bioassay negative. In conclusion, the bridge immunoassay and both bioassays are highly sensitive for the detection of TSHR-Ab. The bridge assay is, however, also positive in the presence of TSHR blocking antibodies detected in a TBAb bioassay.

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