Kurzfassung

Autoantibodies (Abs) to the thyroid stimulating hormone receptor (TSHR) are responsible for the clinical phenotype of Graves’ hyperthyroidism (GD) and are specific biomarkers of this autoimmune thyroid disease (AITD). TSHR-Abs can also be present in a minority of patients with Hashimoto’s thyroiditis (HT). TSHR Abs can be measured either via competitive-binding immunoassays or with cell-based bioassays. Antibody binding assays only report the presence or absence of TSHR binding inhibitory...Autoantibodies (Abs) to the thyroid stimulating hormone receptor (TSHR) are responsible for the clinical phenotype of Graves’ hyperthyroidism (GD) and are specific biomarkers of this autoimmune thyroid disease (AITD). TSHR-Abs can also be present in a minority of patients with Hashimoto’s thyroiditis (HT). TSHR Abs can be measured either via competitive-binding immunoassays or with cell-based bioassays. Antibody binding assays only report the presence or absence of TSHR binding inhibitory immunoglobulins (TBII) and their concentrations but do not indicate their functional activity. Bioassays, in contrast, indicate whether TSHR-Abs have stimulatory (TSAb) or blocking (TBAb) activity. Recent and numerous data demonstrate the clinical utility of TSHR-Abs bioassays in the diagnosis and management of patients with GD and in the characterization of AITD patients with hyper- and hypothyroidism. While the usefulness of TBII for the diagnosis of GD is generally accepted and well-established in the clinical routine, repeated measurements of TBII or their use in outcome prediction was and still is a matter of debate.
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