Thyroid-stimulating hormone-receptor autoantibodies normally causes hyperthyroidism. However, they might have blocking activity causing hypothyroidism. A 11-year-old girl followed due to type 1 diabetes mellitus, celiac disease and euthyroid lymphocytic thyroiditis at diagnosis. Two years after the initial evaluation, thyroid-stimulating hormone was suppressed with normal free T4; nine months later, a biochemical evolution to hypothyroidism with thyroid-stimulating hormone-receptor autoantibodies elevation was seen; the patient remained always asymptomatic. Chinese hamster ovary cells were transfected with the recombinant human thyroid-stimulating hormone -receptor, and then exposed to the patient's serum; it was estimated a 'moderate' blocking activity of these thyroid-stimulating hormone-receptor autoantibodies, and concomitantly excluded stimulating action. In this case, the acknowledgment of the blocking activity of the serum thyroid-stimulating hormone-receptor autoantibodies, supported the hypothesis of a multifactorial aetiology of the hypothyroidism, which in the absence of the in vitro tests, we would consider only as a consequence of the destructive process associated to lymphocytic thyroiditis.
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Front Cell Dev Biol
January 2025
Department of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, Bisha, Saudi Arabia.
Graves disease (GD), an autoimmune disease affects the thyroid gland, results in hyperthyroidisms and goiter. The main cause of GD is not clearly defined; however, stimulating autoantibodies for thyroid stimulating hormone receptor (TSHR) known as thyroid-stimulating immunoglobulins (TSIs) are the primary proposed mechanism. The TSI activation of TSHRs of thyroid gland results in excessive release of thyroid hormones with the subsequent development of hyperthyroidism and goiter.
View Article and Find Full Text PDFEndocrinology
January 2025
Thyroid Research Unit, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
The pathogenesis of Thyroid Eye Disease (TED) has been suggested as due to signal enhancement in orbital fibroblasts as a result of autoantibody-induced, synergistic, interaction between the TSH receptor (TSHR) and the IGF-1 receptor (IGF-1R). This interaction has been explained by a "receptor cross talk", mediated via β-arrestin binding. Here, we have examined if this interaction can be mediated via direct receptor contact using modeling and experimental approaches.
View Article and Find Full Text PDFNat Metab
December 2024
Metabolomics and Cell Biology Platforms, UMS AMMICa, Gustave Roussy Institut, Villejuif, France.
Endocrinol Metab (Seoul)
December 2024
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Graves' hyperthyroidism is characterized by stimulation of the thyroid gland by thyroid-stimulating hormone receptor antibodies (TRAbs). Antithyroid drug (ATD) continuation is recommended as long as the thyroid gland is stimulated. Goiter size, thyroidal 123I uptake, serum thyroglobulin level, and TRAb positivity are reliable markers of thyroid stimulation.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
October 2024
Laboratory Medical Immunology, Department of Immunology, Erasmus MC University Medical Center Rotterdam, Rotterdam, Netherlands.
Background: For the selective detection of thyroid-stimulating hormone receptor antibodies with stimulating properties (thyroid-stimulating immunoglobulins; TSI), a novel and rapid bioassay (Turbo TSI) has been introduced. We evaluate the clinical performance of Turbo TSI in Graves' orbitopathy (GO) patients and compare it to a bridge-based TSI binding immunoassay and third generation TSH-R-binding inhibitory immunoglobulins (TBII) assay. Also, we investigate the association of Turbo TSI and TBII measurements with GO activity and severity, as well as response to intravenous methylprednisolone (IVMP), and compare results to previous findings on the bridge-based TSI binding immunoassay.
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