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]. The autoimmune process that occurs in GD involves both T cells and B cells, which results in the production of autoantibodies to the TSH receptor (TSHR-Ab). The clinical phenotype of GD is induced by unregulated stimulation of thyroid cells and TSHR
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–60 years, with an increased incidence among African Americans [ 8 ]. GD is an organ-specific autoimmune disease whose major manifestations are owing to circulating autoantibodies (Ab) that stimulate the thyroid-stimulating hormone receptor (TSH-R) leading
Internal Medicine, Erasmus MC, University Medical Center Rotterdam
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Department of Ophthalmology, Geneva University Hospitals, Geneva, Switzerland
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Internal Medicine, Erasmus MC, University Medical Center Rotterdam
Rotterdam Eye Hospital, Rotterdam, The Netherlands
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hyaluronan production by orbital fibroblasts, suggesting that TSHR stimulating autoantibodies contribute to development and severity of GO through orbital fibroblast activating properties [ 2 ]. Of the three PDGF-isoforms involved in GO it was found that PDGF-AB
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Introduction Autoantibodies against the thyrotropin receptor (TSH-R-Ab) play an important role in the pathogenesis of autoimmune thyroid diseases [ 1 - 5 ]. These functional antibodies demonstrate different effects on the TSH-R and can either
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Autoantibodies (Ab) to the TSH receptor (TSHR) are responsible for many of the clinical manifestations of Graves' disease (GD) and are specific biomarkers of this autoimmune thyroid disorder (AITD) [ 1 , 2 , 3 ]. These Ab can be measured
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, and the demonstration of a relationship between the level of antibodies to the TSHR (TSHR-Ab) and the development of GO indicates that autoimmune reactions against the TSHR may be a prime cause of GO. TSHR-Ab are present in the serum of the majority of
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Introduction Antibodies (Ab) to the thyroid-stimulating hormone receptor (TSHR) may mimic [ 1 - 3 ] or block [ 4 ] the action of TSH or be functionally neutral [ 5 ]. TSHR stimulating Ab (TSAb) are responsible for many of the clinical
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Introduction TSH-Receptor, Graves’ Disease and Graves’ Orbitopathy The thyrotropin receptor or thyroid-stimulating hormone (TSH) receptor (TSHR) is mainly expressed in follicular epithelial cells of the thyroid gland [ 1 ]. TSHR activation
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-stimulating hormone receptor antibody (TSH-R Ab) titer or radiation absorbed dose ( 2 , 3 , 4 , 5 , 6 , 7 , 8 ). Thyroid peroxidase antibodies (TPO Abs) are associated with autoimmune thyroid disease, and their measurement is helpful in the diagnostic workup
Department of Oto-Rhino-Laryngology – Head and Neck Surgery, University Hospital Essen, Essen, Germany
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Department of Ophthalmology, University Hospital Essen, Essen, Germany
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Introduction Graves disease (GD) is caused by autoantibodies that induce hyperthyroidism by mimicking the action of TSH and activating the TSH receptor (TSHR). The defining component of hyperthyroidism is thyroid follicular hyperplasia