Graves' ophthalmopathy (GO) is characterized by an autoimmune reaction against thyrotropin (TSH) receptors and is diagnosed by TSH receptor antibody (TRAb).
The absence of Graves' orbitopathy and of the CTLA-4 G/G genotype are independent predictors of long-term remission following a first course of antithyroid drugs.
The Thyrotropin receptor antibody (TRAb) is the main driver of Graves' disease (GD) and its most common extra-thyroidal manifestation: thyroid eye disease (TED).
Graves' ophthalmopathy (GO) is a complication of Graves' disease (GD), in which orbital connective tissues become inflamed and increase in volume and orbital fibroblasts within the orbital fat and extraocular muscles differentiate into adipocytes in vitro when stimulated by hormones, several cytokines, and growth factors including TSH, IGF-1, IL-1, interferon γ, and platelet-derived growth factor.
However, no significant differences for rs2294025 and rs7005834 were observed, between the different clinical phenotypes of GD, including gender, Graves' ophthalmopathy (GO), and serum levels of thyrotropin receptor antibody, thyroid peroxidase antibody, and thyroglobulin antibody.
According to the univariate analysis, the relevant factors of higher IOP, larger proptosis, higher clinical activity scoring (CAS), thyroid stimulating hormone-receptor autoantibodies (TRAb), and <sup>131</sup>I therapy were significantly associated with decreased RCDs in GO patients (<i>P</i> < .05).
The expression of IL-1β induced the IL-6, IL-8, intercellular adhesion molecule-1 and cyclooxygenase-2 of GO intraconal OFs, and non-GO nasal OFs were higher than non-GO central OFs and dermal fibroblasts.
Drugs targeting cytokines [anti-TNFα (Etanercept), and anti-IL-6 (Tocilizumab)], and RTX (a chimeric monoclonal antibody vs. CD20) have been used in GO, with promising results.
Whereas elevated thyroid hormone synthesis by the thyroid in Graves' disease can be treated by antithyroid agents, for the pathogenic activation of TSHR in retro-orbital fibroblasts of the eye, leading to Graves' orbitopathy (GO), no causal TSHR directed therapy is available.
AS-IV treatment significantly decreased IL-1β-induced inflammatory cytokine production in orbital fibroblasts in vitro and attenuated GO orbital inflammation, fat accumulation, collagen deposition, and macrophage infiltration in vivo.