Recent insights into the pathogenesis and management of thyroid-associated ophthalmopathy.

摘要: Purpose of review To identify and critique the most recent experimental findings regarding pathogenesis therapy thyroid-associated ophthalmopathy. Recent Much work in this field has focused on identifying genetic alterations associated with phenotypes Graves' disease ophthalmopathy investigating their functional consequences. Identified candidate genes include CD40, cytotoxic T-lymphocyte antigen-4, protein tyrosine phosphatase-22, human leukocyte antigen-major histocompatibility complex those X-chromosome. Efforts to generate a complete rodent model continue little progress. These uniformly involve immunization animals thyrotropin receptor. Studies conducted vitro have actions cytokines orbital fibroblasts, potential role insulin-like growth factor-1 receptor activating antibodies directed against it as fibroblast T cell activation pathway. Reports appear examining relationship between adipogenesis. Regarding for ophthalmopathy, small molecules disrupting cytokine pathways lymphocyte function are currently under examination yielded promising albeit preliminary results. Summary Thyroid-associated remains vexing medical problem, which uncertain. A number obstacles plague major advances, not least is absence robust animal model. few new insights seem represent departure from traditional thinking about may herald important innovation.