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      Pathogenesis of Graves’ orbitopathy: A 2010 update

      research-article
      Journal of endocrinological investigation
      Autoimmune, B cells, fibrocytes, thyroid, TSH receptor

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          Abstract

          The most important of the extra-thyroidal manifestations of Graves’ disease, Graves’ orbitopathy (GO), remains a vexing clinical problem. Treatment of severe active disease has been limited to steroids or radiotherapy. In the relatively rare case where vision is threatened, emergent decompression surgery can be performed. The proptosis, motility, or cosmetic concerns associated with stable GO are commonly remedied with surgical intervention. Substantial obstacles have prevented the development of specific medical therapies for GO, in large part resulting from poor understanding of disease pathogenesis and the absence of pre-clinical animal models. Fundamental aspects of GO’s etiology have been uncovered from studies based in cell culture, extensive analysis of blood constituents, and detailed examination of orbital contents collected at the time of surgical intervention. Many of the published reports resulting from these studies are descriptive and all have failed to yield unifying concepts that integrate the anatomically divergent manifestations of Graves’ disease. This brief review covers recent findings of several research groups. While major breakthroughs continue to occur in closely related autoimmune diseases, progress in identifying the pathogenic mechanisms relevant to GO has been limited. As emerging insights into human autoimmunity becomes applied to the study of Graves’ disease, we anticipate that improved therapeutic strategies will find their way to our patients with GO.

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          Author and article information

          Journal
          7806594
          4766
          J Endocrinol Invest
          J. Endocrinol. Invest.
          Journal of endocrinological investigation
          0391-4097
          1720-8386
          19 December 2018
          June 2010
          07 October 2019
          : 33
          : 6
          : 414-421
          Affiliations
          Departments of Ophthalmology and Visual Sciences and Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA
          Author notes
          Correspondence: T.J. Smith, MD, Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, 1000 Wall Street, Ann Arbor, MI 48105. terrysmi@ 123456med.umich.edu
          Article
          PMC6779038 PMC6779038 6779038 nihpa992085
          10.1007/BF03346614
          6779038
          20631493
          23ef2f58-4ca0-4331-baf0-f8a0e81600de
          History
          Categories
          Article

          fibrocytes,B cells,TSH receptor,Autoimmune,thyroid
          fibrocytes, B cells, TSH receptor, Autoimmune, thyroid

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