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Graves orbitopathy: a perspective
Petros Perros and Gerasimos E. Krassas
Abstract | Advances in the past few years have helped clinicians understand some of the pathogenetic mechanisms of Graves orbitopathy (GO), particularly the role of receptors for TSH and insulin-like growth factor I in the orbit. Optimal treatment strategies have been formulated and published by the European Group on Graves Orbitopathy, which are hoped to improve the management of patients with this condition. The administration of intravenous pulses of steroids has been established as a superior treatment approach compared with other steroid regimens. In addition, orbital radiotherapy was effective in a subgroup of patients with GO who had eye dysmotility. The use of immunotherapies for the treatment of GO is currently being explored; of these, rituximab has emerged as a promising new agent.
Perros, P. & Krassas, G. E. Nat. Rev. Endocrinol. 5, 312318 (2009); published online 5 May 2009; http://www.nature.com/doifinder/10.1038/nrendo.2009.61
Web End =doi:10.1038/nrendo.2009.61
Introduction
Graves orbitopathy (GO) is an eye disease charac terized by inflammation of orbital tissues that develops in around half of patients with Graves disease. This condition has perplexed generations of clinicians and scientists because of its diverse clinical manifestations, obscure patho genesis and the challenges posed by its management.1 GO can cause significant disfigurement of the eye and visual impairment and affects patients psychological well-being and quality of life.2
Clinical symptoms of GO usually appear at approximately the same time that Graves-disease-associated thyrotoxicosis develops, yet 2040% of patients develop orbitopathy several months, or sometimes years, before or after the onset of thyrotoxicosis. Interestingly, GO is not always associated with thyrotoxicosis: sometimes, it occurs in patients who have autoimmune, primary hypothyroidism or in those who have never had thyroid dysfunction. In all patients with GO, however, an auto-immune reaction develops against the thyroid gland, which can be detected by the presence of antithyroid autoantibodies or infiltration of the thyroid gland by lymphocytes.3,4 For this reason, some authors prefer the term thyroid-associated orbitopathy for this condition. In this Review, we provide an overview of the patho
genesis,
diagnosis and management of GO.
Pathogenesis
Autoimmunity
The inflammation of orbital tissues in GO is most likely to be caused by an autoimmune reaction. This hypothe sis is supported by the following findings:...