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Graves’ Ophthalmopathy

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Part of the book series: Contemporary Endocrinology ((COE))

Summary

Graves’ orbitopathy (GO) is one of the extrathyroidal manifestations of Graves’ disease. The incidence of GO apparently is declining in the last few decades, likely as a result of a decreased prevalence of smoking and earlier diagnosis and treatment of hyperthyroidism. Clinical presentation is typically that of a bilateral symmetric eye disease, but why GO is unilateral or occurs in the absence of hyperthyroidism in some patients is not understood. Considerable progress has been made in unraveling the immunopathogenesis of GO. Orbital fibroblasts have been identified as the prime target cells of the autoimmune attack as they are recognized by T lymphocytes, express TSH receptors, and may undergo differentiation into adipocytes. Infiltrating T-cells rather than TSH receptor autoantibodies are likely involved in initiating orbital autoimmunity, via release of cytokines and activation of fibroblasts. Some Graves’ IgG stimulate the IGF-1 receptor on orbital fibroblasts, which raises intriguing questions. The management of GO is based on three lines of intervention: (a) to stop smoking, (b) to restore euthyroidism, and (c) to restore visual functions and appearance. In mild GO, a wait-and-see policy is recommended. In moderate-to-severe GO, intravenous pulses of methylprednisolone is the preferred treatment if the disease is active; if it is inactive, rehabilitative surgery can be done. Dysthyroid optic neuropathy requires urgent medical or surgical treatment.

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Wiersinga, W.M. (2011). Graves’ Ophthalmopathy. In: Eisenbarth, G. (eds) Immunoendocrinology: Scientific and Clinical Aspects. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60327-478-4_29

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