In mild disease, patients present with eyelid retraction. In January 2020, the US Food and Drug Administration approved teprotumumab-trbw for the treatment of Graves’ ophthalmopathy. Many anti-inflammatory biological mediators, such as infliximab, etanercept, and anakinra are being tried. Severe cases are a medical emergency, and are treated with glucocorticoids (steroids), and sometimes ciclosporin. Mild disease will often resolve and merely requires measures to reduce discomfort and dryness, such as artificial tears and smoking cessation if possible. Cigarette smoking, which is associated with many autoimmune diseases, raises the incidence 7.7-fold. About 3–5% have severe disease with intense pain, and sight-threatening corneal ulceration or compression of the optic nerve. Veins become compressed and are unable to drain fluid, causing edema. Fat cells and muscles expand and become inflamed. The autoantibodies target the fibroblasts in the eye muscles, and those fibroblasts can differentiate into fat cells ( adipocytes). It is part of a systemic process with variable expression in the eyes, thyroid, and skin, caused by autoantibodies that bind to tissues in those organs. It occurs most commonly in individuals with Graves' disease, and less commonly in individuals with Hashimoto's thyroiditis, or in those who are euthyroid. Graves’ ophthalmopathy, also known as thyroid eye disease ( TED), is an autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, redness ( erythema), conjunctivitis, and bulging eyes ( exophthalmos). Thyroid eye disease (TED), dysthyroid/thyroid-associated orbitopathy (TAO), Graves' orbitopathy (GO)īulging eyes and lid retraction from Graves' disease
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