<p>Thyroid Eye Disease: How A Novel Therapy May Change The Treatment Paradigm</p>

Abstract

Thyroid eye disease (TED) is a complex, debilitating autoimmune disease that causes orbital inflammation and tissue remodeling, resulting in proptosis, diplopia, and in severe cases, loss of vision. TED can lead to facial disfigurement and severely impact patients' quality of life. Although the course of TED was identified over 60 years ago, effective treatment options have proved to be challenging. Current treatments such as glucocorticoid therapy and orbital radiation focus on reducing orbital inflammation. However, these therapies fail to modify the disease outcomes, including proptosis and diplopia. Recent advances in the understanding of the molecular basis of TED have facilitated the development of targeted molecular therapies such as teprotumumab, an insulin-like growth factor-1 receptor inhibiting monoclonal antibody. In recent phase 2 and phase 3 randomized placebo-controlled trials, teprotumumab rapidly achieved improvement in clinical endpoints defining TED, including improved proptosis and diplopia. Dramatic improvement in clinical outcomes achieved after teprotumumab therapy during active TED are heretofore singular and comparable only to surgical therapies achieved during the inactive phase of TED. The advent of effective medical therapy can lead to a paradigm shift in the clinical management of TED. This review will provide an overview of TED, its epidemiology, insight into the molecular biology of the disease, clinical characteristics and diagnosis, and current and emerging treatment modalities.

Thyroid eye disease: Redefining its management—A review

“…Periorbital edema can be improved with reduced sodium intake, head of the bed elevation when sleeping and a compressive dressing to the lower lids. Diplopia can be helped with prisms 64,65 …”

“…Patients with moderate‐to‐severe active disease that is not considered vision‐threatening have traditionally been treated symptomatically on an elective basis with glucocorticoids, immunosuppressive therapy and/or orbital radiation. Patients with vision‐threatening diseases require urgent intervention, which can include glucocorticoids, orbital radiotherapy and/or orbital decompression 65 …”

“…Mourtis et al found an improvement in diplopia score but no reduction of proptosis and thus concluded radiotherapy only benefited patients with motility impairment 78 . General dosing recommendations for orbital radiation are 2 Gy daily for approximately 2 weeks (20 Gy total) 65 . Side effects of treatment most commonly included transient periorbital edema and conjunctival injection.…”

“…Diplopia can be helped with prisms. 64,65 Other dietary and lifestyle modifications can be helpful. Oxidative stress has been implicated in the pathogenesis of TED, though no studies to date have quantified the benefits of antioxidant supplementation.…”

Evidence That Baseline Levels of Low-Density Lipoproteins Cholesterol Affect the Clinical Response of Graves’ Ophthalmopathy to Parenteral Corticosteroids

“…Those data suggest the possibility that cholesterol might not only increase the risk of GO but also its activity, corroborating previous data showing that chronically elevated cholesterol increases systemic inflammation and modulates innate and adaptive immunity ( 10 ). However, the possible impact of cholesterol levels on the clinical efficacy of ivGC therapy in patients with active GO is not known ( 8 , 11 , 12 ).…”