Abstract
Thyroid-associated ophthalmopathy (TAO) is a condition associated with a wide spectrum of ocular changes, usually in the context of the autoimmune syndrome, Graves’ disease. In this topical review, we attempted to provide a roadmap of the recent advances in current understanding the pathogenesis of TAO, important aspects of its clinical presentation, its impact on the ocular surface, describe the tissue abnormalities frequently encountered, and describe how TAO is managed today. We also briefly review how increased understanding of the disease should culminate in improved therapies for patients with this vexing condition.
Highlights
Thyroid-associated ophthalmopathy (TAOa, aka thyroid eye disease or Graves’ ophthalmopathy) refers to several ocular manifestations related to the systemic autoimmune process, Graves’ disease (GD) [1]
Tear proteins were markedly different in those with TAO versus other forms of dry eye syndrome (DES). These include proteins involved in inflammatory response, cell-to cell signaling and interaction, cellular motility and cell death. These findings suggest that different mechanisms induce Lacrimal gland (LG) and ocular surface (OS) alterations in TAO [56]
Efficacy of intravenous and oral GCs were compared in moderately severe TAO patients; parenteral steroids were more effective in reducing clinical activity score (CAS) by at least 3 points, improvement in visual acuity, and decreasing disease activity at 3 months [62, 65]
Summary
Thyroid-associated ophthalmopathy (TAOa, aka thyroid eye disease or Graves’ ophthalmopathy) refers to several ocular manifestations related to the systemic autoimmune process, Graves’ disease (GD) [1]. Many clinical signs and symptoms of TAO arise from expansion of soft-tissues within the orbit, leading to exophthalmos [9, 25, 26]. Gupta et al [7] detected conjunctival and episcleral inflammation localized over the extraocular muscles in their entire series of patients and considered it to represent a presenting sign of TAO.
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