Abstract
Graves’ ophthalmopathy (GO), an autoimmune condition associated with Graves’ disease (GD), occurs at a prevalence of nearly 40% in patients diagnosed with GD. Ocular involvement is probably due to the presence of autoantibodies in the orbital tissues, regardless of the control state of thyroid hormones in individuals with GD, even during euthyroid or hypothyroid states, which are associated with thyroid hormone treatment. In addition to the immunological role present in the pathophysiology of GO, the genetic component, proteins and cytokines, minerals (e.g., selenium), and environmental factors (e.g., smoking) also contribute to its development and occurrence of clinical manifestations in varying degrees. Until now, the interaction of causal, intermediary, and triggering factors of GO is still unclear, so the purpose of this article is to review literature on the theme.
Highlights
Graves’ ophthalmopathy (GO), an autoimmune condition associated with Graves’ disease (GD), occurs at a prevalence of nearly 40% in patients diagnosed with GD
Ocular involvement is probably due to the presence of autoantibodies in the orbital tissues, regardless of the control state of thyroid hormones in individuals with GD, even during euthyroid or hypothyroid states, which are associated with thyroid hormone treatment
Graves’ ophthalmopathy (GO), an autoimmune condition associated with Graves’ disease (GD), occurs at a prevalence of nearly 40% in patients diagnosed with GD [1] [2] [3] [4]
Summary
Graves’ ophthalmopathy (GO), an autoimmune condition associated with Graves’ disease (GD), occurs at a prevalence of nearly 40% in patients diagnosed with GD [1] [2] [3] [4]. It is usually seen in people who have had GD for some time, and are likely to be included in a more advanced age group than those who do not present with ocular changes. The purpose of this article is to review literature on the theme
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