Thyroid ophthalmopathy
Overview
Thyroid-associated orbitopathy (TAO), frequently termed Graves ophthalmopathy, is part of an autoimmune process that can affect the orbital and periorbital tissue, the thyroid gland, and, rarely, the pretibial skin or digits (thyroid acropachy)
Pathophysiology
In simplest terms, the underlying pathophysiology of thyroid-associated orbitopathy is thought to be an antibody-mediated reaction against the thyroid-stimulating hormone (TSH) receptor with orbital fibroblast modulation of T-cell lymphocytes. T-cell lymphocytes are believed to react against thyroid follicular cells with shared antigenic epitopes in the retroorbital space. An active phase of inflammation is initially present.
Lymphocytic infiltration of the orbital tissue causes a release of cytokines (eg, tumor necrosis factor [TNF], interleukin 1 [IL-1]) from CD4+ T cells stimulating the orbital fibroblasts to produce mucopolysaccharides, which, by hyperosmotic shift, cause tissue edema in the extraocular muscles.
Symptoms
Patients may complain of the following ocular symptoms:
- Dry eyes, Puffy eyelids, Angry-looking eyes, Bulging eyes
- Diplopia, Visual loss, Dyschromatopsia, Photopsia on upgaze, Ocular pressure or pain
Management
Monitor for visual loss from corneal exposure and optic neuropathy and for strabismus development