Abstract

Thyroid-associated orbitopathy (TAO) is caused by T-cell activation of retro-ocular fibroblasts and autoantibodies against thyroid-stimulating hormone receptor (TSHR) leading to accumulation of glycosaminoglycans and inflammation. The condition can present with soft tissue inflammation, proptosis, restrictive myopathy, and optic neuropathy. Although typically associated with Graves disease, TAO is occasionally seen in Hashimoto thyroiditis. We report a case of TAO presenting with unilateral periorbital edema in a patient with Hashimoto disease. A 63-year-old female with hypothyroidism was referred to our dermatology clinic by the ophthalmology service with a 2-year history of persistent and progressive right-sided nontraumatic periorbital swelling, associated with blurry vision, pain upon eye movement, and facial paresthesia. The patient was treated with high-dose systemic corticosteroids and radiotherapy for suspected Graves ophthalmopathy with partial response. Physical examination was remarkable for right-sided erythema and edema of the upper and lower eyelids. Skin biopsy revealed a superficial and deep lymphocytic infiltration with mucin. An orbital CT scan revealed right-sided hypertrophy of the medial rectus muscle and proptosis. Laboratory findings demonstrated elevated thyroglobulin, thyroid peroxidase, and TSHR antibodies. TSH and free T4 levels were normal. Clinicopathologic correlation supported a diagnosis of TAO in the setting of Hashimoto disease. TAO affects 2-5% of patients with Hashimoto thyroiditis. As seen in our patient, asymmetrical ophthalmopathy may be present, and in fact, these symptoms may precede endocrine manifestations. Prompt recognition and management of this condition may spare permanent neurological damage, including vision loss.

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