Graves Ophthalmopathy

For 1 month, a 25-year-old woman had experienced discomfort in and around the left eye and diplopia. She was in good health; she reported no weight loss, excessive nervousness, heat intolerance, decreased strength, changes in the texture of hair or skin, or altered bowel habits. There was no personal or family history of goiter or other thyroid disease.

Results of the physical examination were unremarkable, except for moderate obesity and ocular findings. The thyroid was palpable, smooth, normal in size, and free of nodules. The left eye was mildly proptotic; there was superior and lateral deviation. Moderate chemosis was noted in the right eye; there was no conjunctival infection (A). Visual acuity and visual fields were normal; there was no evidence of corneal damage.

Results of routine laboratory tests-including the fasting plasma glucose concentration-were within normal limits. Thyroid evaluations were normal.

Dr Roy T. Rapp of Quincy, Ill, diagnosed infiltrative ophthalmopathy associated with Graves disease; tumor of the eye had been considered in the differential. The usual triad of manifestations of Graves disease are hyperthyroidism, pretibial skin changes, and eye involvement; this patient exhibited only the ocular signs and symptoms. Between 5% and 10% of patients with Graves disease have ophthalmic or euthyroid Graves ophthalmopathy; no laboratory evidence of thyroid dysfunction is found.¹

The patient was referred to an endocrinologist, who prescribed oral prednisone, 60 mg/d for 1 week followed by 20 mg/d for 6 weeks. Artificial tears were used twice a day. Patients who do not respond to this regimen are occasionally given cyclosporine and radiation therapy.

The patient's right eye cleared after 4 weeks of treatment; the left remained deviated (B). Following completion of the corticosteroid regimen, the Graves ophthalmopathy resolved (C). There has been no recurrence 5 years after treatment.

The associated diplopia, which results from compression of the optic nerve by swollen tissue and may lead to blindness, can be managed nonsurgically with prisms or occlusion therapy. In some patients, operative procedures, such as orbital decompression or extraocular muscle and eyelid surgery, may be required. No such treatment was needed for this patient.

REFERENCE:
1. Weetman AP. Thyroid-associated ophthalmopathy. Autoimmunity. 1992;12:215-222.