A 38-year-old, otherwise healthy man presented to the clinic for evaluation of his progressive Graves ophthalmopathy. His diagnosis dated back to 1992 when he was told that he may have hyperthyroidism. No therapy was instituted at the time, and he had never taken antithyroid medications or received radioactive iodine. He was followed up annually by an endocrinologist and had yearly measurements of thyrotropin and thyrotropin-receptor antibodies, which had always been normal. From the ophthalmic standpoint, the right eye became proptotic in 1992 at the same time when he was diagnosed with “hyperthyroidism.” His proptosis was treated with oral steroids and responded promptly to this therapy. In view of his symptoms and prompt resolution with the established therapy, a presumed diagnosis of Graves ophthalmopathy was made. The patient remained asymptomatic for 3 years, at which time he once again noted proptosis, this time in both eyes with the right more prominent than the left. Therapy with steroids was once again instituted and he improved promptly. From this point on, he experienced yearly recurrent proptosis, which was treated with oral steroids each time. Most recently, the episodes became increasingly severe and he experienced recurrent proptosis approximately 3 times a year. A bilateral 2-wall orbital decompression performed at this point provided him with minimal relief from his symptoms for only 6 months before he experienced proptosis again. Since his decompression, the patient had diplopia in primary gaze when he was tired and in extremes of gaze at all times. He presented to our practice for further evaluation. In addition to the earlier-mentioned details (Figure 1), the patient denied any other significant medical history and was not taking any medications at the time of our consultation. He denied tobacco use.
Figure 1. Proptosis and conjunctival hyperemia with no evidence of upper eyelid retraction or eyelid lag.
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