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Retinal Changes Mimicking Diabetic Retinopathy in Two Nondiabetic, Growth Hormone-Treated Patients¹

U.S. Food and Drug Administration-CDER (E.A.K., L.G., S.N.M.), Rockville, Maryland 20857; New York Hospital, Cornell Medical Center, Pediatric Endocrinology (J.M.G.), New York, New York 10021; and Central University Hospital-Department of Pediatrics (M.B.), Grenoble cedex 09, France

Address all correspondence and requests for reprints to: Elizabeth Koller, U.S. Food and Drug Administration-CDER, Parklawn Building, HFD 510, Room 14B04, 5600 Fishers Lane, Rockville, Maryland 20857. E-mail: kollere{at}cder.fda.gov

A role for GH in the pathogenesis of diabetic retinopathy has long been postulated. Previous clinical studies, however, have been confounded by hyperglycemia. We have identified 2 cases of retinopathy associated with exogenous GH therapy in nondiabetic patients. Cases were identified through the MedWatch drug surveillance system of the U.S. Food and Drug Administration. Causality by concomitant medications was excluded by a search of the literature and the FDA data base. The first patient, an obese, 31-yr-old male with traumatic hypothalamic injury, presented with nonproliferative retinopathy and macular edema, resulting in decreased visual acuity (OD 20/40–1; OS count fingers), which required laser surgery. Human GH had been initiated at 0.009 mg/kg·day, 14 months earlier, and titrated to 0.017 mg/kg·day. The second patient, a nonobese, 11-yr-old girl receiving GH for the management of short stature in Turner’s Syndrome, presented with neovascularization. GH doses were 0.033 mg/kg·day for the first 17 months and 0.043 mg/kg·day for the following 5 months. Cumulative laboratory and clinical observations suggest that GH and related peptides have a role in retinal pathology independent of the degree of glucose tolerance.

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