Eye Physicians of Sussex County (R.H.), Newton, New Jersey 07860 Division of Metabolism and Endocrine Drug Products (E.A.K., S.M.), Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20857
Previously, we reported on two nondiabetic
patients who developed retinal changes mimicking diabetic retinopathy
after GH exposure (1). One of the patients, a 31-yr-old male,
presented with new-onset impairment of visual acuity: right eye,
20/40-1; left eye, count fingers after 14 months of treatment. His
funduscopic examination was notable for bilateral cotton wool spots,
dot hemorrhages, microaneurysms, and macular edema (Fig. 1, A and B). Fluorescein angiography
demonstrated dye leakage in both eye-grounds. Emergent laser surgery
was performed on the left eye, and visual acuity improved to 20/100.
Surgery was not undertaken in the right eye.
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The development of retinal pathology during GH therapy and in the absence of diabetes, followed by the normalization of the patients retinal findings after GH therapy discontinuation, strongly suggest a role for GH in retinopathy. Recently, additional support for this hypothesis has been provided by Hellstrom et al. (2), who investigated the number of retinal branch points in congenitally GH-deficient children using digital image analysis. Such children, whether or not they had been treated with GH, had a lower number of branch points than normal children.
Footnotes
Revision received March 19, 2000. Accepted March 19, 2000.
Address all correspondence and requests for reprints to: Elizabeth A. Koller, M.D., Division of Metabolism and Endocrine Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration, 5600 Fishers Lane, Rockville, Maryland 20857.
1 This communication was written by the authors in their private
capacity. No official support or endorsement by the U.S. Food and Drug
Administration is intended or should be inferred.
Received December 15, 1999.
References