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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 7 2627
Copyright © 2000 by The Endocrine Society

Letters to the Editor

Full Remission of Growth Hormone (GH)-Induced Retinopathy after GH Treatment Discontinuation: Long-Term Follow-Up1

Richard Hansen, Elizabeth A. Koller and Saul Malozowski

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. 1Go, 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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  		Figure 1. A and B, Right and left eye-grounds during GH therapy. C and D, Right and left eye-grounds 3.5 yr after discontinuation of GH. E and F, Angiographic studies of the right and left eyes 3.5 yr after discontinuation of GH.

 
GH was discontinued. In the absence of additional treatment, the patient’s visual findings in both eyes improved. Changes were clearly evident 13 months later. Approximately 3.25 yr after the initial presentation, the patient’s visual acuity is normal (right eye, 20/25; left eye, 20/20) and his funduscopic examination was notable for the absence of cotton wool spots, dot hemorrhages, and microaneurysms in either eye (Fig. 1Go, C and D). An iv fluorescein angiogram was completely normal for the right eye (Fig. 1EGo). Residual laser marks, but no dye leakage, were present in the left eye (Fig. 1FGo).

The development of retinal pathology during GH therapy and in the absence of diabetes, followed by the normalization of the patient’s 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. Back

Received December 15, 1999.

References

  1. Koller EA, Green L, Gertner JM, et al. 1998 Retinal changes mimicking diabetic retinopathy in two nondiabetic, growth hormone-treated patients. J Clin Endocrinol Metab. 83:2380–2383.[Abstract/Free Full Text]
  2. Hellstrom A, Svensson E, Carlsson B, et al. 1999 Reduced retinal vascularization in children with growth hormone deficiency. J Clin Endocrinol Metab. 84:795–798.[Abstract/Free Full Text]



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