To the Editor.
—Platelet hypersensitivity and increased prostaglandin levels have been implicated in the development of diabetic retinopathy.1 Dipyridamole is an inhibitor of thromboxane A2 synthesis and platelet aggregation. Microangiopathy and a breakdown of the blood-retinal barrier have been correlated with fluorescein leakage into the posterior vitreous.2 We have studied the effect of dipyridamole on the blood-retinal barrier of patients with diabetes mellitus by vitreous fluorophotometry.
Patients and Methods.
—Forty maturity-onset diabetic patients with background retinopathy were recruited from the medical diabetic clinic at Mount Sinai Hospital, New York. The patients underwent a general physical and ophthalmic examination, including gonioscopy and fundus photography. Excluded from the study were brittle diabetics, women of childbearing potential, hypertensive subjects with diastolic blood pressures greater than 100 mm Hg while on medication, and patients with proliferative retinopathy, previous photocoagulation therapy, or opaque media. Also excluded were patients taking the following medications:
Howard-Williams JR, Siegel MJ, Podos SM, Brown V. Alteration of the Blood-Retinal Barrier by Dipyridamole. Arch Ophthalmol. 1986;104(4):488-490. doi:10.1001/archopht.1986.01050160040006