The Therapeutic Effects of Angiotensin-Converting Enzyme Inhibitors in Severe Non-proliferative Diabetic Retinopathy

Abstract

PurposeTo evaluate the effects of angiotensin-converting enzyme inhibitors (ACE-I) in retarding progression of severe non-proliferative diabetic retinopathy (NPDR) in normotensive type 2 diabetic patients.MethodsThis was a retrospective case control study of 128 patients with normotensive type 2 diabetes with lower than +1 dipstick proteinuria and severe NPDR who were classified into either an ACE-I treated group (Enalapril maleate 10 mg, n=12 , Ramipril 5 mg, n=17) or an ACE-I untreated group (n=99). Medical records were reviewed for endpoints of (a) occurrence of proliferative diabetic retinopathy (PDR) or macular edema (ME) for which laser phototherapy was necessary or (b) development of proteinuria of higher than +1 level requiring medication of ACE-I.ResultsFrom the total of 128 patients, there were 29 ACE-I treated patients and 99 ACE-I untreated patients. There were no differences in the average age, duration of diabetes, body mass indices, blood pressure and levels of hyperglycemia or HbA1C between the two groups. Blood pressure and HbA1C levels in both groups remained unchanged during the study. The mean follow-up period was 41.6 months. In the ACE-I group, 6 patients progressed to PDR, 5 to ME and 6 developed proteinuria of greater than +1 over the follow-up period. In the control group, 30 patients progressed to PDR, 6 to ME and 9 developed proteinuria of greater than +1 over the follow-up period.ConclusionsSmall doses of ACE-I did not yield any beneficial effects in retarding the progression of severe NPDR.

Impact of ocular hypotensive lipids on clinically significant diabetic macular edema

“…These include increased age, increased duration of diabetes, poor blood glycemic control, systemic hypertension, renal disease, and dyslipidemia (1). Certain systemic medications have also been hypothesized to have an impact on diabetic macular edema, including angiotensin-converting enzyme (ACE) inhibitors (3,4) and glitazones (5,6). Certain topical medications have also been implicated in the development of macular edema, namely the ocular hypotensive lipids (OHL) (8)(9)(10)(11).…”