Abstract

To evaluate the association between angiotensin I-converting enzyme insertion/deletion (ACE I/D) gene polymorphism and retinal vein occlusion (RVO). A total of 80 patients with retinal vein occlusion who was admitted to the Eye Department of Kartal Training and Research Hospital between 2008 and 2011, and 80 subjects were enrolled in this retrospective case–control study. Patients who experienced RVO within one week to six months of study enrolment were included, and those with coronary artery diseases, prior myocardial infarction history and coagulation disturbances were excluded from the study. The diagnosis was made by ophthalmoscopic fundus examination and fluorescein angiography. The ACE gene I/D polymorphism was determined by polymerase chain reaction, and the ACE gene was classified into three types: I/I, I/D and D/D. In multivariate logistic regression analysis, ACE D/D genotype (p = 0.035), diabetes-mellitus (p = 0.019) and hypertension (p = 0.001) were found to be independent predictive factors for RVO. The results of the present study reveal that ACE D/D polymorphism is an independent predictive factor for RVO. However, one cannot definitely conclude that ACE gene polymorphism is a risk factor for retinal vein occlusion.

Highlights

  • Angiotensin I-converting enzyme (ACE), dipeptidyl peptidase, is a membrane-bound enzyme, which is present in endothelial and epithelial cells of various tissues, and innards including lungs and kidneys

  • Whole blood samples from the patients were collected in ethylenediaminetetraacetic acid (EDTA) tubes

  • The main finding of the present study is that ACE D/D gene polymorphism is an independent predictive factor for retinal vein occlusion (RVO)

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Summary

Introduction

Angiotensin I-converting enzyme (ACE), dipeptidyl peptidase, is a membrane-bound enzyme, which is present in endothelial and epithelial cells of various tissues, and innards including lungs and kidneys. Angiotensin I-converting enzyme converts Angiotensin I to Angiotensin II, a very potent vasoconstrictor agent [1]. Angiotensin II is a hormone as well as a locally produced cellular factor, directly affecting vascular endothelial cells and smooth muscles [2]. It has been demonstrated that receptors of Angiotensin II are found in the atherosclerotic vessel walls [3]. It is pointed out that Angiotensin II can promote vasoconstriction, inflammation and thrombosis in the vascular endothelium and vessel walls [4]. Besides being a potent vasoconstrictor, Angiotensin II is a proatherogenic agent, which elevates plasminogen activator inhibitor-1 (PAI-1) levels, which results in a decrease in the fibrinolytic activity [5,6]

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