Angiotensin converting enzyme genetic polimorphizm in patients with age related macular degeneration

Aim: To determine the association between the age related macular degeneration (ARMD) and angiotensin-converting enzyme insertion/deletion (l/D) polymorphism, serum ACE levels in Turkish patients.Methods: 79 patients, who was examined in Celal Bayar University Ophtalmology Department between April 2009- October 2009 and diagnosed as ARMD (neovascular or non-neovascular form), were included the study. Also 68 patients, aged over 64, without senil macular degeneration were examined as control group of the study. Detailed ophtalmologic examination, including best corrected visual acuity, ıntraocular pressure, biomicroscopic and fundoscopic examinations, was performed to all participants. Fundus photographs of the patients with ARMD were taken. In patients with neovascular ARMD fundus fluorescein angiograpy was performed. The treatment and follow-up strategies of these patients were arranged in the retina department of the same clinic. Serum samples were taken from all participants and stored at -20 ºC until biochemical and genetic axaminations were performed. Genetic analyse of insertion/deletion polymorphism was performed by using PCR technique. Serum ACE levels were determined in biochemistry labarotuary by using ELİSA method for all participants. The results were statistically assessed.Results: 79 patients with ARMD and 68 patients without ARMD were examined in our study. There was no statistically significiant difference about age(p:0,155) and gender(p:0,187) between two groups. Serum levels of ACE was determined 175,63±57,67(n:78) in ARMD group, and 191,20±57,92(n:68) in control group. The difference was not statisticially significiant (p:0,107). Also there was no statisticially significiant difference in ACE I/D genetic polimorphizm between two groups ( p:0,218).Conclusion: According to our findings, l/D polymorphism in the angiotensin-converting enzyme gene and serum levels of ACE does not play any role in the pathogenesis of ARMD.