血管紧张素-1转化酶(ACE)基因多态性缺失和原发性开角型青光眼眼部体征的关系

来源 :世界核心医学期刊文摘.眼科学分册 | 被引量 : 0次 | 上传用户:dexter001
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Background: Primary open-angle glaucoma (POAG) is a leading cause of blindnes s. High intraocular pressure (IOP) has been shown to be a key risk factor for PO AG. Topical application of angiotensin 1-converting enzyme (ACE) inhibitors has been shown to lower IOP, and angiotensin-induced increase in vascular tone has been implicated as a pathogenetic mechanism in glaucomatous cupping and damage to the optic nerve. The objective of this study was to investigate the associati on between the deletion polymorphism in the ACE gene and ocular signs of POAG. M ethods: Baseline data from the Rotterdam Study was used. The ACE genotype was de termined in 6,462 subjects. We used univariate and multiple variable statistical techniques to examine associations between ACE genotype and each of ocular hype rtension, glaucomatous optic neuropathy, glaucomatous visual field defects and P OAG diagnosis. Results: We found no consistent evidence between ACE genotype and ocular signs of POAG.We did, however, find evidence of an association betweenAC E genotype and optic disc area, subjects homozygous for the deletion allele tend ing to have fractionally smaller optic disc areas than those with a single delet ion allele subjects, who in turn tended to have fractionally smaller optic discs than those with no deletion alleles (P=0.01) Conclusions: The data provided lit tle evidence of any association between ocular signs of POAG and the deletion po lymorphism of ACE. Therewas, however, evidence that ACE may be associated with o ptic disc size-this was an unexpected finding. Background: Primary open-angle glaucoma (POAG) is a leading cause of blindnes s. High intraocular pressure (IOP) has been shown to be a key risk factor for PO AG. Topical application of angiotensin 1-converting enzyme (ACE) inhibitors has has shown to lower IOP, and angiotensin-induced increase in vascular tone has been implicated as a pathogenetic mechanism in glaucomatous cupping and damage to the optic nerve. The objective of this study was to investigate the associati on between the deletion polymorphism in the ACE gene M ethods: Baseline data from the Rotterdam Study was used. The ACE genotype was de termined in 6,462 subjects. We used univariate and multiple variable statistical techniques to investigate associations between ACE genotype and each of ocular hypertension, glaucomatous optic neuropathy, glaucomatous visual field defects and P OAG diagnosis. We found no consistent evidence between ACE genotype and ocular signs of POAG. We did, however, find evidence of an association between AC E genotype and optic disc area, subjects homozygous for the deletion allele tend to have fractionally smaller optic disc areas than those with a single delet ion allele subjects, who in turn tended to have fractionally smaller optic discs than those with no deletion alleles (P = 0.01) Conclusions: The data provided lit tle evidence of any association between ocular signs of POAG and the deletion of po lymorphism of ACE. Therewas, however, evidence that ACE may be associated with o ptic disc size-this was an unexpected finding.
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