advertisement
Abstract #12132 Published in IGR 7-1
Associations between the deletion polymorphism of the angiotensin 1-converting enzyme gene and ocular signs of primary open-angle glaucoma
Bunce C; Hitchings RA; Van Duijn CM; De Jong PT; Vingerling JRGraefe's Archive for Clinical and Experimental Ophthalmology 2005; 243: 294-299
BACKGROUND: Primary open-angle glaucoma (POAG) is a leading cause of blindness. High intraocular pressure (IOP) has been shown to be a key risk factor for POAG. 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 association between the deletion polymorphism in the ACE gene and ocular signs of POAG. METHODS: Baseline data from the Rotterdam Study was used. The ACE genotype was determined in 6,462 subjects. We used univariate and multiple variable statistical techniques to examine associations between ACE genotype and each of ocular hypertension, glaucomatous optic neuropathy, glaucomatous visual field defects and POAG diagnosis. RESULTS: We found no consistent evidence between ACE genotype and ocular signs of POAG. We did, however, find evidence of an association between ACE genotype and optic disc area, subjects homozygous for the deletion allele tending to have fractionally smaller optic disc areas than those with a single deletion 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 little evidence of any association between ocular signs of POAG and the deletion polymorphism of ACE. There was, however, evidence that ACE may be associated with optic disc size-this was an unexpected finding.
Dr. C. Bunce, Moorfields Eye Hospital, City Road, London, EC1V 2PD, UK. c.bunce@ucl.ac.uk
Classification:
3.4.1 Linkage studies (Part of: 3 Laboratory methods > 3.4 Molecular genetics)
