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• W2086744890 abstract "Retinal vein occlusion (RVO) is one of the leading causes for a severe visual loss in patients older than 60 years. Hypofibrinolysis because of increased plasminogen activator inhibitor-1 (PAI-1) plasma concentrations has been identified as a risk factor [1-3]. Yet only very limited and at least partly conflicting data on the role of gene polymorphism known to affect PAI-1 plasma levels are available [2-4]. Recently, Gori et al. [2] investigating 112 patients with RVO suggested both homozygosity for the angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism and the combined presence of the PAI-1 4G/4G and ACE DD genotypes as novel risk factors. Homozygosity for the PAI-1 4G/5G gene polymorphism itself was not associated with an increased risk for RVO [2]. No significant difference in the PAI-1 4G/5G genotype distribution was also found in another study including 72 patients with either retinal artery or vein occlusion [4]. These findings, however, are in contrast to Glueck et al. [3], who observed a significantly higher prevalence of the PAI-1 4G-allele among 17 patients with RVO. In the present study genotyping for the ACE I/D and PAI-1 4G/5G gene polymorphisms was performed in 556 patients with RVO (308 females and 248 males) and 322 control subjects (186 females and 136 males). Because of second eye involvement, branch retinal vein occlusion (BRVO) was diagnosed in 348 eyes, and 235 eyes were affected by central retinal vein occlusion (CRVO). Control subjects were recruited from the same geographical area and were seen at the Department of Ophthalmology for other reasons than retinal vascular occlusion. Genomic DNA was isolated from venous blood by standard methods and stored at −20°C. Genotyping for the ACE polymorphism was carried out by size-analysis of polymerase chain reaction products [5], and the PAI-1 4G/5G polymorphism was determined as described by Margaglione et al. [6]. The mean age of patients was 67.3 ± 12.7 years (range: 17.5–92.9 years) and 70.2 ± 11.7 years (range: 24.1–91.1 years) in control subjects. As expected, arterial hypertension, hypercholesterolemia and ever-smoking status were found significantly more often among patients with RVO. Genotype distribution and allelic frequencies of the ACE I/D and the PAI-1 4G/5G gene polymorphisms are shown in Table 1. Genotype frequencies of both polymorphisms were in line with those predicted by the Hardy–Weinberg equilibrium, and were similar to those previously reported by other investigators [7, 8]. In contrast to the findings of Gori et al. [2], neither the prevalence of the ACE DD genotype nor the ACE D-allele frequency were significantly higher in patients with RVO than among control subjects. In a multivariate logistic regression analysis homozygosity for the ACE D-allele was associated with a non-significant odds ratio of 0.76 (95% CI: 0.52–1.11; P = 0.159) for RVO. Separate analysis of patients with CRVO and BRVO revealed similar results (data not shown), suggesting that the ACE I/D polymorphism is not a major risk factor for either type of RVO. As for the PAI-1 4G/5G gene polymorphism, no significant difference in either the prevalence of the PAI-1 4G/4G genotype or PAI-1 4G-allele frequency was observed between both groups (Table 1). Homozygosity for the PAI-1 4G allele was associated with a non-significant odds ratio of 0.93 for RVO (95% CI: 0.64–1.35; P = 0.701). Again separate analysis of patients with CRVO and BRVO yielded similar results (data not shown). Approximately 10% of patients with RVO are younger than 50 years, and thrombophilic risk factors may be more relevant in this subgroup of patients. In the present study, however, neither the ACE DD nor the PAI-1 4G/4G genotypes were found significantly more often among those patients younger than 50 years at the time of presentation with RVO (Table 1). Both the ACE DD and the PAI-1 4G/4G genotypes increase plasma PAI-1 concentrations [9], and synergistic effects have been reported in patients with diabetic nephropathy, recurrent spontaneous miscarriage and RVO [2, 10, 11]. In the present study including 556 patients the combined presence of the PAI-1 4G/4G and ACE DD genotypes did not significantly differ between patients with RVO and control subjects. A non-significant odds ratio of 1.45 (95% CI: 0.72–2.92; P = 0.297) for RVO was found in subjects carrying both genotypes. This is in contrast to Gori et al. [2], who studied 112 patients with RVO and reported an odds ratio of 4.82 for RVO in those carrying both the ACE DD and the PAI-1 4G/4G genotypes. Conflicting results may at least in part be explained by different ethnic background and the number of patients enrolled. However, as the present study had a statistical power of 0.8 to detect an odds ratio as low as 1.53 for RVO in either ACE DD or PAI-1 4G/4G homozygotes, we consider it unlikely that the investigated gene polymorphisms are major independent risk factors for RVO." @default.
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• W2086744890 title "Role of angiotensin-converting enzyme insertion/deletion and plasminogen activator inhibitor-1 4G/5G gene polymorphisms in retinal vein occlusion" @default.
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• W2086744890 doi "https://doi.org/10.1111/j.1538-7836.2005.01591.x" @default.
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