Role of the ABO blood groups as a risk factor for retinal vein occlusion.

Introduction A recent study suggested that non-O blood groups had an increased risk for the presence of RVO. In this study we investigated (i) an association between blood group and the presence of RVO and (ii) whether this association correlated to other RVO risk factors. Methods We included 485 RVO patients and 295 control subjects who were recruited in this case-control study. We determined ABO genotypes rs8176719 as a marker for the O allele and rs8176746 for the B allele by polymerase chain reaction. Results We did not find an association between ABO blood group and the presence of RVO. In detail, the proportion of ABO blood groups was similar among RVO patients and control subjects (p=0.527). In a logistic regression, non-O blood group was associated with 1.06-fold higher odds of being a RVO patient (95%CI: 0.78-1.45, p=0.693), and this lack of association prevailed upon multivariable adjustment for age, gender, history of stroke and venous thromboembolism and co-medication with lipid-lowering agents. Discussion Although non-O blood groups are a known risk factor for thrombotic and cardiovascular disease, they do not seem to be a major risk factor for the development of RVO.

Heme oxygenase-1 gene rs2071746 polymorphism in retinal vein occlusion.

BACKGROUND: Heme oxygenase-1 (HO-1) is an important cytoprotective enzyme due to its ability to degrade pro-inflammatory heme. The common single nucleotide polymorphism (SNP) rs2071746 on the HMOX1 gene has been associated with HO-1 activity and a variety of cardiovascular diseases. This study was performed to investigate the association between the rs2071746 SNP and retinal vein occlusion (RVO). METHODS: We included 496 RVO patients and 297 control subjects in this case-control study. Genotypes of the rs2071746 polymorphism were determined by TaqMan assays. RESULTS: There was no association between the rs2071746 genotype and the presence of RVO (p = .443). The lack of association was found in all three logistic regression models, namely the dominant (p = .560), the recessive (p = .373) and the co-dominant model (p = .444). The distribution of the rs2071746 genotype was 30% (AA), 51% (AT), and 19% (TT). Baseline characteristics were similar between these genotypes, except for diabetes mellitus, which was less prevalent in the AA genotype (p < .001). CONCLUSION: The rs2071746 polymorphism does not seem to be a major risk factor for the presence of RVO.

ENDOTHELIN-1 AS A RISK FACTOR IN RETINAL VEIN OCCLUSION.

PURPOSE: Retinal vein occlusion (RVO) risk factors largely coincide with cardiovascular risk factors. Endothelin-1 (ET-1), the most potent vasoconstrictor with proinflammatory properties, is a known cardiovascular risk factor. In this study, we explore the role of serum ET-1 as a potential risk factor for RVO. METHODS: Endothelin-1 serum levels were measured in patients with RVO and control subjects. Samples were measured using the sandwich enzyme-linked immunosorbent assay for the quantitative determination of human big endothelin-1 (Biomedica Group, Austria). RESULTS: The study consisted of 147 RVO patients and 150 control subjects. Median serum ET-1 was significantly higher in RVO patients (0.26 pmol/L; range, 0.19-0.37 pmol/L) compared with control subjects (0.10 pmol/L; range, 0.05-0.22 pmol/L) (P < 0.0001) independent of the occlusion site. The difference remained significant after adjusting for arterial hypertension, diabetes mellitus, history of stroke, history of myocardial infarction, history of venous thromboembolism, glomerular filtration rate, and c-reactive protein. CONCLUSION: In conclusion, our results suggest that ET-1 is a potential risk factor for all types of RVO.

SERUM LEVELS OF ANTIBODIES AGAINST OXIDATION-SPECIFIC EPITOPES ARE DECREASED IN PATIENTS WITH RETINAL VEIN OCCLUSION.

PURPOSE: Oxidative stress and inflammation have been implicated in the development of retinal vein occlusion (RVO). Oxidation-specific epitopes (OSEs) represent products of oxidative stress that can trigger vascular inflammation and thrombosis. Natural occurring antibodies have been shown to bind oxidation-specific epitopes thereby inhibiting their inflammatory potential and promoting their removal. METHODS: This prospective cross-sectional study included 270 patients with RVO and 81 in-hospital control patients. We measured three types of serum levels of oxidation-specific epitope-specific immunoglobulin M and immunoglobulin G antibodies (anti-copper-oxidized LDL [CuOx-LDL], antiphosphocholine [PC], anti-malondialdehyde-modified LDL [MDA-LDL]). History of arterial hypertension, hyperlipidemia, myocardial infarction, diabetes mellitus, stroke, smoking status, and several laboratory parameters were determined to control for potential confounders. RESULTS: Compared with controls, patients with RVO had significantly lower levels of immunoglobulin M and immunoglobulin G antibodies against CuOx-LDL and PC, and significantly lower levels of immunoglobulin G but not immunoglobulin M antibodies against MDA-LDL. The association between RVO patients and lower levels of these antibodies prevailed upon multivariable adjustment. CONCLUSION: These prospective data show that antibodies against oxidation-specific epitope are lower in patients with RVO compared with control patients and support the concept that oxidative stress and inflammation play key roles in the development and subsequent complications in RVO.

Role of the tissue-type plasminogen activator -7351C > T and plasminogen activator inhibitor 1 4G/5G gene polymorphisms in central serous chorioretinopathy.

BACKGROUND: Central serous chorioretinopathy (CSC) is a common chorioretinal disease, characterized by choroidal hyperpermeability leading to neurosensory and/or retinal pigment epithelial detachments. Hypofibrinolysis due to higher plasma concentrations of plasminogen activator type 1 (PAI-1) or lower activity of tissue-type plasminogen activator (t-PA) has been implicated in the pathogenesis of CSC. Functional polymorphisms in the PAI-1 (SERPINE1) and t-Pa (PLAT) are thus potential risk factors for CSC. The aim of the present study was therefore to investigate a hypothesized association between the PAI-1 4G/5G and the t-PA -7351C > T gene variants and the presence of CSC. METHODS: The present study comprised 172 CSC patients and 313 control subjects. Genotypes of the PAI-1 4G/5G and the t-PA -7351C > T polymorphisms were determined by TaqManTM fluorogenic 5'-exonuclease assays. RESULTS: Allelic frequencies or genotype distributions of neither the PAI-1 4G/5G nor the t-PA -7531C > T polymorphisms were significantly different between patients with CSC and control subjects (PAI-1 4G/4G: 24.4% vs. 20.4, p = 0.36; t-PA -7351CC: 42.4% vs. 46.0%, p = 0.50). After adjusting for age and gender presence of the PAI-1 4G/4G genotype was associated with a non-significant odds ratio (OR) of 1.21 (95% confidence interval [95% CI]: 0.77-1.92, p = 0.41), while homozygosity for the t-PA -7351C allele yielded a non-significant OR of 0.91 (95% CI: 0.62-1.33, p = 0.62) for CSC. CONCLUSION: The present study suggests that both the t-PA -7351C > T and the PAI-1 4G/5G gene variants are unlikely major risk factors for CSC.