Impact of internal carotid endarterectomy on visual fields: a non-randomised prospective cohort study in Austria.

PURPOSE: The goal of this study was to determine whether internal carotid endarterectomy is associated with visual field changes. METHODS: Between March 2007 and December 2010, a cohort study involved 29 patients with stenosis of the carotid artery. All patients underwent ophthalmoscopy and kinetic visual field examination (Goldmann perimetry) preoperatively and postoperatively. Furthermore, a detailed area calculation was performed. On both the operated and the contralateral side, the areas surrounded by the different isopters (isopter areas) were determined and preoperative and postoperative values compared. The three isopters were classified from the centre to the periphery (I, II and III). Isopter area values are given as ratio compared with total perimetric circle. p Values <0.05 were considered to be statistically significant. RESULTS: 1) The ophthalmologists assessment (paragraph is missing in the proof!)Eight of eleven patients with precarotid endarterectomy impairments experienced focal or concentric improvement. Six cases with preoperative concentric narrowing of the isopters returned to normal or improved substantially. Three out of 18 patients with normal preoperative visual field presented with deteriorations after surgery, two cases with ipsilateral and one with contralateral focal impairment. In 15 cases, there was no preoperative or postoperative abnormality.2) Area calculation (preoperative area, postoperative area, P) (paragraph is missing in the proof)Ipsilateral: isopter area I (0.015, 0.018, 0.131), isopter area II (0.107, 0.120, 0.087), isopter area III (0.392, 0.425, 0.015)Contralateral: isopter area I (0.017, 0.021, 0.222), isopter area II (0.119, 0.125, 0.333), isopter area III (0.416, 0.434, 0.171) CONCLUSIONS: We found a statistically significant extension of the ipsilateral peripheral isopter area (III). Further studies will focus on the question which subgroup is most likely to profit from internal carotid endarterectomy with respect to visual field changes.

Role of the vitamin K epoxide reductase complex subunit 1 (VKORC1) -1639G>A gene polymorphism in patients with retinal vein occlusion.

PURPOSE OF THE STUDY: Retinal vein occlusion (RVO) is a major vision-threatening disease. Vitamin K epoxide reductase recycles reduced vitamin K, which is essential for the gamma carboxylation of clotting factors II, VII, IX, X and proteins C and S. Recently, the vitamin K epoxide reductase complex subunit 1 (VKORC1) -1639G>A (rs9923231) polymorphism has been reported as a novel risk factor for RVO in a Turkish population. The present study was set to confirm or to refute this association in a larger cohort of patients with RVO. MATERIALS AND METHODS: The present case-control study comprised 285 patients with central RVO, 401 patients with branch RVO and 333 control subjects. Genotypes of the VKORC1 -1639G>A polymorphism were determined by 5' exonuclease assay (TaqMan). RESULTS: No significant differences in either genotype distributions or allele frequencies of the vitamin K epoxide reductase complex subunit 1 -1639G>A polymorphism were found between patients and control subjects (p > 0.05). In a logistic regression analysis neither branch nor central RVO was predicted by the vitamin K epoxide reductase complex subunit 1 -1639G>A genotypes, but by arterial hypertension, ever-smoking status and in case of central RVO additionally by diabetes mellitus. CONCLUSIONS: Our data suggest that the vitamin K epoxide reductase complex subunit 1 -1639G>A gene polymorphism is unlikely a major risk factor for patients with either central or branch RVO.

Combination treatment of photodynamic therapy with verteporfin and intravitreal ranibizumab in patients with retinal angiomatous proliferation.

PURPOSE: To investigate the efficacy and safety of initial photodynamic therapy (PDT) with a ranibizumab loading dose of three monthly intravitreal injections and a subsequent PRN ranibizumab regimen in the treatment of retinal angiomatous proliferation (RAP). METHODS: In this 12-month prospective case series, 15 patients underwent PDT followed by 3 intravitreal ranibizumab injections at monthly intervals. At monthly follow-up examinations, further single ranibizumab injections were given in case of any intra- or subretinal fluid on optical coherence tomography (OCT), visual loss ≥5 letters or signs of activity on fluorescein or indocyanine green angiography. RESULTS: Best-corrected visual acuity (BCVA) improved from 58.1 ± 13.2 at baseline by 9.2 letters (SD ± 8.5; p = 0.004) at 6 months and by 8.7 letters (SD ± 11.4; p = 0.017) at 12 months. Neither at 6 nor at 12 months, any patient had lost ≥15 letters. The mean number of injections per patient was 4.8 (SD ± 1.4) in the first year of therapy after PDT. The average time to first retreatment was 3.7 months (range 1-7 months). No serious adverse events, such as endophthalmitis or retinal detachment, were noted. CONCLUSION: PDT with 3 ranibizumab loading injections and subsequent ranibizumab as needed resulted in a significant gain of 8.7 ± 11.4 letters at month 12. This regimen is safe and efficacious, but even in a population of mostly early stages of RAP, retreatment rates remained high.

Role of inflammation-related gene polymorphisms in patients with central retinal vein occlusion.

OBJECTIVE: Central retinal vein occlusion (CRVO) is a vision-threatening disease, primarily occurring among patients aged more than 60 years. Several risk factors, including arterial hypertension and diabetes mellitus, have been identified. Compression of the central retinal vein by an atherosclerotic retinal artery at the lamina cribrosa also has been implicated in the pathogenesis of the disease. Functional gene polymorphisms of cytokines or chemokines previously shown to affect atherogenesis or hemostasis are potential risk factors for CRVO. The present study investigates a hypothesized association between inflammation-related gene polymorphisms and the presence of CRVO in a relatively large cohort of patients. DESIGN: Case-control study. PARTICIPANTS: The study group consisted of 315 patients with CRVO and 335 control subjects. METHODS: Determination of genotypes was done by 5' exonuclease assay (TaqMan). MAIN OUTCOME MEASURES: Genotypes of interleukin (IL)1ß -511C>T, IL1 receptor antagonist (IL1RN) 1018T>C, IL4 -584C>T, IL6 -174G>C, IL10 -592C>A, IL18 183A>G, tumor necrosis factor (TNF)-α -308G>A, monocyte chemoattractant protein (MCP)-1/CCL2 -2518A>G, IL8 -251A>T, and RANTES (CCL5) -403G>A polymorphisms. RESULTS: Genotype distributions and allele frequencies of the investigated gene polymorphisms did not significantly differ between both groups (P>0.05). Arterial hypertension, diabetes mellitus, and cigarette smoking were significantly more frequent in patients with CRVO than among control subjects (arterial hypertension: 67.0% vs. 52.2%, P<0.001; diabetes mellitus: 16.8% vs. 6.3%, P<0.001, cigarette smoking: 32.1% vs. 23.6%, P = 0.02). In a logistic regression analysis, the presence of arterial hypertension was associated with an odds ratio (OR) of 1.75 (95% confidence interval [CI], 1.26-2.44) in those with CRVO, whereas an OR of 2.52 (95% CI, 1.46-4.35) was found in those with diabetes mellitus. A history of cigarette smoking was associated with an OR of 1.57 (95% CI, 1.09 - 2.25) for CRVO. CONCLUSIONS: Our data suggest that the investigated inflammation-related gene polymorphisms are unlikely major risk factors for CRVO. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Twenty-three-gauge and 20-gauge vitrectomy in epiretinal membrane surgery.

PURPOSE: The purpose of this study was to investigate the safety profile of the 23-gauge sutureless vitrectomy system in the treatment of epiretinal membranes compared with standard 20-gauge vitrectomy. METHODS: A retrospective case comparison of 20-gauge and 23-gauge vitrectomy performed in 167 and 64 eyes, respectively, by the same surgeon. Intraoperative and postoperative complications, duration of surgery, and postoperative visual acuity results were evaluated. RESULTS: Postoperative hypotony occurred significantly more often in the 23-gauge group [9.4% (n = 6) vs. 0% (n = 0), P < 0.001]. With the 23-gauge system, the incidence of retinal detachment was 1.6% (n = 1), vitreous hemorrhage was 0%, and endophthalmitis was 1.6% (n = 1). Patients with 20-gauge vitrectomy developed retinal detachments in 1.8% (n = 3), vitreous hemorrhages in 1.2% (n = 2), and endophthalmitis in 2.4% (n = 4). The mean overall duration of surgery was significantly shorter in the 23-gauge procedures with 23.1 +/- 6.5 minutes compared with 34.5 +/- 9.1 minutes in the 20-gauge procedures (P < 0.05). At postoperative Day 2, patients with 23-gauge vitrectomy regained preoperative mean best-corrected visual acuity of 20/60. Patients who had 20-gauge vitrectomy experienced a statistically significant decrease of visual acuity from 20/80 to 20/100 (P < 0.05). CONCLUSION: Twenty-three-gauge vitrectomy in epiretinal membrane surgery is comparable with 20-gauge vitrectomy and is a safe method with a low complication rate. However, the incidence of postoperative hypotony is more frequent using the 23-gauge system.

Analysis of inflammation- and atherosclerosis-related gene polymorphisms in branch retinal vein occlusion.

PURPOSE: Branch retinal vein occlusion (BRVO) is a common vision-threatening disease. Compression of the underlying retinal vein due to increased rigidity of the crossing artery has been implicated in the pathogenesis of BRVO. Among others, arterial hypertension and hypercholesterolemia, both of which contribute to atherogenesis, have been identified as risk factors. Atherosclerosis itself is a chronic low-grade inflammatory disease with a distinct pro-inflammatory cytokine pattern. In addition to their role in atherogenesis, some cytokines have been shown to exert procoagulatory effects, and may thus contribute to the development of BRVO by a second mechanism. Gene polymorphisms affecting the expression of inflammation-related cytokines are therefore candidates as potential risk factors for BRVO. The purpose of the present study was to investigate hypothesized associations between cytokine gene polymorphisms and the presence of BRVO. METHODS: The study comprised 398 patients with BRVO and 355 control subjects. Using 5'exonuclease assays (TaqMan), genotypes of the following functional single nucleotide polymorphisms were determined: interleukin 1 beta (IL1B) -511C>T, interleukin 1 receptor antagonist (IL1RN) 1018T>C, interleukin 4 (IL4) -584C>T, interleukin 6 (IL6) -174G>C, interleukin 8 (IL8) -251A>T, interleukin 10 (IL10) -592C>A, interleukin 18 (IL18) 183A>G, tumor necrosis factor (TNF) -308G>A, monocyte chemoattractant protein 1 (CCL2) -2518A>G, and RANTES (CCL5) -403G>A. RESULTS: Neither genotype distributions nor allele frequencies of any of the investigated polymorphisms differed significantly between BRVO patients and controls (p>0.05). Arterial hypertension was found to be significantly more prevalent in BRVO patients than in controls (p<0.001). In a logistic regression analysis presence of arterial hypertension was associated with an odds ratio of 3.33 (95% confidence interval: 2.42-4.57) for BRVO. CONCLUSIONS: As none of the investigated gene variants was significantly more prevalent in BRVO patients than among control subjects, our data suggest that these polymorphisms themselves are unlikely major risk factors for BRVO.

Analysis of three pigment epithelium-derived factor gene polymorphisms in patients with exudative age-related macular degeneration.

PURPOSE: Exudative age-related macular degeneration (exudative AMD) is a common vision-threatening disease, with both environmental and genetic factors contributing to its development. Recently, homozygosity for the 72Met variant of the pigment epithelium-derived factor (PEDF) Met72Thr gene polymorphism (rs1136287) was identified as a novel risk factor for exudative AMD in Chinese patients from Taiwan. The role of this polymorphism, however, has not yet been determined in a white European population. In addition, two other PEDF gene polymorphisms, -5736T>C (rs12150053) and -5304C>T (rs12948385), have been associated with increased risk of diabetic retinopathy, but have not yet been studied among patients with exudative AMD. The purpose of the present study was thus to investigate a hypothesized association between these PEDF polymorphisms and the presence of exudative AMD in a white European population. METHODS: The present case-control study comprised 269 patients with exudative AMD and 155 control subjects. Genotypes of the PEDF polymorphisms were determined by 5'-exonuclease assays (TaqMan). RESULTS: PEDF genotype and allele frequencies were not significantly different between AMD patients and control subjects. The two promoter polymorphisms, -5736T>C (rs12150053) and -5304C>T (rs12948385), were in complete association. Presence of the homozygous PEDF 72 Met/Met genotype was associated with a nonsignificant odds ratio of 1.00 (95% confidence interval: 0.67-1.49, p=0.99). Similarly, presence of the homozygous PEDF -5736 TT genotype or -5304 CC genotype was associated with a nonsignificant odds ratio of 0.99 (95% confidence interval: 0.56 - 1.75, p=0.97). Both promoter polymorphisms were in linkage disequilibrium with the Met72Thr (rs1136287) polymorphism (D'=0.83) and formed three common and one rare haplotype. Haplotype frequencies were similar between AMD patients and control subjects (p>0.05). CONCLUSIONS: Our data suggest that none of the investigated PEDF polymorphisms is likely a major risk factor for exudative AMD in a white European population.

Association of the HTRA1 -625G>A promoter gene polymorphism with exudative age-related macular degeneration in a Central European population.

PURPOSE: Exudative age-related macular degeneration (AMD) is one of the most common causes of severe visual loss. Both environmental and genetic factors, such as the complement factor H (CFH) 402H allele, have been associated with AMD. Recently, the HTRA1 -625A allele was identified as a novel risk marker in both a North American and a Chinese population. The present study was performed to evaluate the association of the HTRA1 -625A allele with exudative AMD in a Central European population. METHODS: The present case-control study included 242 patients with exudative AMD and 157 control subjects. Genotypes of the HTRA1 -625G>A polymorphism were determined by a 5'-exonuclease assay (TaqMan). Determination of CFH Y402H genotypes was done by allele specific digestion of polymerase chain products. RESULTS: Carriers of the HTRA1 -625AA genotype were found significantly more often in AMD patients than among control subjects (27.7% versus 5.1%; p<0.001). Binary logistic regression analysis binary logistic regression analysis revealed an odds ratio (OR) of 2.7 (95% confidence interval (CI): 1.1-6.8) for AMD among subjects heterozygous for the HTRA1 -625A allele compared to those with the wildtype genotype, when adjusted for CFH Y402H genotypes (p=0.034). The OR increased to 10.2 (95% CI: 3.0-34.5) among subjects homozygous for the HTRA1 -625A allele (p<0.001). The OR for AMD among heterozygous carriers of the CFH 402H variant was 3.6 (95% CI: 1.6-7.8) compared to those with the wildtype genotype, when adjusted for HTRA1 -625G>A genotypes (p=0.001). The OR increased to 9.8 (95% CI: 3.7-25.9) among subjects homozygous for the CFH 402HH genotype (p<0.001). Interaction terms between CFH and HTRA1 genotypes were not significantly associated with AMD. CONCLUSIONS: Our data suggest that both the HTRA1 -625A allele and the CFH 402H allele are independently associated with exudative AMD in a Central European population.

Association of complement factor H Y402H gene polymorphism with different subtypes of exudative age-related macular degeneration.

OBJECTIVE: Exudative age-related macular degeneration (AMD) is a common cause for a severe central visual loss. The complement system has been implicated in the pathogenesis of drusen. Recently, a complement factor H (CFH) polymorphism, which is characterized by a tyrosine (Y)-to-histidine (H) exchange at position 402 of the CFH gene, has been suggested as a major risk factor for AMD in a North American population. The aim of the present study was to investigate a hypothesized association between the CFH Y402H polymorphism and the presence of exudative AMD in a Central European population of Caucasoid descent as well as to determine the genotype distribution among different types of exudative AMD. DESIGN: Retrospective case-control study. PARTICIPANTS: The study cohort consisted of 179 patients with exudative AMD and 163 controls. METHODS: Determination of genotypes was carried out by allele-specific digestion of polymerase chain reaction products. MAIN OUTCOME MEASURES: Genotypes of CFH Y402H polymorphism. RESULTS: The prevalence of the CFH 402HH genotype was significantly higher in patients with exudative AMD than among controls (35.2% vs. 8.6%; P<0.001). Homozygosity for the CFH Y402H polymorphism was associated with an odds ratio of 5.78 (95% confidence interval, 3.09-10.83) for exudative AMD. Subgroup analysis revealed that the CFH 402HH genotype was significantly more prevalent in eyes with predominantly classic with no occult choroidal neovascularization (CNV) than in those with either retinal angiomatous proliferation, occult with no classic CNV, or predominantly classic with occult CNV. CONCLUSION: Our data suggest that the CFH Y402H polymorphism is a major risk factor for exudative AMD in a Central European population.

Haplotype-tagging interleukin-10 promoter polymorphism is associated with reduced risk of retinal artery occlusion.

PURPOSE: Pro- and anti-inflammatory cytokines, including interleukin 10 (IL-10), play an essential role in atherogenesis. Increased IL-10 production has been found among carriers of the IL10 [TCATA] haplotype, which is formed by five polymorphisms at position -3575, -2763, -1082, -819, and -592 in the promoter region of the IL10 gene. Due to linkage disequilibrium, the presence of the [TCATA] haplotype can be unequivocally determined by analysis of the IL10-592C>A polymorphism. The purpose of the present study was to investigate a hypothesized association between the haplotype-tagging IL10 -592C>A polymorphism and the presence of retinal artery occlusion (RAO). METHODS: The present case-control study was comprised of 194 patients with RAO and 257 normal control subjects. Genotypes of the IL10 -592C>A polymorphism were determined by fluorogenic exonuclease (TaqMan) assay. RESULTS: Carriers of the IL10 -592A-allele, indicating the presence of the IL10 [TCATA] haplotype, were found significantly more often in controls than among patients with RAO (48.6% versus 36.1%; p=0.008). In a logistic regression analysis after adjusting for age, sex, arterial hypertension, diabetes mellitus, hypercholesterolemia, and smoking habits, carriage of the IL10 -592A-allele was associated with an odds ratio of 0.65 (95% CI: 0.44-0.97) for RAO. CONCLUSIONS: Our data suggest that the IL10 [TCATA] haplotype, identified by the presence of the IL10 -592A-allele, may exert a protective effect against RAO.

Angiotensin-converting enzyme insertion/deletion polymorphism and retinal artery occlusion.

PURPOSE: An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting enzyme (ACE) is associated with higher ACE plasma levels and activity. This enzyme is known to play an important role in blood pressure regulation and the ACE I/D gene polymorphism has been suggested as a risk factor for atherosclerotic vascular diseases. The purpose of the present study was to investigate a hypothesized association between the ACE I/D polymorphism and retinal artery occlusion (RAO). METHODS: A total of 159 patients with RAO and 304 control subjects were enrolled in the present retrospective case-control study. ACE I/D genotypes were determined by polymerase chain reaction. RESULTS: Allelic frequencies and genotype distribution of the ACE I/D polymorphism did not significantly differ between patients and control subjects (ACE DD 25.8% versus 28.0%; p = 0.36). A logistic regression analysis predicted the presence of RAO by arterial hypertension and current smoking status, but not by ACE I/D genotypes. CONCLUSION: Our data suggest that the ACE I/D polymorphism is not a major risk factor for RAO.

Methylenetetrahydrofolatereductase (MTHFR) 677C>T polymorphism and open angle glaucoma.

PURPOSE: Increased plasma homocysteine levels have been found in patients with primary open angle glaucoma (POAG) and glaucoma secondary to pseudoexfoliation syndrome (PEXG). A common polymorphism of the methylenetetrahydrofolatereductase (MTHFR 677C>T) leads to moderately elevated plasma homocysteine levels particularly under conditions of impaired folate status. It was the aim of this study to investigate a hypothesized association between this polymorphism and the presence of either POAG or PEXG. METHODS: The present retrospective case-control study included a total of 553 participants comprising 204 patients with POAG, 138 patients with PEXG, and 211 control subjects. Genotyping for the MTHFR 677C>T polymorphism was performed by polymerase chain reaction (PCR). RESULTS: No significant difference in the genotype distribution of the MTHFR 677C>T polymorphism was found between control subjects and patients with POAG or PEXG. The prevalence of the MTHFR 677TT genotype was 6.9% in patients with POAG, 11.6% in patients with PEXG, and 9.5% in control subjects. CONCLUSIONS: The present data suggest that the MTHFR 677C>T polymorphism itself is not a major genetic risk factor for POAG and PEXG in a central European population.

Impairment of homocysteine metabolism in patients with retinal vascular occlusion and non-arteritic ischemic optic neuropathy.

Mild hyperhomocysteinemia is established as an independent risk factor for atherothrombotic disease, including ocular pathologies such as retinal vascular occlusion and non-arteritic ischemic optic neuropathy (NAION). Low intake or low status of B-vitamins explains elevated total homocysteine (tHcy) concentrations only in part. The underlying cause for disturbed homocysteine metabolism requires further insight. We investigated whether the combined determinations of plasma tHcy, methylmalonic acid (MMA) and cystathionine provide more information on the causes of impaired homocysteine metabolism as compared with vitamin B12, vitamin B6 and folate in patients with ocular ischemic vascular disease. A total of 51 hyperhomocysteinemic (>12 micromol/L) patients with retinal vascular occlusion (n=42) and NAION (n=9) were included. Mild renal dysfunction was an important determinant of tHcy, indicated by the positive correlation between creatinine and tHcy (r=0.47, p=0.001). The assessment of MMA in addition to tHcy identified at least 12 out of 51 patients (23%) who were most likely to have a functional vitamin B12 deficiency. An additional 14 patients (27%) with elevated MMA and cystathionine levels also had slightly elevated concentrations of creatinine, pointing to the need for discrimination between renal dysfunction and vitamin B12 deficiency in this group. In contrast, measurement of cystathionine is very sensitive for renal dysfunction and this marker was strongly related to serum creatinine (r=0.56, p<0.001) and to tHcy (r=0.50, p<0.001). Measurement of the vitamins folate, vitamin B12 and vitamin B6 in plasma did not provide sufficient information on intracellular disturbances in homocysteine metabolism. In conclusion, the metabolites homocysteine, cystathionine and MMA are sensitive indicators and valuable for discrimination of the underlying cause of mild to moderate hyperhomocysteinemia, with implications for therapeutic targeting.

Role of thrombophilic gene polymorphisms in branch retinal vein occlusion.

OBJECTIVE: Branch retinal vein occlusion (BRVO) is a common cause of severe visual loss. Numerous risk factors, including arterial hypertension, diabetes mellitus, and arteriosclerosis, have been identified. Gene polymorphisms affecting hemostasis may also play a role in the pathogenesis of BRVO. The present study was therefore done to determine the prevalence of genetic polymorphisms in factors implicated in hypercoagulability among patients with BRVO. DESIGN: Retrospective case-control study. PARTICIPANTS: The study cohort consisted of 294 patients with BRVO and 294 control subjects, matched for age and gender. METHODS: Determination of genotypes was done by allele-specific digestion of polymerase chain reaction products, or by 5' exonuclease assay (TaqMan). MAIN OUTCOME PARAMETERS: Genotypes of factor V R506Q (factor V Leiden), prothrombin 20210G>A, fibrinogen beta -455G> A, factor XII (FXII) 46C>T, and ITGA2 807C>T (platelet glycoprotein Ia [GPIa] 807C>T) and ITGB3 L59P (platelet GPIIIa PlA1/PlA2) polymorphisms. RESULTS: Genotype distributions of the investigated gene polymorphisms did not differ significantly between patients and control subjects. In contrast, significantly increased prevalences of arterial hypertension and hypercholesterolemia were found among patients with BRVO. In a logistic regression analysis, the presence of arterial hypertension was associated with an odds ratio (OR) of 2.32 (95% confidence interval [CI], 1.62-3.32), whereas hypercholesterolemia yielded an OR of 2.54 (95% CI, 1.74-3.70) for BRVO. CONCLUSION: Our data indicate that the prevalences of the investigated gene polymorphisms do not differ significantly in patients with BRVO and control subjects. This suggests that these polymorphisms are not major risk factors for BRVO.

Role of the interleukin-6 -174 G>C gene polymorphism in retinal artery occlusion.

BACKGROUND AND PURPOSE: Proinflammatory cytokines including interleukin-6 (IL-6) are supposed to play a pivotal role in the development of atherosclerosis. A common polymorphism in the promoter of the IL-6 gene (IL-6 -174G>C) affects plasma IL-6 concentrations and has been suggested as a risk factor for cardiovascular disease. The aim of the present case-control study was to investigate the role of this polymorphism for retinal artery occlusion (RAO). METHODS: One hundred eighty-two patients with RAO and 307 control subjects were genotyped for the IL-6 -174G>C polymorphism. Genotypes were determined by fluorogenic exonuclease (TaqMan) assay. RESULTS: The prevalence of the CC genotype was significantly lower in patients with RAO than in control subjects (10.4% versus 19.9%; P=0.006). Homozygosity for the C allele was associated with an odds ratio of 0.50 (95% CI, 0.28 to 0.89) for RAO. CONCLUSIONS: The CC genotype of the IL-6 -174G>C polymorphism may be associated with a protective effect against RAO.