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Purpose: The purpose of this study was to evaluate health-related quality of life in patients with retinal vein occlusion (RVO) and investigate the possible risk factors for poor quality of life in patients with RVO. Methods: Participants in the study were 67 patients with RVO, 42 male and 25 female, mean-aged 73.1 ± 10.9 years, and 70 sex- and age-matched controls. Demographic data, lifestyle factors and medical history were recorded. All patients underwent best-corrected visual acuity measurement, dilated fundoscopy and optical coherence tomography. All participants completed two questionnaires assessing quality of life (EQ-5D, NEI VFQ-25). Risk factors for health-related quality of life in RVO patients were investigated. Results: Patients with RVO exhibited significantly lower composite score for VFQ-25 compared to controls (74.1 ± 3.8 vs. 91.7 ± 3.9 for patients and controls, respectively, p <.001). In addition, RVO patients had significantly lower EQ-5D Index score compared to controls (0.88 ± 0.15 vs. 0.92 ± 0.12 for patients and controls, respectively, p =.043). Risk factors associated with quality of life in patients with RVO were found the alcohol consumption, the presence of thyroidopathy, coagulation disorders, visual acuity in the eye with RVO, central retinal thickness, the type of edema, the presence of ischemia and the condition of external limiting membrane. In multivariate analysis, only alcohol consumption and visual acuity in the eye with RVO were found to be independent risk factors, affecting quality of life in RVO patients. Conclusions: Patients with RVO presented lower quality of life in comparison with controls. Potential risk factors should be taken into account and their early detection may improve quality of life in such patients and lead to targeted health policies. [ABSTRACT FROM AUTHOR]

Mechanisms that favor Hepatitis C virus (HCV) persistence over clearance are unclear, but involve defective innate immunity. Chronic infection is characterized by hepatic iron overload, hyperferraemia and hyperferittinaemia. Hepcidin modulates iron egress via ferroportin and its storage in ferritin. Chronic HCV patients have decreased hepcidin, while HCV replication is modified by HAMP silencing. We aimed to investigate interactions between HCV and hepcidin, during acute and chronic disease, and putative alterations in cellular iron homeostasis that enhance HCV propagation and promote viral persistence. Thus, we used HCV JFH-1-infected co-cultures of Huh7.5 hepatoma and THP-1 macrophage cells, HCV patients’ sera and Huh7 hepcidin-expressing cells transfected with HCV replicons. Hepcidin levels were elevated in acutely infected patients, but correlated with viral load in chronic patients. HAMP expression was up-regulated early in HCV infectionin vitro, with corresponding changes in ferritin and FPN. Hepcidin overexpression enhanced both viral translation and replication. In HCV-infected co-cultures, we observed increased hepcidin, reduced hepatoma ferritin and a concurrent rise in macrophaghic ferritin over time. Altered iron levels complemented amplified replication in hepatoma cells and one replication round in macrophages. Iron-loading of macrophages led to enhancement of hepatic HCV replication through reversed ferritin “flow.” Viral transmissibility from infected macrophages to naïve hepatoma cells was induced by iron. We propose that HCV control over iron occurs both by intracellular iron sequestration, through hepcidin, and intercellular iron mobilisation via ferritin, as means toward enhanced replication. Persistence could be achieved through HCV-induced changes in macrophagic iron that enhances viral replication in these cells. [ABSTRACT FROM PUBLISHER]