OBJECTIVE Men with gout have been found to have an increased risk of acute myocardial infarction (AMI), but no corresponding data are available among women. We evaluated the potential independent association between gout and the risk of AMI among elderly women, aged ≥65 years. METHODS We conducted a population-based cohort study using the British Columbia Linked Health Database and compared incidence rates of AMI between 9,642 gout patients and 48,210 controls, with no history of ischemic heart disease. Cox proportional hazards models stratified by gender were used to estimate the relative risk (RR) for AMI, adjusting for age, co-morbidities, and prescription medication use. RESULTS Over 7-year median follow-up, we identified 3,268 incident AMI cases, 996 among women. Compared to women without gout, the multivariate RRs among women with gout were 1.39 (95% CI, 1.20–1.61) for all AMI and 1.41 (95% CI, 1.19–1.67) for non-fatal AMI. These RRs were significantly larger than those among men (multivariate RRs for all AMI and non-fatal AMI, 1.11 and 1.11; P-values for interaction, 0.003 and 0.005, respectively). CONCLUSION These population-based data suggest that women with gout have an increased risk for AMI and the magnitude of excess risk is higher than in men.

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BackgroundHepatitis C virus (HCV) genotype-3a infection is now the dominant strain in South Asia and the UK. Characteristic features include a favourable response to therapy; the reasons for this are unknown but may include distinct genotype-3a-specific T cell immunity. In contrast to genotype-1 infection, T cell immunity to this subtype is poorly defined.ObjectivesThe aims of the study were to (1) define the frequency, specificity and cross-reactivity of T cell immunity across the whole viral genome in genotype-3a infection and (2) assess the impact of interferon (IFN)-α/ribavirin on T cell immunity.DesignT cell responses in chronic and resolved HCV genotype-3a were analysed in comparison with genotype-1 infection (total n=85) using specific peptide panels in IFN-γ ELISpot assays. T cell responses were followed longitudinally in a subset of genotype-3a infected patients receiving therapy. Responses were further defined by CD4 and CD8 subset analysis, sequencing of autologous virus and cross-reactivity of genotype-3a with genotype-1a/-1b antigens.ResultsCD8 T cell responses commonly targeted the non-structural (NS) proteins in chronic genotype-3a infection whereas in genotype-1 infection CD4 responses targeting HCV core predominated (p=0.0183). Resolved infection was associated with CD4 T cells targeting NS proteins. Paradoxically, a sustained response to therapy was associated with a brisk decline in virus-specific and total lymphocyte counts that recovered after treatment.ConclusionHCV genotype-3a exhibits a distinct T cell specificity with implications for vaccine design. However, our data do not support the theory that genotype-3a viral clearance with therapy is associated with an enhanced antiviral T cell response. Paradoxically, a reduction in these responses may serve as a biomarker of IFN responsiveness.