ObjectiveTo identify risk alleles relevant to the causal and biologic mechanisms of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis (AAV).MethodsA genome‐wide association study and subsequent replication study were conducted in a total cohort of 1,986 cases of AAV (patients with granulomatosis with polyangiitis [Wegener's] [GPA] or microscopic polyangiitis [MPA]) and 4,723 healthy controls. Meta‐analysis of these data sets and functional annotation of identified risk loci were performed, and candidate disease variants with unknown functional effects were investigated for their impact on gene expression and/or protein function.ResultsAmong the genome‐wide significant associations identified, the largest effect on risk of AAV came from the single‐nucleotide polymorphism variants rs141530233 and rs1042169 at the HLA–DPB1 locus (odds ratio [OR] 2.99 and OR 2.82, respectively) which, together with a third variant, rs386699872, constitute a triallelic risk haplotype associated with reduced expression of the HLA–DPB1 gene and HLA–DP protein in B cells and monocytes and with increased frequency of complementary proteinase 3 (PR3)–reactive T cells relative to that in carriers of the protective haplotype. Significant associations were also observed at the SERPINA1 and PTPN22 loci, the peak signals arising from functionally relevant missense variants, and at PRTN3, in which the top‐scoring variant correlated with increased PRTN3 expression in neutrophils. Effects of individual loci on AAV risk differed between patients with GPA and those with MPA or between patients with PR3‐ANCAs and those with myeloperoxidase‐ANCAs, but the collective population attributable fraction for these variants was substantive, at 77%.ConclusionThis study reveals the association of susceptibility to GPA and MPA with functional gene variants that explain much of the genetic etiology of AAV, could influence and possibly be predictors of the clinical presentation, and appear to alter immune cell proteins and responses likely to be key factors in the pathogenesis of AAV.

Background Cataracts is the major global causes of blindness and a vision-affecting disease of the eye. Cataract surgery is a curative and cost-effective intervention. The number of people who undergo cataract surgery has increased rapidly. Hence, this study was aimed to determine predictors and the time of recovery of cataract patients after cataract surgery by using Simi parametric models of survival analysis. Methods A retrospective cohort study was conducted from January/01/2015 and January/30/2019. STATA version14.0 statistical software was used for analysis. The Kaplan-Meier survival method and log-rank test curves were applied. Weibull regression was used and adjusted hazard ratio 95% CI with a value of p less than 0.05 was used to identify a significant association. Results Two hundred twenty three cataract patients were recovered from cataract, 72.6% (95% CI 69.8%–75.9%). The overall median survival time was 23 weeks (IQR = 16 to 35) with (95% CI, 21%–25%). aged between 16 and 30year (AHR = 1.20 CI; 1.07–2.36), age 31 to 45 (AHR = 1.24 CI; 1.08–1.54), urban dwellers (AHR = 1.59; 95% CI, 1.18–2.14), medium visual acuity (AHR = 4.14 CI; 2.57–6.67), high visual acuity (AHR = 5.23 CI; 3.06–8.93), Secondary cataract (AHR = 2.59 CI; 1.01–3.02), traumatic cataract (AHR = 1.75 CI; 1.01–3.02), extra capsular cataract extraction surgery (AHR = 1.43 CI; 1.07–1.94),and diabetes mellitus (AHR = 0.75, CI; 0.41–0.96) were notably associated with time to recovery. Conclusion Time to recovery in the study area was slightly higher as compared with the global cut of time. Cataract patients with comorbidity of DM had lower recovery time.