https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15139 Wed 11 Apr 2018 14:39:08 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14944 Wed 11 Apr 2018 14:30:16 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25744 T), a single nucleotide polymorphism encoding substitution of arginine for tryptophan in PTPN22 (R620W), in 193 patients with PAD and 148 control subjects from an Australian cohort. We also performed a subgroup analysis according to the presence of autoimmunity and B-cell phenotypes. Results: C/T and T/T PTPN22 genotypes were more common in patients with PAD than in the matched control subjects (C/T, 18.1% vs 9.5%; T/T, 1.04% vs 0.6%). The T allele was associated with an increased risk of PAD relative to control subjects (odds ratio, 2.10; 95% CI, 1.11-4.00). The distribution of genotypes in control subjects was similar to those reported previously and did not deviate significantly from Hardy-Weinberg equilibrium. We found a strong association between the 1858T allele and PAD with coexistent autoimmune diseases. In patients with PAD and autoimmunity, 16 (43.2%) of 37 had at least one T allele of PTPN22 compared with 27 (17.3%) of 156 with the C/C genotype (P = .0014; odds ratio, 3.64; 95% CI, 1.68-7.88). We found no evidence that this effect was mediated by enrichment of CD21low B cells. Conclusion: The 1858T PTPN22 allele is strongly associated with autoimmunity in patients with PAD.]]> Sat 24 Mar 2018 07:30:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24254 Sat 24 Mar 2018 07:15:08 AEDT ]]>