https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2100 Wed 24 Jul 2013 22:55:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35106 Wed 21 Jun 2023 11:30:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19510 40 U/ml) ACA-IgG OR 4.60, 95% CI:1.02–20.8, p=0.047). Both ACA-IgM (OR 2.04, 95% CI: 1.4-3.0, p<0.0001) and ACA-IgG (OR 1.84, 95% CI: 1.2-2.8, p=0.005) were associated with interstitial lung disease (ILD). Increasing ACA-IgM and IgG titres were associated with increased likelihood of ILD. ACA-IgG was a marker of coexistent pulmonary hypertension and ILD (ILD-PH) (OR 2.10, 95% CI: 1.1-4.2, p=0.036). We also found an association between ACA-IgG and digital ulcers (OR 1.76, 95% CI: 1.16-2.67, p=0.008) and ACA-IgM and Raynaud`s phenomenon (OR 2.39, 95% CI: 1.08-5.27, p=0.031). There was no association between APLA and SSc disease subtype, peak skin score, presence of other autoantibodies, mortality or other disease manifestations. CONCLUSIONS: The association of APLA with PAH, ILD, ILD-PH, Raynaud`s phenomenon and digital ulcers suggests that endothelial abnormalities and small vessel thrombosis may be important in the pathogenesis of these disease features.]]> Sun 09 Aug 2015 09:58:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8133 Sat 24 Mar 2018 08:40:03 AEDT ]]>