Royal College of Surgeons Bowling Green, KY, United States
Eric Schwender1, Dylan Hansen2, Wendy Stevens2, Laura Ross3, Nava Ferdowsi2, Susanna Proudman4, Jenny Walker5, Jo Sahhar6, Gene-Siew Ngian7, Lauren Host8, Gabor Major9, Mandana Nikpour10 and Kathleen Morrisroe2, 1Royal College of Surgeons, Dublin, Ireland, 2St Vincent's Hospital Melbourne, Melbourne, Australia, 3The University of Melbourne at St. Vincent's Hospital, Brunswick, Australia, 4Rheumatology Unit, Royal Adelaide Hospital, and Discipline of Medicine, University of Adelaide, Adelaide, Australia, 5Royal Adelaide Hospital, Adelaide, Australia, 6Monash Health, Melbourne, Australia, 7Melbourne Health, Northcote, Australia, 8Fiona Stanley Hospital, London, United Kingdom, 9Hunter New England Health Service, Rankin Park - Newcastle, New South Wales, Australia, 10The University of Melbourne at St. Vincent's Hospital Melbourne, Melbourne, Australia
Background/Purpose: To characterise a cohort of Australian scleroderma patients with inflammatory arthritis including patient characteristics, autoantibody profile, therapy and impact on function and quality of life.
Methods: 1717 scleroderma (SSc) patients, meeting ACR/EULAR criteria, were recruited from the Australian SSc Cohort Study (ASCS). Inflammatory arthritis (IA) was defined clinically as the presence of synovitis on examination. Patient reported outcome measures including quality of life (QoL) using the Medical Outcomes Study Short Form-36 and physical function using the health assessment questionnaire (HAQ) were recorded. Associations between IA and demographics, disease manifestations and autoantibody profile were investigated using logistic regression analysis.
Results: IA was a common manifestation in SSc affecting one third (33.3%) of SSc patients, more commonly found in limited SSc (lcSSc) than diffuse SSc (dcSSc) (69.9% vs 30.1%, p=0.001). A third of SSc patients, regardless of the presence of IA, had a positive rheumatoid factor (RF) (31.7% in those with IA vs 29.5% in those without IA, p=0.354), whereas the presence of anti-CCP antibody, although of low frequency, was significantly associated with IA (7.5% in those with IA vs 1.5% without IA, p< 0.001). The presence of IA was associated with higher unemployment (25.9% vs 19.2%, p=0.014) and reduced physical function (HAQ 1.25 vs 0.88, p< 0.001). In multivariate regression analysis (Table 1), IA was associated with female gender (OR 1.4, p=0.03), myositis (OR 2.0, p< 0.001), joint contractures (OR 1.7, p< 0.001), elevated CRP (OR 1.01, p< 0.001), and the absence of vascular complications of SSc renal crisis (SRC) and pulmonary arterial hypertension (PAH) (OR 0.5, p=0.03 and OR 0.5, p< 0.001 respectively) (Table 1). Those with IA, compared with those without IA, were more likely to be treated with immunosuppressive medications including prednisolone (61.9% vs 38.6%, p< 0.001), hydroxychloroquine (44.9% vs 13.1%, p< 0.001), methotrexate (46.0% vs 14.0%, p< 0.001), leflunomide (4.2% vs 0.3%, p< 0.001), rituximab (3.0% vs 0.5%, p< 0.001), tocilizumab (1.6% vs 0.3%, p=0.002) and abatacept (1.6% vs 0.0%, p< 0.001). Unsurprisingly, the presence of IA was associated with a lower QoL as reflected in both the physical and mental component scores (p< 0.001).
Conclusion: IA is a common disease manifestation in SSc which negatively impacts upon employment and QoL. In contrast to rheumatoid arthritis, the presence of a positive RF in SSc, despite its high prevalence, was not significantly associated with IA, whilst anti-CCP, despite its low prevalence, was strongly associated with IA. Additionally, the presence of IA in our cohort was associated with a lower prevalence of vascular complications. Table 1. Associations of inflammatory arthritis on multivariate regression analysis Abbreviations rheumatoid factor (RF), Scleroderma (SSc), pulmonary arterial hypertension (PAH), scleroderma renal crisis (SRC), c-reactive protein (CRP), antinuclear antibody (ANA) Disclosures: E. Schwender, None; D. Hansen, None; W. Stevens, None; L. Ross, None; N. Ferdowsi, None; S. Proudman, Janssen, Boehringer-Ingelheim; J. Walker, Boehringer-Ingelheim; J. Sahhar, Boehringer-Ingelheim; G. Ngian, None; L. Host, The limbic; G. Major, None; M. Nikpour, Janssen, AstraZeneca, GlaxoSmithKlein(GSK), Boehringer-Ingelheim, Bristol-Myers Squibb(BMS); K. Morrisroe, None.