2166: Inflammatory Arthritis in an Australian Scleroderma Cohort – Patient Characteristics, Associations and Treatments

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.