Background The association between smoking and radiographic progression has been established in axial spondyloarthritides and rheumatoid arthritis (RA) but this association has not been established in psoriatic arthritis (PsA).
Objectives The aim of this study was to determine the effects of cigarette smoking on clinical joint damage in patients with psoriatic arthritis.
Methods From 1306 PsA patients followed prospectively between 1978 and 2014 as part of an observational cohort, a total of 1107 that started treatment after the first visit was included in the current study. We defined clinical damage as limitation of movement of more than 20% of the range that is not related to a joint effusion, the presence of flexion contractures, fused or flail joints, or evidence of surgery in a particular joint. We used clinical damage as it is assessed at each protocol visit and we have previously demonstrated that clinical joint damage in linked to radiological joint damage. We evaluated the smoking status at the baseline visit up until the first development of clinical joint damage. Smoking status was defined as “non-smoker”, “past smoker” and “current smoker”. Time to development of joint damage was assessed using a Cox Regression Analysis to determine the factors predictive of clinical damage, including age, sex, dactylitis and smoking status, joint counts, treatment and HLA B*27 status.
Results Among the 1107 patients, 55.6% were males, with a mean age of 46 years, duration of psoriasis 17.4 years and the duration of PsA 8.4 years at baseline. 55.6% of the patients were non-smokers, 24.4% were past-smokers and 12.4% were current smokers. 7.9% of the patient had clinical joint damage and 26% had dactylitis at baseline. Males, HLA-B*27 positivity, higher age at diagnosis of PsA, clinical damage at baseline, dactylitis and swollen joints were associated with a higher probability of developing clinically damaged joints whereas current and past-smokers at baseline were associated with a lower probability of developing clinically damaged joints compared to nonsmokers.
Conclusions Unlike what occurs in RA and ankylosing spondylitis, the clinical damage in PsA was not associated with smoking status but was associated with disease-specific features.
Disclosure of Interest None declared