Session Information
Date: Tuesday, November 15, 2016
Title: Spondylarthropathies and Psoriatic Arthritis – Clinical Aspects and Treatment - Poster III
Session Type: ACR Poster Session C
Session Time: 9:00AM-11:00AM
Background/Purpose: Smoking is a major modifiable risk factor for various inflammatory diseases including rheumatoid arthritis 1, 2 and psoriasis 3,4,5. The presence of cyclic citrullinated peptide antibody (CCP) has been associated with smoking in rheumatoid arthritis 1. Presence of CCP has also been shown to be associated with severe Psoriatic arthritis (PsA) in a few retrospective studies 6,7. Our aim is to assess the association of smoking and CCP Ab positivity in PsA, with the hypothesis that smoking is associated with severe PsA, and CCP may also be associated with severe arthritis.
Methods: Medical records of patients with PsA followed in our clinic from 2010 to 2015, identified by ICD 9 code were analyzed for demographic characteristics, body mass index (BMI), smoking status, CCP positivity and clinical characteristics for severe PsA. Severe disease was defined as treatment with biologics and/or joint erosions identified on hand and foot radiographs. Chi square statistic was used to assess the relationship between smoking and disease severity. The association of CCP positivity with severe PsA was determined by Fisher’s exact test.
Results: One hundred and twelve patients who were ever smokers and one hundred and thirteen never smokers were identified. 30.4% were found to have more severe disease in the ever smoker group and 36.3% were found to have more severe disease in the never smoker group with a relative risk of 0.84 (0.58-1.21, 95% CI)
Conclusion: A relationship between smoking status and disease severity was not identified. There were insufficient numbers of CCP positive patients to establish statistical significance for either positive association with smoking or disease severity. However, CCP positive patients were more likely to be on biologic medications, further studies are needed to establish relationship. References: 1. Klareskog et al. A new model for an etiology of rheumatoid arthritis: Smoking may trigger HLA–DR (shared epitope)–restricted immune reactions to auto antigens modified by citrullination. Arthritis and Rheumatism 2006;54:38–46 2. Stolt et al. Quantification of the influence of cigarette smoking on rheumatoid arthritis:results from a population based case-control study, using incident cases. Ann Rheum Dis 2003;62:835-841 3. Mills et al. Smoking habits in Psoriasis: a case control study. British Journal of dermatology 1992;127:18-21 4. Setty et al. Smoking and risk of Psoriasis in Women: Nurses’ Health Study II. Am J Med 2007;120:953-959 5. Armstrong et al. Smoking and pathogenesis of Psoriasis: a review of oxidative, inflammatory and genetic mechanisms. British Journal of dermatology 2011;165:1162-1168 6. Bogliolo et al. Antibodies to cyclic citrullinated peptides in psoriatic arthritis. Jrheum 2005; 32:511-515 7. Perez-Alamino et al. Are anti CCP antibodies in Psoriatic arthritis patients a biomarker of erosive disease. J Med Life 2013;6(4):376-82
To cite this abstract in AMA style:
Jarugula S, Libman B, Kennedy A, Howard D. Smoking and Severity of Psoriatic Arthritis [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/smoking-and-severity-of-psoriatic-arthritis/. Accessed .« Back to 2016 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/smoking-and-severity-of-psoriatic-arthritis/