Background:Smoking has been proposed to be associated with the development of anti-citrullinated peptide antibodies (ACPA) in rheumatoid arthritis (RA) patients.Objectives:To study the relationship between smoking and ACPA as well as smoking and RF in patients with RA in Kuwait Registry for Rheumatic Diseases (KRRD).Methods:Data on RA patients were extracted from KRRD from four major hospitals from February 2013 through December 2019. As females rarely smoke in Kuwait with a smoking prevalence of 3% in female RA patients in KRRD, females were excluded from the study population to reach the minimum statistical percentage needed to perform chi square test and assess the association between smoking and other variables. Statistical tests were applied where appropriate. Logistic regression was conducted to adjust for possible confounders including age, disease duration, comorbidities, family history of a rheumatic disease, ANA, treatment agents and disease activity and quality of life assessment tools.Results:A total of 863 RA male patients were studied with a mean age of 53.9±12.5 years and a mean disease duration 7.3±5.5 years. 652 (75.6%) had positive RF and 624 (72.3%) had positive ACPA. 431 (50%) had at least one comorbidity. 640 (74.2%) were on conventional disease modifying agents (cDMARD’s) and 223 (25.8%) were on biologic therapy. 183 (21.2%) were smokers. After adjustment of other factors, logistic regression showed that smokers were significantly different than non-smokers in terms of a positive ACPA (β=-1.051,p<0.001, odds=4.019) and a positive RF (β=-0.804,p=0.019, odds=2.517).Conclusion:Smokers have a higher risk of expressing a positive RF and a positive ACPA in a male population. Smoking should be considered as a possible risk factor for RA and efforts should be done to educate the population to cease smoking to possibly lower that risk.References:[1]Benowitz, N.L., 2009. Pharmacology of nicotine: addiction, smoking-induced disease, and therapeutics. Annual review of pharmacology and toxicology, 49, pp.57-71.[2]Firestein, G.S., 2003. Evolving concepts of rheumatoid arthritis. Nature, 423(6937), p.356.[3]Heliövaara, M., Aho, K., Aromaa, A., Knekt, P. and Reunanen, A., 1993. Smoking and risk of rheumatoid arthritis. The Journal of rheumatology, 20(11), pp.1830-1835.[4]Hoy, K. W., 2009. Quantitative Research in Education: A Primer. SAGE. pp. 69-86.[5]Kerlan-Candon, S., Combe, B., Vincent, R., Clot, J., Pinet, V. and Eliaou, J.F., 2001. HLA-DRB1 gene transcripts in rheumatoid arthritis. Clinical & Experimental Immunology, 124(1), pp.142-149.[6]Kuada, J., 2012. Research Methodology: A Project Guide for University Students. Samfundslitteratur. pp. 45-56.[7]Kumar, R., 2010. Research Methodology: A Step-by-Step Guide for Beginners. SAGE. pp. 148-159.[8]Masdottir, B., Jonsson, T., Manfreðsdóttir, V., Víkingsson, A., Brekkan, Á. and Valdimarsson, H., 2000. Smoking, rheumatoid factor isotypes and severity of rheumatoid arthritis. Rheumatology, 39(11), pp.1202-1205.[9]Neuman, W., 2009. Understanding research. Boston: Pearson. pp. 230- 255.Disclosure of Interests:None declared
Anticyclic Citrullinated Peptide Antibodies in Patients with Rheumatic Diseases other than Rheumatoid Arthritis: Clinical or Pathogenic Significance?
