D P C de Rooy1, J A B van Nies1, M C Kapetanovic2, H Kristjansdottir3, M L E Andersson4, K Forslind5, D M F M van der Heijde1, P K Gregersen6, E Lindqvist2, T W J Huizinga1, G Gröndal3, B Svensson7, A H M van der Helm-van Mil1. 1. Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands. 2. Section of Rheumatology, Department of Clinical Sciences, Lund University, Lund, Sweden Department of Rheumatology, Skåne University Hospital, Lund, Sweden. 3. Department of Rheumatology and Center for Rheumatology Research, Landspítali-The National University Hospital of Iceland, Reykjavik, Iceland. 4. R and D Centre, Spenshult Hospital, Oskarström, Sweden Section of Rheumatology, Department of Clinical Sciences, Lund University, Sweden for the BARFOT study group, Lund, Sweden. 5. Section of Rheumatology, Department of Clinical Sciences, Lund University, Sweden for the BARFOT study group, Lund, Sweden Section of Rheumatology, Department of Medicine, Helsingborg's lasarett, Helsingborg, Sweden. 6. Feinstein Institute for Medical Research and North Shore-Long Island Jewish Health System, Manhasset, New York, USA. 7. Section of Rheumatology, Department of Clinical Sciences, Lund University, Sweden for the BARFOT study group, Lund, Sweden.
Abstract
BACKGROUND: Smoking is a risk factor for the development of anti -citrullinated protein antibodies (ACPA) positive rheumatoid arthritis (RA). Whether smoking predisposes to severe joint damage progression is not known, since deleterious, protective and neutral observations have been made. OBJECTIVE: To determine the effect of smoking on joint damage progression. METHODS: Smoking status was assessed in 3158 RA patients included in six cohorts (Leiden Early Arthritis Clinic (Leiden-EAC), BARFOT, Lund, Iceland, NDB and Wichita). In total 9412 radiographs were assessed. Multivariate normal regression and linear regression analyses were performed. Data were summarised in a random effects inverse variance meta-analysis. RESULTS: When comparing radiological progression for RA patients that were never, past and current smokers, smoking was significantly associated with more severe joint damage in Leiden-EAC (p=0.042) and BARFOT (p=0.015) RA patients. No significant associations were found in the other cohorts, though a meta-analysis on the six cohorts showed significantly more severe joint damage progression in smokers (p=0.01). Since smoking predisposes to ACPA, analyses were repeated with ACPA as additional adjustment factor. Then the association was lost (meta-analysis p=0.29). CONCLUSIONS: This multi-cohort study indicated that the effect of smoking on joint damage is mediated via ACPA and that smoking is not an independent risk factor for radiological progression in RA. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
BACKGROUND: Smoking is a risk factor for the development of anti -citrullinated protein antibodies (ACPA) positive rheumatoid arthritis (RA). Whether smoking predisposes to severe joint damage progression is not known, since deleterious, protective and neutral observations have been made. OBJECTIVE: To determine the effect of smoking on joint damage progression. METHODS: Smoking status was assessed in 3158 RApatients included in six cohorts (Leiden Early Arthritis Clinic (Leiden-EAC), BARFOT, Lund, Iceland, NDB and Wichita). In total 9412 radiographs were assessed. Multivariate normal regression and linear regression analyses were performed. Data were summarised in a random effects inverse variance meta-analysis. RESULTS: When comparing radiological progression for RApatients that were never, past and current smokers, smoking was significantly associated with more severe joint damage in Leiden-EAC (p=0.042) and BARFOT (p=0.015) RApatients. No significant associations were found in the other cohorts, though a meta-analysis on the six cohorts showed significantly more severe joint damage progression in smokers (p=0.01). Since smoking predisposes to ACPA, analyses were repeated with ACPA as additional adjustment factor. Then the association was lost (meta-analysis p=0.29). CONCLUSIONS: This multi-cohort study indicated that the effect of smoking on joint damage is mediated via ACPA and that smoking is not an independent risk factor for radiological progression in RA. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Authors: Jeremy Sokolove; Catriona A Wagner; Lauren J Lahey; Harlan Sayles; Michael J Duryee; Andreas M Reimold; Gail Kerr; William H Robinson; Grant W Cannon; Geoffrey M Thiele; Ted R Mikuls Journal: Rheumatology (Oxford) Date: 2016-07-31 Impact factor: 7.580
Authors: Xinyi Liu; Sara K Tedeschi; Medha Barbhaiya; Cianna L Leatherwood; Cameron B Speyer; Bing Lu; Karen H Costenbader; Elizabeth W Karlson; Jeffrey A Sparks Journal: Arthritis Care Res (Hoboken) Date: 2019-07 Impact factor: 4.794
Authors: Kathleen Chang; So Min Yang; Seong Heon Kim; Kyoung Hee Han; Se Jin Park; Jae Il Shin Journal: Int J Mol Sci Date: 2014-12-03 Impact factor: 5.923
Authors: Saedis Saevarsdottir; Hamed Rezaei; Pierre Geborek; Ingemar Petersson; Sofia Ernestam; Kristina Albertsson; Kristina Forslind; Ronald F van Vollenhoven Journal: Ann Rheum Dis Date: 2014-04-04 Impact factor: 19.103
Authors: Emil Rydell; Kristina Forslind; Jan-Åke Nilsson; Lennart T H Jacobsson; Carl Turesson Journal: Arthritis Res Ther Date: 2018-05-02 Impact factor: 5.156