Effects of cigarette smoking on early arthritis: a cross-sectional study—data from the Argentine Consortium for Early Arthritis (CONAART)

Salinas, María Jezabel Haye; Retamozo, Soledad; Álvarez, Ana Cecilia; Ficco, Hernán Maldonado; Pra, Fernando Dal; Citera, Gustavo; Benegas, Mariana; Moral, Rafael Chaparro del; Rillo, Oscar; Secco, Anastasia; Claverie, Lucila Marino; Pellet, Antonio Catalán; Marcos, Josefina; García, Mercedes; Marcos, Juan Carlos; Barbaglia, A. L.; Bellomio, Verónica; Berman, Alberto; Quiroz, Cristian; Soriano, Enrique R.; Ceccato, Federico; Paira, Sergio; Vazquez, Doralia; Juárez, Vicente; Velozo, E.; Salvatierra, Gabriela; Caeiro, Francisco

doi:10.1007/s00296-014-3188-7

Cited by 12 publications

(11 citation statements)

References 32 publications

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“…The association of smoking with development and severity of RA was documented almost 30 years ago [10] and confirmed in many subsequent studies [11][12][13][14][15][16][17][18][19][20][21]. A recent dose-response meta-analysis (encompassing 4,552 RA patients) reported relative risks of 1.26 and 1.96 for the associations of RA with smoking histories of 1-10 and >20 pack years respectively [19].…”

Section: Smoking and Ramentioning

confidence: 76%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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Smoking is now well recognised not only as a risk factor for rheumatoid arthritis (RA), but also as a determinant of disease activity, severity, response to therapy, and possibly mortality. Recent studies have provided significant insights into the molecular and cellular mechanisms which underpin the pathogenesis of smokingrelated RA. These involve release of the enzymes, peptidylarginine deiminases (PADs) 2 and 4 from smoke-activated, resident and infiltrating pulmonary phagocytes. PADs, in turn, mediate the conversion of various endogenous proteins to putative citrullinated autoantigens. In genetically susceptible individuals, these autoantigens trigger the production of anti-citrullinated peptide/protein pathogenic autoantibodies (ACPA), an event which precedes the development of RA. This review is focused primarily on smoking-mediated harmful chronic inflammatory responses, both local and systemic, which promote the formation of ACPA, as well as the possible involvement of other types of outdoor and indoor pollution in the pathogenesis of RA. This is preceded by a brief overview of the evidence implicating smoking as a risk factor for development of ACPA-positive RA.Keywords: Anti-citrullinated peptide/protein antibodies; airway microbiota; atmospheric pollution; heavy metals; peptidylarginine deiminases; smoking cessation strategies. ImplicationsChronic inflammatory mechanisms operative in the lungs of smokers lead to the production of anti-citrullinated protein antibodies which, in turn, drive the development of rheumatoid arthritis. These mechanistic insights not only reinforce the association between smoking and risk for rheumatoid arthritis, but also the necessity to increase the level of awareness in those at highest risk.

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Section: Smoking and Ramentioning

confidence: 76%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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“…Finally, in the assessment of multiple variables, type 1 statistical error may arise from chance such as the association of smoking with arthropathy. However, with the variable of arthritis, biological plausibility of smoking affecting joints is present in current smokers with rheumatoid/undifferentiated arthritis having increased joint disease activity and radiological joint erosions . Strengths of this study include its large number of patients, inclusion of both CD and UC patients, the extended follow‐up period and the width of clinical outcomes interrogated; ensuring comprehensive characterisation of disease course in smokers, ex‐smokers and never smokers.…”

Section: Discussionmentioning

confidence: 99%

“…However, with the variable of arthritis, biological plausibility of smoking affecting joints is present in current smokers with rheumatoid/undifferentiated arthritis having increased joint disease activity and radiological joint erosions. 59 Strengths of this study include its large number of patients, inclusion of both CD and UC patients, the extended follow-up period and the width of clinical outcomes interrogated; ensuring comprehensive characterisation of disease course in smokers, ex-smokers and never smokers. Translatable outcomes from this study include the association between arthritis and smoking in CD suggesting another possible avenue for treating this disabling extra-intestinal manifestation, and the lack of benefit of ongoing smoking on the natural history of UC, recommending cessation of smoking be offered to all patients with IBD.…”

Section: Discussionmentioning

confidence: 99%

Smoking prevalence and its influence on disease course and surgery in Crohn's disease and ulcerative colitis

Lunney

Kariyawasam

Wang

et al. 2015

Aliment Pharmacol Ther

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Summary Background Smoking demonstrates divergent effects in Crohn's disease (CD) and ulcerative colitis (UC). Smoking frequency is greater in CD and deleterious to its disease course. Conversely, UC is primarily a disease of nonsmokers and ex‐smokers, with reports of disease amelioration in active smoking. Aim To determine the prevalence of smoking and its effects on disease progression and surgery in a well‐characterised cohort of inflammatory bowel diseases (IBD) patients. Methods Patients with smoking data of the Sydney IBD Cohort were included. Demographic, phenotypic, medical, surgical and hospitalisation data were analysed and reported on the basis of patient smoking status. Results 1203 IBD patients were identified comprising 626 CD and 557 UC with 6725 and 6672 patient‐years of follow‐up, respectively. CD patients were more likely to smoke than UC patients (19.2% vs. 10.2%, P < 0.001). A history of smoking in CD was associated with an increased proportional surgery rate (45.8% vs. 37.8%, P = 0.045), requirement for IBD‐related hospitalisation (P = 0.009) and incidence of peripheral arthritis (29.8% vs. 22.0%, P = 0.027). Current smokers with UC demonstrated reduced corticosteroid utilisation (24.1% vs. 37.5%, P = 0.045), yet no reduction in the rates of colectomy (3.4% vs. 6.6%, P = 0.34) or hospital admission (P = 0.25) relative to nonsmokers. Ex‐smokers with UC required proportionately greater immunosuppressive (36.2% vs. 26.3%, P = 0.041) and corticosteroid (43.7% vs. 34.5%, P = 0.078) therapies compared with current and never smokers. Conclusions This study confirms the detrimental effects of smoking in CD, yet failed to demonstrate substantial benefit from smoking in UC. These data should encourage all patients with IBD to quit smoking.

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“…CONAART also informed about work disability and its main associated factors in patients with ERA [ 43 ]. They also analyzed the effects of cigarette smoking on disease activity, functional capacity, radiographic damage, serology, and presence of extra-articular manifestations in patients not only with ERA, but also with undifferentiated arthritis, and found that neither was tobacco exposure related to the presence of extra-articular manifestations or to the degree of disability in any of the two groups of patients [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Rheumatoid arthritis in Latin America: the importance of an early diagnosis

et al. 2015

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The generalization of the early rheumatoid arthritis (ERA) concept and the existence of a window of therapeutic opportunity—a time span in which the institution of a proper therapeutic method for the disease would determine clinical improvement—have set the notion that early diagnosis and treatment may modify the course of the disease. Although in several regions of the world, especially in North America and Europe, since the year 2000, a significant reduction in diagnostic delay was observed in cohorts of patients with rheumatoid arthritis (RA), probably reflecting a stronger awareness of the importance of early diagnosis, this is not a reality in Latin America (LA). LA is a region of great economic inequality, with disparities in access to the public healthcare system and limited access to private medicine, being widely difficult to obtain a specialized medical evaluation in both scenarios. This paper aims to briefly review the main difficulties in the management of ERA in LA, based on the review of the literature, on the evaluation of a survey conducted among 214 rheumatologists of LA, members of Pan-American League of Associations for Rheumatology (PANLAR) and the experience of the authors. The paper also aims to propose solutions to the difficulties in managing ERA in LA.

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Effects of cigarette smoking on early arthritis: a cross-sectional study—data from the Argentine Consortium for Early Arthritis (CONAART)

Cited by 12 publications

References 32 publications

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Smoking prevalence and its influence on disease course and surgery in Crohn's disease and ulcerative colitis

Rheumatoid arthritis in Latin America: the importance of an early diagnosis

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