Smoking is a major preventable risk factor for rheumatoid arthritis: estimations of risks after various exposures to cigarette smoke

Källberg, Henrik; Ding, Bo; Padyukov, Leonid; Bengtsson, Camilla; Rönnelid, Johan; Klareskog, Lars; Alfredsson, Lars

doi:10.1136/ard.2009.120899

Cited by 313 publications

(227 citation statements)

References 21 publications

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“…RA autoantibodies levels, especially anti-CCP, were very strongly positive in the BRRA group significantly more so than among RA controls. However, tobacco consumption (a well-recognised environmental risk factor for anti-CCP positive RA 29 ) was low, suggesting that other factors must drive the very high levels of anti-CCP positivity. The very high levels of anti-CCP antibodies in our BRRA group, in addition to recent findings of high levels of antibodies to citrullinated peptides in bronchiolar lavage fluid 30 , subclinical HRCT lung abnormalities at diagnosis of RA 17 and .…”

Section: Discussionmentioning

confidence: 99%

Increased disease activity, severity and autoantibody positivity in rheumatoid arthritis patients with co‐existent bronchiectasis

et al. 2015

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AimPatients with rheumatoid arthritis (RA) and co‐existent bronchiectasis (BRRA) have a five‐fold increased mortality compared to rheumatoid arthritis alone. Yet previous studies have found no difference in clinical and serological markers of RA disease severity between BRRA patients and RA alone. However, RA disease activity measures such as Disease Activity Score of 28 joints – C‐reactive protein (DAS28‐CRP) and anti‐cyclic citrullinated peptide antibodies (anti‐CCP) have not been studied, so we assessed these parameters in patients with BRRA and RA alone.MethodsBRRA patients (n = 53) had high‐resolution computed tomography proven bronchiectasis without any interstitial lung disease and ≥ 2 respiratory infections/year. RA alone patients (n = 50) had no clinical or radiological evidence of lung disease. DAS28‐CRP, rheumatoid factor (immunoglobulin M) and anti‐CCP were measured in all patients, together with detailed clinical and radiology records.ResultsIn BRRA, bronchiectasis predated RA in 58% of patients. BRRA patients had higher DAS28 scores (3.51 vs. 2.59), higher levels of anti‐CCP (89% vs. 46%) and rheumatoid factor (79% vs. 52%) (P = 0.003) compared to RA alone. Where hand and foot radiology findings were recorded, 29/37 BRRA (78%) and 13/30 (43%) RA alone had evidence of erosive change (P = 0.003). There were no significant differences between groups in smoking history or disease‐modifying anti‐rheumatic drug/biologic therapy.ConclusionsIncreased levels of RA disease activity, severity and RA autoantibodies are demonstrated in patients with RA and co‐existent bronchiectasis compared to patients with RA alone, despite lower tobacco exposure. This study demonstrates that BRRA is a more severe systemic disease than RA alone.

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Section: Discussionmentioning

confidence: 99%

Increased disease activity, severity and autoantibody positivity in rheumatoid arthritis patients with co‐existent bronchiectasis

et al. 2015

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“…[1] Smoking may be a negative predictor of response to TNF-α inhibitors as observed in our study, even though no biologically plausible reason was clearly elucidated. Meanwhile, smoking is a well-recognized risk factor for the development of RA or CD [3,4] with an association with more severe disease state such as higher levels of disability and extra-articular manifestations. [36,37] The proposed mechanisms for this phenomenon are as follows.…”

Section: Discussionmentioning

confidence: 99%

“…[2] Many epidemiology studies show evidence that smoking is a risk factor for several autoimmune diseases such as rheumatoid arthritis (RA) and Crohn's disease (CD). [3,4] In addition, smok-TCP Transl Clin Pharmacol ing can affect the outcomes of pharmacological agents such as TNF-α inhibitors including infliximab, adalimumab, and etanercept, which are used for the treatment of RA or CD. TNF-α inhibitors produce excellent clinical responses for patients with these diseases, but there are limited therapeutic alternatives for patients who fail to respond to TNF-α inhibitors.…”

Section: Introductionmentioning

confidence: 99%

Impact of smoking on the effectiveness of TNF-α inhibitors in patients with rheumatoid arthritis or Crohn's disease

Song

Sohn

Kim

et al. 2014

Transl Clin Pharmacol

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These authors contributed equally as co-first authorsCigarette smoking may be associated with the augmentation of pro-inflammatory cytokines including Tumor Necrosis Factor-alpha (TNF-α), which may affect the outcomes of pharmacological agents such as TNF-α inhibitors. The purpose of this study was to investigate the impact of smoking on the effectiveness of TNF-α inhibitors in patients with rheumatoid arthritis (RA) or Crohn's disease (CD). We used systematic literature review methods. A total of 1,147 articles were selected after exclusion of duplicates through a database search. Among them, 28 articles were finally selected through a review of titles and abstracts and a subsequent review of full articles. The effectiveness of TNF-α inhibitors in patients with RA or CD among the selected articles was summarized by their smoking status. Meta-analysis was performed with random effect model. When current smokers were compared with non-smokers for response after adjustments through meta-analysis among patients with RA, current smokers had 59% less response than non-smokers with statistical significance (Pooled adjusted OR=0.41, 95% CI=0.17-0.95). In patients with CD, current smokers tended to have lower clinical response than non-smokers, but statistical significance was not shown. In subgroup analyses for luminar CD or fistulizing CD, current smokers tended to have a lower response in luminar CD (Pooled OR=0.62, 95% CI=0.34-1.14), but smoking status was not associated with drug response in fistulizing CD. This study raises awareness of the adverse effects of smoking in terms of clinical response in patients treated with TNF-α inhibitors.

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“…Smoking is the major known environmental risk factor for RA. Smoking and genetic risk factors interact in providing an increased risk of RA [26]. Immune responses with several inflammatory cascades lead toward a final common pathway with persistent synovial inflammation and associated damage to articular cartilage and underlying bone as a consequence.…”

Section: Rheumatoid Arthritis and Anti-citrullinated Protein Antibodiesmentioning

confidence: 99%

Rheumatoid arthritis and periodontitis; a possible link via citrullination

et al. 2011

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a b s t r a c tRheumatoid Arthritis (RA) and chronic and aggressive periodontitis are chronic inflammatory disorders characterized by deregulation of the host inflammatory response. Increased secretion of pro-inflammatory mediators results in soft and hard tissue destruction of the synovium and periodontium respectively. Both diseases share risk factors and have pathological pathways in common, resulting in loss of function and disability as a final clinical outcome. This article discusses possible interactions, particularly related to the periodontal pathogen Porphyromonas gingivalis, which could explain the observed association between these two prevalent diseases.

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Smoking is a major preventable risk factor for rheumatoid arthritis: estimations of risks after various exposures to cigarette smoke

Cited by 313 publications

References 21 publications

Increased disease activity, severity and autoantibody positivity in rheumatoid arthritis patients with co‐existent bronchiectasis

Increased disease activity, severity and autoantibody positivity in rheumatoid arthritis patients with co‐existent bronchiectasis

Impact of smoking on the effectiveness of TNF-α inhibitors in patients with rheumatoid arthritis or Crohn's disease

Rheumatoid arthritis and periodontitis; a possible link via citrullination

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