Relationship Between Pack-year History of Smoking and Response to Tumor Necrosis Factor Antagonists in Patients with Rheumatoid Arthritis

Mattey, Derek L.; Brownfield, Ann; Dawes, P. T.

doi:10.3899/jrheum.081096

Cited by 83 publications

(63 citation statements)

References 43 publications

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“…Harty and Veale have confirmed our finding of higher tender joint counts and overall DAS scores in ever-smokers compared with never-smokers in patients with RA receiving anti-TNF therapy 1 . However, in contrast to our findings, they also suggest that ever-smokers have marginally higher mean swollen joint counts than never-smokers at both 3 and 12 months.…”

Section: To the Editorsupporting

confidence: 78%

Dr. Mattey, et al reply

Mattey¹,

Brownfield²,

Dawes³

2010

J Rheumatol

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Section: To the Editorsupporting

confidence: 78%

Dr. Mattey, et al reply

Mattey¹,

Brownfield²,

Dawes³

2010

J Rheumatol

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“…In addition, others have reported that RAaffected male, current smokers were less likely to experience remission than their 4 never-or former-smoking counterparts, an association that was not detected in females [22]. These observations are in keeping with several reports on the negative impact of smoking on the response to tumour necrosis factor (TNF) antagonists in particular [23][24][25][26], as well as methotrexate [26], in patients with RA [23][24][25][26].…”

Section: Smoking and Rasupporting

confidence: 77%

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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“…A majority of studies classified smoker or non-smoker by smoking status at the time of drug initiation, but some studies considered ex-smoking status. [7,8,[10][11][12] Some studies defined the amount of smoking as more than 5 cigarettes per day within 6 months from initiation of drug administration, [16,19,20,28,29] more than 7 cigarettes per week, [18,26] more than 1 cigarette per day, [17] or the presence of smoking without considering cigarette numbers. [13][14][15][22][23][24][25]27,[31][32][33][34] These variable smoking definitions could contribute to the discrepancy in the study results.…”

Section: Discussionmentioning

confidence: 99%

“…A total of 28 articles were finally selected. Among them, 6 articles were for RA [7][8][9][10][11][12] and 22 articles were for CD. Figure 1 shows the literature selection flows.…”

Section: Literature Selectionmentioning

confidence: 99%

“…They were all observational studies and reported outcomes using [7,9,10,12] without the other two articles (Canhao and Saevarsdottir) [8,11] categorizing outcomes as good responders and non-responders. Results of meta-analyses based on the smoking status and outcome presentation methods (i.e., ORs or percentage) are shown in Fig.…”

Section: Impact Of Smoking On Drug Response In Patients With Ramentioning

confidence: 99%

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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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Relationship Between Pack-year History of Smoking and Response to Tumor Necrosis Factor Antagonists in Patients with Rheumatoid Arthritis

Abstract: RA patients with a history of smoking were more likely to show a poor response to TNF antagonists. Response failure was associated with the intensity of previous smoking, irrespective of smoking status at initiation of anti-TNF therapy.

Cited by 83 publications

References 43 publications

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

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

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