Cigarette smoking and rheumatoid arthritis severity

Saag, Kenneth G.; Cerhan, James R.; Kolluri, Sheela; Ohashi, Kousaburo; Hunninghake, Gary W.; Schwartz, David

doi:10.1136/ard.56.8.463

Cited by 262 publications

(175 citation statements)

References 38 publications

(12 reference statements)

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“…Del Rincon et al (21) examined cardiovascular events and reported significant associations with both diabetes and hypertension. Smoking is an established risk factor for atherosclerosis and is also associated with the development and severity of RA (47,(55)(56)(57). In our study, we demonstrated, by univariate analysis, that a history of smoking prior to the RA incidence date increased the risk of cardiovascular death in a dose-dependent manner, but the association was no longer significant when other cardiovascular variables were considered.…”

Section: Discussionmentioning

confidence: 50%

Cardiovascular death in rheumatoid arthritis: A population‐based study

Kremers¹,

Nicola²,

Crowson³

et al. 2005

Arthritis & Rheumatism

847

532

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Objective. To determine whether systemic inflammation confers any additional risk for cardiovascular death among patients with rheumatoid arthritis (RA), after adjusting for traditional cardiovascular risk factors and comorbidities.Methods. Using the population-based data resources of the Rochester Epidemiology Project, we assembled an incidence cohort of all Rochester, Minnesota residents ages >18 years who first fulfilled the American College of Rheumatology 1987 criteria for RA between January 1, 1955 and January 1, 1995. All subjects were followed up longitudinally through their complete (inpatient, outpatient) medical records, beginning at age 18 years and continuing until death, migration, or January 1, 2001. Detailed information on the occurrence of various cardiovascular risk factors (personal history of coronary heart disease [CHD], congestive heart failure, smoking, hypertension, dyslipidemia, body mass index [BMI], diabetes mellitus, menopausal status) as well as indicators of systemic inflammation and RA disease severity (rheumatoid factor [RF] seropositivity, erythrocyte sedimentation rate [ESR], joint swelling, radiographic changes, RA nodules, RA complications, RA treatments, disease duration) and comorbidities were collected on all subjects. Causes of death were ascertained from death certificates and medical records. Cox regression models were used to estimate the independent predictors of cardiovascular death.Results. This inception cohort comprised a total of 603 RA patients whose mean age was 58 years, of whom 73% were women. During a mean followup of 15 years, 354 patients died and cardiovascular disease was the primary cause of death in 176 patients. Personal history of CHD, smoking, hypertension, low BMI, and diabetes mellitus, as well as comorbidities, including peripheral vascular disease, cerebrovascular disease, chronic pulmonary disease, dementia, ulcers, malignancies, renal disease, liver disease, and history of alcoholism, were all significant risk factors for cardiovascular death (P < 0.01 for each

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Section: Discussionmentioning

confidence: 50%

Cardiovascular death in rheumatoid arthritis: A population‐based study

Kremers¹,

Nicola²,

Crowson³

et al. 2005

Arthritis & Rheumatism

847

532

View full text Add to dashboard Cite

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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: 80%

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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“…There is evidence from cross-sectional studies that smoking is associated with longterm erosive damage [2][3][4][5] , although some longitudinal studies failed to find an association 6,7 . However, the longitudinal studies have been carried out mainly in patients with earlier disease.…”

Section: To the Editormentioning

confidence: 99%