Smoking: keeping the joint alight

The topic of smoking seems to be quite controversial of late, with the health hazards being advertised across the board, from smoking cartons to billboards. Despite the increased publicity and warnings, people at large continue to smoke. This is of significant concern considering the health risks of smoking. Smokers reduce their life expectancy by ten years compared to non-smokers, with death being attributable to cardiac, vascular, pulmonary and cancer-related conditions.

Smoking is a recognised risk factor in atherosclerosis, cardiovascular disease, chronic obstructive pulmonary disease (COPD), lung cancer and rheumatoid arthritis (RA). Rheumatoid arthritis alone can contribute to cardiovascular disease. Patients with RA have a two-fold risk of developing a myocardial infarct or a stroke.¹ Therefore, the combination of smoking and RA significantly increases cardiovascular risk.

A recent spot audit to assess the efficacy of the clinician providing smoking cessation advice was performed in our rheumatology clinic. The results proved dismal and potentially reflect current medical practice across London. Twenty-five sets of patient notes of RA patients and 25 sets of patient notes of psoriatic arthritis patients were audited. The objective was to assess whether the patients were active smokers and whether smoking cessation advice had been encouraged and documented. Cessation advice was given in 0% of cases. However, this may be an inaccurate figure, reflecting flaws in the documentation of verbal advice given to patients in the pressured outpatient setting. In reality, one would hope that doctors and health clinicians encourage smoking cessation more frequently in this environment.

The audit was performed to highlight the importance of smoking cessation in patients with inflammatory types of arthritis, especially RA. In keeping with National Rheumatoid Arthritis Society (NRAS) educational material, smoking increases the risk of developing RA by 50%, as well as decreasing the efficacy of treatment, leading to more severe RA in smokers rather than non-smokers.²

Although the pathogenesis is unclear, the pro-inflammatory effect of cigarette smoke on tissue joints is one contributing factor. Smoking upregulates cyclooxygenase (COX)-2 in the oral mucosa in response to increased epidermal growth factor signalling. The upregulation of COX-2 receptors may also occur in the joints.³ Smoking also induces the expression of rheumatoid factor, even in patients without RA.⁴ A nationwide study from Denmark highlighted that patients who smoke heavily and are homozygous for the shared epitope have an increased risk of anti-CCP antibody positive RA.⁵ The strongest association is noted between PTPN22, smoking and anti-CEP-1.⁶

The benefits gained from treating RA are reduced by the effect of smoking. Saevarsdottir et al demonstrated that at three months smokers had a lower response rate to treatment than non-smokers.⁷ Further studies showed that active smoking could be used as a predictor of poor response to treatment, even at 12 months.⁸

Smoking not only contributes to the susceptibility of RA and accelerates cardiovascular risk, it also decreases the efficacy of treatments. Education is paramount, as 60% of smokers do not perceive increased health risks secondary to smoking.⁹ We would urge clinicians to encourage their patients to stop smoking and provide them with smoking cessation advice in verbal and written form. There can be no doubt about the benefit of stopping smoking and we should be actively promoting smoking cessation in our rheumatology clinics and outpatient practices.

• © 2012 Royal College of Physicians