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There is a well recognised association between rheumatoid arthritis (RA) and bronchiectasis. Walker observed a 10-fold increased prevalence of bronchiectasis in RA.1 The increased incidence of pulmonary disease in his study could not be explained by the greater susceptibility to infection by patients with RA because the symptoms of bronchiectasis preceded those of arthritis in the majority of the cases. Earlier reports found the prevalence of bronchiectasis in RA to be between 1 and 10%.1 However, with the advent of high resolution computed tomography (HRCT) of the lung, later studies reported a prevalence of 25–30%.2,3 This is important as HRCT is a more sensitive method of detecting bronchiectasis, and it is generally accepted that a chest radiograph may be normal in patients with bronchiectasis. Secondly, later studies investigated principally lifelong non-smoking patients with RA as opposed to the earlier studies, which investigated patients with RA irrespective of their smoking history. Cigarette smoking, particularly heavy cigarette smoking, is associated with the development of seropositive RA.4 Likewise, it has been suggested that bronchiectasis may be a trigger for the development of RA.5 To determine if these two potential risk factors for the development of RA are distinct we used HRCT to study patients with RA to determine if there are differences in the prevalence of smoking in patients with RA and bronchiectasis.
METHODS AND RESULTS
Using HRCT, we identified 22 patients with RA with bronchiectasis (group I). We then matched these patients (group I) for age and sex with a cohort of patients with RA who had undergone HRCT of the chest as part of a larger study undertaken earlier by the department6 (group II). All patients in group II had no HRCT evidence of bronchiectasis. Table 1 shows the results obtained.
This study disclosed a significant difference in smoking between the two groups, with a greater tendency for those in the group with bronchiectasis to be non-smokers. There was also a significant difference in smoking when expressed as pack-years between the two groups. This is in keeping with previous studies showing a high incidence of bronchiectasis on HRCT in non-smoking patients with RA.2 Patients with bronchiectasis in the population generally tend to be non-smokers. A study investigating the predisposing factors for the development of bronchiectasis in 69 patients found that 50 of them were non-smokers.6 This is presumably because the symptoms of bronchiectasis,7 such as production of copious amounts of sputum daily, frequent severe chest infections, and wheezing, are not conducive to a desire to smoke. A survey of publications between 1985 and 2001 did show an irrefutable link between smoking and RA.8 Possibly, patients with RA and bronchiectasis stop smoking because of deteriorating lung function. However, significantly more of the patients in the study group were non-smokers than ex-smokers.
There are a number of potential mechanisms by which bronchiectasis might trigger RA. The presence of bronchiectasis is consistent with a persistently active inflammatory process, and increases in CD 4+ T lymphocytes, macrophages, and neutrophils, and interleukin 8 positive cells have been found in the airways of patients with bronchiectasis.9 The priming of these inflammatory cells within the bronchiectatic lung might result in an increase of circulating proinflammatory cells and predispose to RA. Based on the results of this study and others, it is tempting to speculate that bronchiectasis is a strong risk factor for the development of RA, particularly in those who have never smoked.
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