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Rheumatoid arthritis (RA) affects the respiratory system in a number of ways, including interstitial lung disease, nodules, pleural effusion, bronchiolitis obliterans, and bronchiectasis.1Isolated small airways obstruction has been described in patients with RA.2-6 Some of the studies, however, included a predominance of smokers2 or patients who were ex-smokers in the analysis.3 4 One study found no evidence of an increase in airways obstruction.7 The incidence and frequency, therefore, of small airways obstruction in non-smoking patients with RA still remains unclear and the natural history of the condition is unknown.
We obtained detailed medical and smoking histories from 54 unselected patients with RA (ARA criteria) in 1988. Patients were questioned specifically regarding the presence of cough, wheeze, dyspnoea or sputum production and had a full respiratory examination. All patients had respiratory function tests and chest radiography. The history, examination, and pulmonary function tests were repeated on those patients available for study eight years later in 1996. The pulmonary function tests performed included forced expiratory volume in one second (FEV1), forced vital capacity (FVC), FEV1/FVC, forced expiratory flow between 25% and 75% of vital capacity (FEF25–75), and total lung diffusion capacity (TLCO). Observed values were compared with those predicted for age, sex, and height. Isolated small airways obstruction was defined as FEF25–75 < 65% predicted.
In the initial study of 54 patients, 24 were lifelong non-smokers of whom six (25%) had isolated small airways obstruction. At follow up eight years later 34 patients were available for study (10 patients had died and eight patients were lost to follow up). Twenty were lifelong non-smokers. Of the six patients who had previously documented isolated small airways obstruction, one had died, one had an improvement in FEF25–75 while the remaining four patients had a further deterioration in their small airways obstruction with a mean reduction of FEF25–75 of 14.7% predicted (range 2–32%).
At follow up a further two non-smokers (with previously normal respiratory function) had developed a reduction in FEF25–75 <65%, resulting in a total of six non-smoking patients (30%) having isolated small airways obstruction. The mean value (SD) of FEF25–75 in these six patients was significantly reduced from baseline after eight years, 63.6 (19.4) compared with 48.0 (12.9); p<0.01 (paired t test). None of the patients with small airways obstruction had symptoms or clinical signs of pulmonary disease and all had normal chest radiographs. There was no significant difference in the FEF25–75 after eight years in non-smoking patients with >65% predicted at baseline, 91 (26.9) compared with 92 (21.4); p<0.7. At initial evaluation only one non-smoking patient had a significant reduction in TLCO (35% predicted). This patient had clinical and radiographic evidence of pulmonary fibrosis and at follow up had a further reduction in TLCO (20% predicted). Interestingly, there was no significant difference in the mean TLCO between baseline and follow up in the non-smoking patients, 90 (21.3) compared with 85 (25.8); p<0.12, in keeping with the findings of Linstow.8 Table 1 shows the clinical features and pulmonary function of those patients having small airways obstruction at follow up.
There was no significant difference in mean age at study (60v 60 years), sex, mean age at disease onset (39v 38 years), mean disease duration (19 v 18 years), titre of rheumatoid factor or the presence of extra-articular features (nodules, vasculitis or sicca symptoms) between non-smoking patients with isolated airways obstruction and those with normal respiratory function and there was no increase in episodes of recurrent bronchitis. There was no difference in the number or type of disease modifying agents, or use of NSIADs, between patients with airways obstruction and those without.
Pulmonary infection, α1 antitrypsin deficiency, and drug treatment have been proposed as possible predisposing factors for small airways obstruction in RA, however the exact mechanism is not yet known. Mucosal oedema secondary to pre-existing airways inflammation in RA leading to bronchial narrowing and airways obstruction has been proposed as a mechanism.9
This study confirms the existence of a subgroup of non-smoking patients with RA who have isolated small airways obstruction. The abnormalities seem to be progressive and the number of patients with airways obstruction may increase over time.
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