[Respiratory involvement in ankylosing spondylarthritis: relations to alpha-1-antitrypsin phenotypes and tobacco consumption].

The distribution of alpha-1-antitrypsin phenotypes was similar in 555 controls and 98 patients with ankylosing spondylitis: the MM phenotype (including "main" MM subtypes, i.e., M2M2 and M3M3, and "secondary" MM subtypes) was found in 86% of subjects and "rare" phenotypes combining M, F, S, and Z in 14%. Six per cent of the controls and none of the ankylosing spondylitis patients had the M4M4 phenotype (p < 0.01). Respiratory function tests were performed in 49 patients with axial ankylosing spondylitis and 30 controls matched on sex, age, body mass index, smoking status, nonsteroidal antiinflammatory drug use and distribution of "main" and "secondary" phenotypes (no subjects in this study had "rare" phenotypes); the significant reduction in chest expansion seen in the ankylosing spondylitis group (5.6 +/- 2.7 cm versus 8.7 +/- 1.2; p < 0.001) was correlated with total capacity (p < 0.04) and vital capacity (p < 0.001). Restrictive ventilatory dysfunction was seen in four ankylosing spondylitis patients versus no controls (p < 0.02). Proximal airway obstruction, pulmonary distension and decreases in the diffusing capacity for carbon monoxide were seen in similar proportions of ankylosing spondylitis patients and controls. In the ankylosing spondylitis group, evidence of pulmonary distension included increases in mean residual functional capacity and mean residual volume (105.6 +/- 21.2% versus 94.8 +/- 17.4, p < 0.03, and 100.3 +/- 22.8% versus 88.6 +/- 17.9, p < 0.04, respectively) and bullous emphysema in the lung bases in two patients (versus no controls). In the small subgroup of ankylosing spondylitis patients with lung distension or a decreased diffusing capacity for carbon monoxide, smokers and nonsmokers were evenly balanced but subjects with "secondary" phenotypes outnumbered those with "main" phenotypes (p < 0.02); in contrast, our data suggested that smoking may play the central role in the proximal airway obstruction. Our findings suggest that in addition to previously established causes of pulmonary involvement in ankylosing spondylitis a "secondary" MM phenotype (i.e., neither M2M2 nor M3M3) may be a risk factor for lung distension and impaired diffusing capacity for carbon monoxide.