SUBCLINICAL ALVEOLITIS IN SPONDYLOARTHROP ATHIES

Restrictive ventilatory dysfunction, lowered diffusing capacity, and a pical fibrosis have been reported in ankylosing spondylitis. TO invest igate the pathogenesis of these abnormalities, we studied distal airsp ace cytology by performing bronchoalveolar lavage in 34 spondyloarthro pathy patients (ankylosing spondylitis, n=16; reactive arthritis, n=4; axial psoriatic arthritis, n=2; and undifferentiated spondyloarthropa thy with HLA B27-positivitY in every case but one, n=12). Mean age was 32.4 +/- 13.7 years. None of the study patients had apical fibrosis, lower respiratory tract infection, or exposure to airborne pollutants other than tobacco smoke. The control group was composed of nine subje cts who had no lung or inflammatory diseases and were not using medica tions. Significantly higher proportions of lymphocytes were found in b ronchoalveolar lavage specimens from patients, as compared with contro ls. This difference was not influenced by smoking or medication use (n on steroidal antiinflammatory drugs, sulfasalazopyridine). Alveolar ly mphocytosis was not correlated with laboratory tests for disease activ ity (erythrocyte sedimentation rate, serum IgA levels) or with the pre sence of restrictive ventilatory dysfunction. Increases in the proport ion of lymphocytes were of similar magnitude in patients with ankylosi ng spondylitis and in those with other spondyloarthropathies. Absolute total cell counts and relative neutrophil counts were similar in pati ents and controls. However, among the patients with spondyloarthropath ies, those with a disease duration of more than five years had a signi ficantly higher proportion of neutrophils than those with a disease du ration of less than five years. These findings demonstrate that spondy loarthropathy patients have subclinical lymphocyte alveolitis. Althoug h of unclear significance, this alveolitis may be related to the devel opment of apical fibrosis in some patients with ankylosing spondylitis .