The main finding in this study is that patients with rheumatoid arthritis who are HLA-DQwl positive have a significant reduction in pulmonary function compared to DQwl-negative individuals. The findings of a reduced FEVj, FVC, and D are consistent with an abnormal pattern of interstitial pulmonary disease in patients with rheumatoid arthritis who manifest the DQwl allele. The TLC was well preserved in this group, a finding in other cohorts of patients with rheumatoid arthritis with abnormal pulmonary function. DQw3-positive subjects showed evidence of airflow obstruction associated with an increased prevalence of keratoconjunctivitis sicca and HLA-DR4. Analysis of subgroups showed that the majority of these subjects with airflow obstruction were heterozygotes for DQwl and DQw3.
In addition, DQw2-positive patients had better pulmonary function than DQw2-negative patients. Whether the presence of the DQw2 allele confers some protective attribute against the development of pulmonary disease in this subgroup or merely represented the absence a deleterious attribute of the DQwl and DQw3 alleles cannot be answered. Although pulmonary function was influenced, we did not find differences among different DQw phenotypes in terms of clinical activity of rheumatoid arthritis or laboratory tests. A high ESR independently predicted a low FEVi and FVC, but the cause of the association is unclear. in detail
In order to determine the predictive value of possible risk factors for abnormal pulmonary function in patients with rheumatoid arthritis, we used a stepwise multiple regression analysis which included HLA-DR4 status, smoking, keratoconjunctivitis sicca, clinical parameters, and DQw phenotypes as independent variables. The presence of the heterozygotic phenotype, DQwl/DQw3, was the strongest predictor of a low percent predicted FEV^ Furthermore, defining obstructive pulmonary disease as an FEV^FVC ratio less than 70 percent, five of 17 DQwl/DQw3-positive patients were abnormal, while only two of 30 DQwl/DQw3-negative patients were abnormal. Thus, DQwl/DQw3 heterozygotes are at particular risk to develop obstructive pulmonary disease, especially smokers.