The effect of α-antitrypsin deficiency combined with increased bacterial loads on chronic obstructive pulmonary disease pharmacotherapy: A prospective, parallel, controlled pilot study.

Chronic obstructive pulmonary disease (COPD) is caused by α1-antitrypsin deficiency (AATD) genetic susceptibility and exacerbated by infection. The current pilot study aimed at studying the combined effect of AATD and bacterial loads on the efficacy of COPD conventional pharmacotherapy. Fifty-nine subjects (29 controls and 30 COPD patients) were tested for genetic AATD and respiratory function. The bacterial loads were determined to the patients' group who were then given a long acting beta-agonist and corticosteroid inhaler for 6 months. Nineteen percent of the studied group were Pi∗MZ (heterozygote deficiency variant), Pi∗S (5%) (milder deficiency variant), Pi∗ZZ (10%) (the most common deficiency variant), and Pi∗Mmalton (2%) (very rare deficiency variant). The patients' sputum contained from 0 to 8 × 10 CFU/mL pathogenic bacteria. The forced vital capacity (FVC) values of the AAT non-deficient group significantly improved after 3 and 6 months. Patients lacking AATD and pathogenic bacteria showed significant improvement in forced expiratory volume (FEV), FEV/FVC, FVC, and 6 min walk distance (6MWD) after 6 months. However, patients with AATD and pathogenic bacteria showed only significant improvement in FEV and FEV/FVC. The findings of this pilot study highlight for the first time the role of the combined AATD and pathogenic bacterial loads on the efficacy of COPD treatment.