Accelerated decline of lung function in COPD patients with chronic hepatitis C virus infection - A preliminary study based on small numbers of patients

Study objectives: It has been suggested that chronic viral infection may increase the risk for development of COPD. This prospective study was designed to determine that chronic hepatitis C virus (HCV) infection is associated with accelerated decline of lung function in patients with COPD, and that antiviral therapy against HCV is effective for such patients. Design: Prospective 5-year follow-up study. Setting: University hospital. Patients: Fifty-nine patients with COPD (group A, 15 HCV-negative ex-smokers; group B, 14 HCV-negative current smokers; group C, 14HCV-positive ex-smokers; group D, 16 HCV-positive current smokers). Interventions: After a 5-year follow-up period, 21 HCV-positive patients received *'interferon (IFN)-alpha therapy. Measurements and results: The rate of annual decline in FEV1 and diffusing capacity of the lung for carbon monoxide (D-LCO) during the 5-year follow-up period were significantly higher in group B (DeltaFEV(1) 59.7 mL/yr [SD, 17.5], p = 0.0008; DeltaD(LCO), 3.50%/yr [SD, 0.44], p < 0.0001) and group C (DeltaFEV(1), 54.0 mL/yr [SD, 15.3], p = 0.0128; DeltaD(LCO), 3.36%/yr [SD, 0.28], p < 0.0001) than in group A (DeltaFEV(1), 33.5 mL/yr [SD, 7.7]; DeltaD(LCO), 2.66%/yr [SD, 0.34]). Moreover, these parameters in group D (DeltaFEV(1), 79.5 mL/yr [SD, 20.6]; DLCO, 4.5%/yr [SD, 0.40]) were also significantly higher than those in group B and group C. We evaluated the DeltaFEV(1), after IFN therapy during the 3-year follow-up period in the 8 IFN responders and 13 IFN nonresponders. DeltaFEV(1) in the IFN nonresponders did not significantly change during the 3-year follow-up period (before, 65.5 mL/yr [SD, 23.5]; after, 66.1 mL/yr [SD, 24.01). However, DeltaFEV(1) in the IFN responders significantly decreased (before, 68.4 mL/yr [SD, 26.2]; after, 57.3 mL/yr [SD, 23.6), p = 0.0116). Conclusions: Our findings suggest that chronic HCV infection might accelerate decline in lung function in patients who already have COPD.