title: Accelerated decline of lung function in COPD patients with chronic hepatitis C virus infection: a preliminary study based on small numbers of patients.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  Prospective 5-year follow-up study.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Fifty-nine patients with COPD (group A, 15 HCV-negative ex-smokers; group B, 14 HCV-negative current smokers; group C, 14 HCV-positive ex-smokers; group D, 16 HCV-positive current smokers).
  
  
  METHODS
  After a 5-year follow-up period, 21 HCV-positive patients received interferon (IFN)-alpha therapy.
  
  
  RESULTS
  The rate of annual decline in FEV(1) and diffusing capacity of the lung for carbon monoxide (DLCO) 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; DeltaDLCO, 3.50%/yr [SD, 0.44], p < 0.0001) and group C (DeltaFEV(1), 54.0 mL/yr [SD, 15.3], p = 0.0128; DeltaDLCO, 3.36%/yr [SD, 0.28], p < 0.0001) than in group A (DeltaFEV(1), 33.5 mL/yr [SD, 7.7]; DeltaDLCO, 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, 24.0]). 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.
authors.affiliation: Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Japan. kanazawa-h@med.osaka-cu.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kanazawa
authors.forename: Kazuto
authors.initials: K
authors.lastname: Hirata
authors.forename: Junichi
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000187:drug effects / Q000502:physiology*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011653:Pulmonary Diffusing Capacity / Q000187:drug effects / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects; D016896:Treatment Outcome
chemical_list: D016898:Interferon-alpha