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Preliminary Reports |

Accelerated Decline of Lung Function in COPD Patients With Chronic Hepatitis C Virus Infection*: A Preliminary Study Based on Small Numbers of Patients

Hiroshi Kanazawa, MD; Kazuto Hirata, MD; Junichi Yoshikawa, MD
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*From the Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Correspondence to: Hiroshi Kanazawa MD, Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, 1–4-3, Asahi-machi, Abenoku, Osaka, 545-8585, Japan; e-mail address: kanazawa-h@med.osaka-cu.ac.jp.



Chest. 2003;123(2):596-599. doi:10.1378/chest.123.2.596
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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, 14 HCV-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)-α therapy.

Measurements and results: The rate of annual decline in FEV1 and diffusing capacity of the lung for carbon monoxide (Dlco) during the 5-year follow-up period were significantly higher in group B (ΔFEV1, 59.7 mL/yr [SD, 17.5], p = 0.0008; ΔDlco, 3.50%/yr [SD, 0.44], p < 0.0001) and group C (ΔFEV1, 54.0 mL/yr [SD, 15.3], p = 0.0128; ΔDlco, 3.36%/yr [SD, 0.28], p < 0.0001) than in group A (ΔFEV1, 33.5 mL/yr [SD, 7.7]; ΔDlco, 2.66%/yr [SD, 0.34]). Moreover, these parameters in group D (ΔFEV1, 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 ΔFEV1 after IFN therapy during the 3-year follow-up period in the 8 IFN responders and 13 IFN nonresponders. ΔFEV1 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, ΔFEV1 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.

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