Hepatitis C and pulmonary fibrosis

authors:

avatar Rasoul Aliannejad 1 , avatar Mostafa Ghanei 2 , *

Respiratory Diseases and TB Research Center of Guilan University of Medical Science, IR.Iran
Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, m.ghanei@bmsu.ac.ir, IR.Iran
Hepatitis Monthly: Vol.11, issue 2; 71-73
article type: Editorial
received: January 4, 2011
accepted: January 12, 2011

how to cite: Aliannejad R, Ghanei M. Hepatitis C and pulmonary fibrosis. Hepat Mon. 2011;11(2): 71-73. 

Abstract

Background: Hepatitis C virus (HCV) is a hepatotropic and lymphotropic virus that causes hepatic and extrahepatic disease. Emerging clinical data suggest that chronic HCV infection can lead to many direct and indirect effects on the lung.
Objectives: This article discusses evidence on the relationship between HCV infection and pulmonary fibrosis to increase knowledge on this topic among clinicians and scientists and highlights the need for further study.
Methods: We searched the MEDLINE, ISI WEB OF KNOWLEDGE, OVID, ELSEVIER, and MDCONSULT databases and top respiratory journals, such as the American Journal of Respiratory and Critical Care, Chest, and Thorax for articles in English using the following keywords: hepatitis C, HCV infection, IPF, pulmonary fibrosis, and interstitial pneumonitis. We reviewed the reference lists of all identified studies.
Results: The evidence for a pathogenetic link between pulmonary fibrosis and HCV is: the higher frequency of HCV markers in IPF patients, an increase in lymphocyte and neutrophil numbers in bronchoalveolar lavage of chronic HCV infection patients, and the development of IPF in HCV-related chronic hepatitis that is treated with interferon. There is a discrepancy between studies on the frequency of HCV in IPF patients, which might be attributed to geographical differences of in the prevalence of HCV infection, selection bias in choosing the control group, and the HCV genome.
Conclusions: BAL studies in HCV infection are associated with increased counts of lymphocytes and neutrophils in BAL fluid. These studies show that HCV infection is associated with nonspecific pulmonary inflammatory reactions that are not compatible with IPF but that it can lead to pulmonary fibrosis. The other factor is interferon therapy. Interstitial pneumonia and sarcoidosis are well-documented complications of IFN therapy. More extensive cohort studies should be conducted to confirm an actual causal relationship between HCV infection and pulmonary fibrosis.

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