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Volume 35, Issue 2, Pages 185-192 (February 2006)


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Fibrosis progression in chronic hepatitis C patients with occult hepatitis B co-infection

Chee-Kin HuiadCorresponding Author Informationemail address, Eva Laub, Helen Wuc, Alexander Montob, Michael Kimb, John M Lukd, George KK Lauad, Teresa Lyn Wrightb

Received 18 March 2005; received in revised form 4 July 2005; accepted 10 July 2005. published online 16 August 2005.

Abstract 

Occult hepatitis B virus (HBV) infection in individuals without hepatitis B surface antigen (HBsAg) can be identified in hepatitis C virus (HCV) infected patients. However, its role in fibrosis progression remains uncertain. This retrospective study compared the fibrosis progression (defined as fibrosis progression by at least one stage) and progression to severe fibrosis (fibrosis stage 3 or 4) in HCV patients with occult HBV infection. Occult HBV infection was diagnosed by the detection of HBV DNA in the serum of 74 consecutive anti-HCV positive patients by PCR. Thirty-one patients (41.9%) had occult HBV infection. All 74 patients had a median of 2 (range 2–3) liver biopsies. The median time between the first and last liver biopsy was 57.7 (range 15.0–132.8) months. Eleven of the 31 patients with occult HBV infection compared with 12 of the 43 patients without occult HBV infection had fibrosis progression (35.5% versus 27.9%, respectively, p=0.608). Six of the 31 patients with occult HBV infection compared with 8 of the 43 patients without occult HBV infection developed severe fibrosis (19.4% versus 18.6%, respectively, p=0.946). In conclusion, chronic HCV patients with occult HBV co-infection does not seem to progress more than patients without occult HBV infection. However, more large-scale studies are needed before a definite conclusion can be obtained.

a Department of Medicine, The University of Hong Kong, Hong Kong SAR, China

b GI Section, Department of Medicine, Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, USA

c Roche Diagnostics, San Jose, CA, USA

d Centre For The Study of Liver Disease, The University of Hong Kong, Hong Kong SAR, China

Corresponding Author InformationCorresponding author. Tel.: +852 28184300; fax: +852 28184030.

PII: S1386-6532(05)00196-4

doi:10.1016/j.jcv.2005.07.003


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