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Development of hepatocellular carcinoma in chronic hepatitis B patients with advanced fibrosis is independent of viral genotype
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Edité par CCSD ; Wiley-Blackwell -
International audience. Hepatitis B is leading cause of liver related morbidity in Asia with predominant genotypes B and C in East-Asia. Data on Serum, intrahepatic viral-markers, and long-term follow-up of prevalent genotypes (GT) B and C in patients with biopsy proven advanced fibrosis are sparse. To compare serum, intrahepatic viral-markers and development of hepatocellular carcinoma (HCC) in GT-B and C in patients with advanced fibrosis (Ishak \textgreater/= 4). Sixty-three treatment-naive patients identified with advanced fibrosis on liver-biopsy performed between 1998 and 2000 at Singapore General Hospital. FFPE tissue was available for 59 patients and serum for 42 patients. HBV-DNA was quantified in serum and liver while qHBsAg quantified in serum. Patients were followed-up till December 2015. The median age was 47 +/- 16 years, with 77.7% males. About 19 were GT-B, 43 patients were GT-C, and 1 had both GT-B and C. Mean follow-up was 13.5 years. The median serum HBV-DNA was 6.25 +/- 2.17 and 6.58 +/- 1.85 log IU/ml, serum HBsAg was 3.29 +/- 0.80 and 3.45 +/- 1.85 log IU/ml, and intrahepatic HBV-DNA was 0.52 +/- 3.73 copies/cell and 0.4 +/- 1.37 copies/cell in the GT-B and C, respectively (P \textgreater 0.1 in all). Complete cirrhosis (Ishak-6) was present in 47.6%, Ishak-5 fibrosis in 33.3%, and Ishak-4 fibrosis in 19% at recruitment. On follow-up HCC developed in 8/43 in GT-C and in 3/19 GT-B (P = 0.86). Advanced age and cirrhosis were significant factors for development of HCC. No difference in serum HBV-DNA, qHBsAg or intrahepatic HBV-DNA was seen in the two genotypes. HCC development seen over long-term follow-up was independent of genotypes in patients with advanced fibrosis. J. Med. Virol. (c) 2016 Wiley Periodicals, Inc
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