Premium
Influence of viral load and genotype in the progression of Hepatitis B‐associated liver cirrhosis to hepatocellular carcinoma
Author(s) -
Mahmood Sabina,
Niiyama Gouichi,
Kamei Ayumi,
Izumi Akiyoshi,
Nakata Keiichi,
Ikeda Hideji,
Suehiro Mitsuhiko,
Kawanaka Miwa,
Togawa Kazumi,
Yamada Gotaro
Publication year - 2005
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2005.01077.x
Subject(s) - hepatocellular carcinoma , medicine , cirrhosis , hepatitis b virus , gastroenterology , odds ratio , hepatitis b , genotype , viral load , univariate analysis , immunology , multivariate analysis , virus , biology , gene , biochemistry
Aim/Background: Hepatitis B virus (HBV) is an important factor in the development of hepatocellular carcinoma (HCC). We studied the influence of HBV viral load on HCC occurrence in HBV related liver cirrhosis (LC). Patients and Methods: Ninety‐one LC patients were followed up over a period of 7 years. Twenty three patients received Interferon (IFN) therapy. Results: In 7 years, 23 patients developed HCC. Of them twenty‐two (95.6%) were of genotype C. HBV DNA was found to be the only significant variable associated with HCC occurrence on both univariate ( P =0.029) and multivariate analysis (odds ratio 2.33; P <0.033). The cumulative survival at 5 years was 83% and the annual rate of hepatitis B surface antigen clearance was 0.9 %. All of 17 HCC patients observed over a period of 5 years or more belonged to the continuously high HBV DNA group (annual average >3.7 log copies/ml) and all but one belonged to the continuously high alanine aminotransferase group (annual average >40 IU/l). Conclusion: Patients with genotype C and a continuously high HBV DNA for 5 years or more are at a high‐risk group for HCC development. Maintaining continuously low HBV DNA for 3 years or more with anti‐viral therapy, may be useful in preventing or delaying HCC occurrence.