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Lower serum viral loads in young patients with hepatitis‐B‐virus‐related hepatocellular carcinoma
Author(s) -
Tsai F.C.,
Liu C.J.,
Chen C.L.,
Chen P.J.,
Lai M.Y.,
Kao J.H.,
Chen D.S.
Publication year - 2007
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2006.00780.x
Subject(s) - hepatocellular carcinoma , hepatitis b virus , medicine , odds ratio , viral load , gastroenterology , genotype , confidence interval , hepatitis b , viral hepatitis , young adult , titer , immunology , virus , biology , gene , biochemistry
Summary. Advanced age and high hepatitis B virus (HBV) DNA level are risk factors associated with the development of HBV‐related hepatocellular carcinoma (HCC). However, little is known about the role of viral load in the carcinogenesis of HCC in young people. A total of 183 HBV‐related HCC patients and 202 HBV carriers were therefore enrolled to compare serum viral loads in young (≤40 years of age) and old (>40 years of age) age groups. Other factors associated with the development of HCC were also analysed. The results showed that serum alanine aminotransferase (38.7 ± 24.1 vs 58.4 ± 65.4 IU/L, P = 0.006) and HBV DNA levels (log 10 titre: 4.20 ± 1.33 vs 4.80 ± 1.39, P = 0.053) were lower in young HCC patients than in old HCC patients. There was a positive correlation between age and serum HBV DNA level in HCC patients but a negative correlation in HBV carriers. Young HCC patients with HBV genotype B infection had higher viral loads than those with genotype C infection (log 10 titre: 4.79 ± 1.34 vs 3.27 ± 0.60, P = 0.001). By multivariate logistic regression analyses, high serum HBV DNA level was associated with the development of HCC in old patients [odds ratio (OR) 1.584, 95% confidence interval (CI) 1.075–2.333] rather than in young patients (OR 0.848, 95% CI 0.645–1.116). In conclusion, viral factors in association with the development of HBV‐related HCC in young patients may be different from their old counterparts. The complicated interplay between host and virus could be responsible for the emergence and aggressive outcome of early‐onset HCC.