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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Characteristics and outcome of patients with dual hepatitis B and C-associated hepatocellular carcinoma: are they different from patients with single virus infection?
Liver International : Official Journal of the International Association for the Study of the Liver 2009 May
BACKGROUND: Patients with hepatocellular carcinoma (HCC) caused by dual hepatitis B and C virus (HBV, HCV) infection may constitute a distinct disease group that is different from patients with single virus infection. This study compared the clinical characteristics and outcomes of patients with HBV, HCV and dual virus infection.
METHODS: A prospective database of 1215 HCC patients with chronic hepatitis B, C or dual virus infection was investigated.
RESULTS: Patients with HCV infection (n=388) were significantly older (mean age, 69 years) than patients with dual virus (n=75, 65 years) and HBV (n=752; 60 years) infection (P<0.0001). The male-to-female ratios for the HBV, dual virus and HCV groups were 5.2, 3.4 and 1.3 respectively (P<0.0001). Patients in the HBV group more often had higher total tumour volume (mean, 409 cm(3)) than those in the dual virus group (244 cm(3)) and HCV (168 cm(3)) group (P<0.0001). No significant differences of the severity of liver cirrhosis, performance status, cancer staging and tumour cell differentiation were noted among the three groups. Patients in the HCV group had a significantly poor survival in comparison with the HBV group only in the subset of patients with small tumour volume (<50 cm(3)) in the Cox proportional hazards model (relative risk, 1.44; P=0.041).
CONCLUSIONS: Dual HBV and HCV virus infection does not accelerate the speed of HCC formation in patients with chronic hepatitis B, and appears to have a modified course of carcinogenesis pathway that is diverted away from the biological behaviour of HBV and HCV infection.
METHODS: A prospective database of 1215 HCC patients with chronic hepatitis B, C or dual virus infection was investigated.
RESULTS: Patients with HCV infection (n=388) were significantly older (mean age, 69 years) than patients with dual virus (n=75, 65 years) and HBV (n=752; 60 years) infection (P<0.0001). The male-to-female ratios for the HBV, dual virus and HCV groups were 5.2, 3.4 and 1.3 respectively (P<0.0001). Patients in the HBV group more often had higher total tumour volume (mean, 409 cm(3)) than those in the dual virus group (244 cm(3)) and HCV (168 cm(3)) group (P<0.0001). No significant differences of the severity of liver cirrhosis, performance status, cancer staging and tumour cell differentiation were noted among the three groups. Patients in the HCV group had a significantly poor survival in comparison with the HBV group only in the subset of patients with small tumour volume (<50 cm(3)) in the Cox proportional hazards model (relative risk, 1.44; P=0.041).
CONCLUSIONS: Dual HBV and HCV virus infection does not accelerate the speed of HCC formation in patients with chronic hepatitis B, and appears to have a modified course of carcinogenesis pathway that is diverted away from the biological behaviour of HBV and HCV infection.
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