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Characteristics and outcome of patients with dual hepatitis B and C‐associated hepatocellular carcinoma: are they different from patients with single virus infection?
Author(s) -
Huo TehIa,
Huang YiHsiang,
Hsia ChengYuan,
Su ChienWei,
Lin HanChieh,
Hsu ChiaYang,
Lee PuiChing,
Lui WingYiu,
Loong CheChuan,
Chiang JenHuei,
Chiou YiYou,
Lee ShouDong
Publication year - 2009
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.1478-3231.2008.01908.x
Subject(s) - hepatocellular carcinoma , medicine , hepatitis b virus , cirrhosis , hepatitis c virus , gastroenterology , virus , liver cancer , hepatitis b , virology
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.