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Viral Load, Genotypes, and Mutants in Hepatitis B Virus-Related Hepatocellular Carcinoma: Special Emphasis on Patients with Early Hepatocellular Carcinoma

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http://www.springerlink.com/content/up2212m88751t534/

Digestive Diseases and Sciences

DOI: 10.1007/s10620-011-1844-2Online Firstâ„¢

Original Article

Viral Load, Genotypes, and Mutants in Hepatitis B Virus-Related Hepatocellular

Carcinoma: Special Emphasis on Patients with Early Hepatocellular Carcinoma

Chia-Ming Chu, Chen-Chun Lin, Shi-Ming Lin, Deng-Yn Lin and Yun-Fan Liaw

Abstract

Background/Aims

The role of viral factors in the pathogenesis of hepatitis B virus (HBV)-related

hepatocellular carcinoma (HCC) is still inconclusive. Whether virological

features such as viral load or mutants might change with the progression of HCC

remains unknown. A case–control study including patients with early HCC and

HBsAg carriers who are presumed to be at the minimal potential of HCC as

controls might better identify factors significantly associated with HCC

development.

Methods

Virological features were compared between 59 patients with early HCC (a

solitary tumor of size ≤3 cm) and 101 patients with non-early HCC. A

case–control study was performed by comparing 59 patients with early HCC and

1:2 age-matched inactive carriers with persistent normal alanine

aminotransferase (ALT) levels.

Results

HBV DNA levels, HBV genotypes, and the frequency of precore A1896 and basal core

promoter T1762/A1764 mutations showed no significant difference between patients

with early HCC and those with non-early HCC. In the case–control study,

patients with early HCC had significantly higher HBV DNA levels, and higher

frequencies of genotype C HBV and basal core promoter T1762/A1764 mutation, but

a similar frequency of precore A1896 mutation. Multiple logistic regression

analysis identified HBV DNA levels ≥2,000 IU/mL and basal core promoter

T1762/A1764 mutation as being independent factors for HCC development.

Additionally, there was a synergistic effect between high viral load and basal

core promoter T1762/A1764 mutation on HCC development.

Conclusions

Virological features did not change significantly with the progression of HCC.

HBV DNA levels ≥2,000 IU/mL and basal core promoter T1762/A1764 mutation were

two independent viral factors for HCC.

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http://www.springerlink.com/content/up2212m88751t534/

Digestive Diseases and Sciences

DOI: 10.1007/s10620-011-1844-2Online Firstâ„¢

Original Article

Viral Load, Genotypes, and Mutants in Hepatitis B Virus-Related Hepatocellular

Carcinoma: Special Emphasis on Patients with Early Hepatocellular Carcinoma

Chia-Ming Chu, Chen-Chun Lin, Shi-Ming Lin, Deng-Yn Lin and Yun-Fan Liaw

Abstract

Background/Aims

The role of viral factors in the pathogenesis of hepatitis B virus (HBV)-related

hepatocellular carcinoma (HCC) is still inconclusive. Whether virological

features such as viral load or mutants might change with the progression of HCC

remains unknown. A case–control study including patients with early HCC and

HBsAg carriers who are presumed to be at the minimal potential of HCC as

controls might better identify factors significantly associated with HCC

development.

Methods

Virological features were compared between 59 patients with early HCC (a

solitary tumor of size ≤3 cm) and 101 patients with non-early HCC. A

case–control study was performed by comparing 59 patients with early HCC and

1:2 age-matched inactive carriers with persistent normal alanine

aminotransferase (ALT) levels.

Results

HBV DNA levels, HBV genotypes, and the frequency of precore A1896 and basal core

promoter T1762/A1764 mutations showed no significant difference between patients

with early HCC and those with non-early HCC. In the case–control study,

patients with early HCC had significantly higher HBV DNA levels, and higher

frequencies of genotype C HBV and basal core promoter T1762/A1764 mutation, but

a similar frequency of precore A1896 mutation. Multiple logistic regression

analysis identified HBV DNA levels ≥2,000 IU/mL and basal core promoter

T1762/A1764 mutation as being independent factors for HCC development.

Additionally, there was a synergistic effect between high viral load and basal

core promoter T1762/A1764 mutation on HCC development.

Conclusions

Virological features did not change significantly with the progression of HCC.

HBV DNA levels ≥2,000 IU/mL and basal core promoter T1762/A1764 mutation were

two independent viral factors for HCC.

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