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

StephenW

Dig Dis Sci. 2011 Aug 12. [Epub ahead of print]

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

Chu CM, Lin CC, Lin SM, Lin DY, Liaw YF.

Source

Department of Gastroenterology and Hepatology, Liver Research Unit, Chang
Gung Memorial Hospital, Chang Gung University College of Medicine, 199,
Tung Hwa North Road, Taipei, 10591, Taiwan, [email protected].

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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StephenW

谷歌翻译不是100％正确。仅作为参考使用。

Digestive Science 科学。 2011年08月12。 [检索提前打印]

病毒载量，基因型，乙型肝炎病毒相关的突变体
肝癌的早期患者特别强调
肝细胞癌。

CM楚，林CC，林SM，林DY，廖YF。

来源

部胃肠病学和肝病，肝研究组，张
长庚医院，张长庚大学医学学院，199，
敦化北路，台北，10591，台湾，[email protected]。

摘要

背景/目的：

病毒因素在B型肝炎病毒的发病机制中的作用
病毒（HBV）相关肝细胞癌（HCC）是仍然没有定论。无论
病毒学，如病毒载量或突变体的功能可能随
肝癌的进展尚不清楚。包括病人的病例对照研究
早期肝癌和乙肝表面抗原携带者被推定为最小
作为对照肝癌的潜在可能更好地识别因素显着
与肝癌发展。

方法：

病毒学特点比较59例早期肝癌患者（一个
孤肿瘤大小≤3厘米）和101非早期肝癌患者。一
比较早期肝癌患者59例进行的病例对照研究
1:2年龄相匹配的持续正常丙氨酸无效运营商
转氨酶（ALT）水平。

结果：

HBV DNA水平，HBV基因型，前C区A1896的频率和基底
核心启动子T1762/A1764突变均无显着差异
早期肝癌和非早期肝癌的患者之间。在
病例对照研究，早期肝癌患者显着高于乙肝
DNA水平和较高的基因型频率彗星HBV和基础核心
T1762/A1764启动子的突变，但类似的前C区A1896频率
突变。多元Logistic回归分析发现HBV DNA水平
≥2000 IU / mL和基础核心启动T1762/A1764突变被
肝癌发展的独立危险因素。此外，有一个
高病毒载量和基础核心启动子之间的协同效应
T1762/A1764突变对肝癌发展。

结论：

病毒学特点并没有改变，显着的进展
肝癌。 HBV DNA水平≥2000 IU / mL和基础核心启动T1762/A1764
突变是肝癌病毒的两个独立的因素。

侬是马甲

发上链接体现对原作者的尊重，真不错
但是不是说现在不能单单发摘要了，要发全文啊。

interdetect

回复 侬是马甲 的帖子

英文的abstract里面包含着有用信息，很多情况下不可能很轻松的获得全文，请理解！

侬是马甲

interdetect 发表于 2011-8-17 16:51
回复 侬是马甲 的帖子

英文的abstract里面包含着有用信息，很多情况下不可能很轻松的获得全文，请理解！

明白了