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本帖最后由 StephenW 于 2015-11-22 18:33 编辑
zgct 发表于 2015-11-21 07:01 
第二，另外一个值得注意的是，在通过抗病毒治疗达到了病毒持续抑制的170例患者中，有60多例仍然会发生 ...
AASLD 131
Even after achieving viral suppression, 36.5% (62/170) of cirrhotic patients with CHB still developed HCC.
即使实现病毒抑制肝硬化患者，36.5％（62/170）慢性乙型肝炎患者仍然发生HCC。
A Study for the Risk Factors of Hepatocellular Carcinoma in Cirrhotic Patients with Chronic Hepatitis B
Yuanqing Zhang1, Lijun Peng1,2, Yirong Cao1, Zhiping Zeng1, Yujing Wu1, Hong Shi1, Shiyao Chen1, Jiyao Wang1, Scott L. Friedman1,3, John J. Sninsky1,4, Jinsheng Guo1;
1Division of Digestive Diseases, Zhong Shan Hospital, Fu Dan University, Shanghai,
China;
2Department of Gastroenterology, Linyi People’s Hospital,
Linyi, China;
3Division of Liver Diseases,, Mount Sinai Hospital, Icahn School of Medicine at Mount Sinai, New York, NY;
4Celera/Quest Diagnostics, Alameda, CA
Background and Aims:
Chronic hepatitis B virus infection and
cirrhosis are important risk factors for hepatocellular carcinoma
(HCC), however the HCC risk can vary widely among individuals. The aim of this study was to identify the clinical factors
and host genetic single nucleotide polymorphisms (SNPs) that
are associated with HCC risk in cirrhotic patients with CHB.
Methods:
Data from 949 Chinese Han patients with chronic
HBV infection were analyzed by single and multivariate logistic
regression analysis in cirrhotic patients without (n = 281) and
with HCC (n = 434) to identify the clinical factors associated
with HCC risk. In a parallel study, DNA was extracted from
879 chronic HBV patients including non-cirrhotic HBV carriers
and CHB patients (n = 234), cirrhotic patients without (n =
257) and with HCC (n = 388) for genotyping of ten candidate SNPs using polymerase chain reaction-ligase detection
reaction method. The correlations between the candidate SNPs
and HCC risk were analyzed by chi-square test followed by
logistic regression analysis.
Results:
1. Ineffective antiviral treatment (OR=5.2), fatty liver (OR=3.4), family history of HCC
(OR=2.3), drinking history (OR=2.2), and age>=50 (OR=1.8)
were independent risk factors for HCC in cirrhotic patients with
CHB. Longer HBV infection increased the HCC risk whereas
sustained virologic suppression significantly lowered HCC
risk compared to those without enough response or untreated
patients, especially in patients with decompensated cirrhosis.
Even after achieving viral suppression, 36.5% (62/170) of cirrhotic patients with CHB still developed HCC. Fatty liver, family history of HCC and HBV infection were significantly associated
with the HCC development in these patients.
2. After adjusted
for influencing factors, TLR4 rs11536889 was found to be a
protective factor (OR for CC vs. GG+GC or GG =0.4 and
0.6, respectively) whereas SPP1 rs2853744 (OR for TT
vs. GG and GT+TT vs. GG =1.9 and 3.1, respectively) and AP3S2
rs2290351 (OR for GA+AA or GA vs. GG =2.5 and 2.9, respectively) were risk factors of HCC in cirrhotic patients with CHB. In cirrhotic patients with CHB and drinking history, MLEC
rs7976497 (OR for TT vs. CC=2.8, CT+TT vs. CC=3.6) and SOCS3 rs4969168 (OR for GG
vs. AA=2.4) were found to be risk factors of HCC.
Conclusion:
Ineffective antiviral treatment, fatty liver, family history of HCC, drinking history and age
≥50 are risk factors for HCC. Sustained suppression of HBV does
not remove the risk of HCC. Specific host genetic factors may
impact on HCC development in cirrhotic patients with CHB
including a protective SNP in TLR4, and risk SNPs in SPP1,
AP3S2, MLEC, and SOCS3. |
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楼主: zgct
发表于 2015-11-22 16:59
