Occult and previous hepatitis B virus infection are not associated with hepatocellular carcinoma in United States patients with chronic hepatitis C.

Occult and previous hepatitis B virus infection are not associated with hepatocellular carcinoma in United States patients with chronic hepatitis C.
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DOI:
10.1002/hep.24257
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发表时间:
2011-08
期刊:
影响因子:
13.5
通讯作者:
Morgan, Timothy R.
Morgan, Timothy R.
中科院分区:
医学1区
文献类型:
--
作者:
Lok, Anna S.;Everhart, James E.;Di Bisceglie, Adrian M.;Kim, Hae-Young;Hussain, Munira;Morgan, Timothy R.

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先前的研究表明,先前暴露于乙型肝炎病毒(HBV)感染可能会增加慢性丙型肝炎患者发生肝细胞癌(HCC)的风险。本研究的目的是比较美国hbsag阴性的组织学晚期慢性丙型肝炎患者中既往或隐性HBV感染的患病率,这些患者发生或未发生HCC。参与HALT-C试验的91例HCC患者和182例匹配对照者的保存血清进行了抗hbc、抗hbs和HBV DNA检测。采用实时荧光定量PCR检测28例HCC患者和55例对照者的冷冻肝脏样本的HBV DNA。41.8%的HCC患者和45.6%的对照组血清中存在抗- hbc(作为既往HBV感染的标志物)(P=0.54);在16.5%的HCC病例和24.7%的对照组中存在单独的抗- hbc。仅1例对照者血清中检测到HBV DNA,无HCC患者血清中检测到HBV DNA。10.7%的HCC患者和23.6%的对照组肝脏中检测到HBV DNA(作为隐匿性HBV感染的标志物)(P=0.18)。尽管在HALT-C试验中几乎有一半的患者有既往HBV感染的血清学证据,但在发生或未发生HCC的患者之间,血清中抗hbc的患病率或肝脏中HBV DNA的患病率没有差异。在美国,既往或隐匿性HBV感染都不是晚期慢性丙型肝炎患者发生HCC的重要因素。
Previous studies have suggested that prior exposure to hepatitis B virus (HBV) infection may increase the risk of development of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C. The aim of this study was to compare the prevalence of previous or occult HBV infection in a cohort of HBsAg-negative patients with histologically advanced chronic hepatitis C in the United States who did or did not develop HCC. Stored sera from 91 patients with HCC and 182 matched controls who participated in the HALT-C Trial were tested for anti-HBc, anti-HBs and HBV DNA. Frozen liver samples from 28 HCC cases and 55 controls were tested for HBV DNA by real-time PCR. Anti-HBc (as a marker of previous HBV infection) was present in the serum of 41.8% HCC cases and 45.6% controls (P=0.54); anti-HBc alone was present in 16.5% of HCC cases and 24.7% of controls. HBV DNA was detected in the serum of only one control subject and no patient with HCC. HBV DNA (as a marker of occult HBV infection) was detected in the liver of 10.7% HCC cases and 23.6% controls (P=0.18). Although almost half the patients in the HALT-C Trial had serological evidence of previous HBV infection there was no difference in prevalence of anti-HBc in serum or HBV DNA in liver between patients who did or did not develop HCC. In the United States, neither previous nor occult HBV infection is an important factor in HCC development among patients with advanced chronic hepatitis C.
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