Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: systematic review and meta-analysis
Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: systematic review and meta-analysis
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DOI：
10.1002/ijc.25321
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发表时间：
2011-01-01
影响因子：
6.4
通讯作者：
Park, Sue K.
中科院分区：
文献类型：
--
作者：
Cho, Lisa Y.;Yang, Jae Jeong;Park, Sue K.
B型肝炎病毒（HBV）和丙型肝炎病毒（HCV）合并感染的亚加性效应是可能的，因为一种病毒的重叠感染倾向于抑制另一种病毒的感染。然而，研究报告了不一致的结果，来自不同国家（1998年）和中国（2005年）的两项荟萃分析报告了肝细胞癌（HCC）风险的超累加效应。因此，我们重新评估HBV/HCV单一感染和合并感染。在411份报告中，我们纳入了59项研究，评估了HBV/HCV单一感染和合并感染与HCC风险之间的关系。由于高/可检测到的HBV DNA和HBeAg感染导致的肝癌风险高于HBsAg感染，而抗-HCV与抗-HCV/HCV RNA没有差异。从地理上看，非流行区的HCC风险显著高于HBV或HCV流行区。在最近发表的研究、队列研究和在HBV/HCV非流行区进行的研究中呈现HCC风险的亚加性效应;在HBV流行区进行的研究中呈现加性效应;在先前发表的研究、病例对照研究和在HCV流行区进行的研究中呈现超加性效应。我们的研究结果表明，HBV/HCV合并感染的肝癌风险并不显着大于HBV/HCV单一感染，和肝癌的风险，由于HBV或HCV是在非流行区高于流行区。除HBV（+）/HCV（+）和HBV生物标志物分析外，大多数分析的p异质性均具有显著性。需要针对HBV或HCV单一感染患者的预防策略。此外，还需要针对性的预防措施，以减少感染性，如HBV标志物（HBeAg，HBV DNA）。
A subadditive effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is possible because superinfection of one virus tends to inhibit infection of the other virus. However, studies have reported inconsistent findings, and two meta-analyses of studies from various countries (1998) and China (2005) reported a supraadditive effect for hepatocellular carcinoma (HCC) risk. Thus, we reevaluate HBV/HCV monoinfection and coinfection. Of 411 reports, we included 59 studies that assessed the association between HBV/HCV monoinfection and coinfection for HCC risk. HCC risk because of high/detectable HBV DNA and HBeAg infection was higher than HBsAg infection, whereas anti-HCV vs anti-HCV/HCV RNA was not different. Geographically, HCC risk was significantly higher in nonendemic than in HBV or HCV endemic areas. Subadditive effect for HCC risk was presented in recently published studies, cohort studies and studies conducted in HBV/HCV nonendemic areas; an additive effect was presented in studies conducted in HBV endemic areas; a supraadditive effect was presented in previously published studies, case-control studies and studies conducted in HCV endemic areas. Our results suggest HBV/HCV coinfection for HCC risk is not significantly greater than HBV/HCV monoinfection, and HCC risk due to HBV or HCV is higher in nonendemic than endemic areas. The p-heterogeneity was significant for most analyses, except HBV(+)/HCV( +) and HBV biomarker analyses. Prevention strategies targeted toward HBV or HCV monoinfected patients are needed. In addition, tailored prevention to reduce infectivity such as HBV markers (HBeAg, HBV DNA) is needed.