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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Occult Hepatitis B Infection and HBV Replicative Activity in Patients with Cryptogenic Cause of Hepatocellular Carcinoma
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Occult Hepatitis B Infection and HBV Replicative Activity in Patients with Cryptogenic Cause of Hepatocellular Carcinoma

机译:隐源性肝细胞癌患者隐匿性乙型肝炎感染和HBV复制活性

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摘要

We aimed to investigate the incidence of occult hepatitis B infection (OBI) in patients with "cryptogenic" hepatocellular carcinoma (HCC) and to study the HBV replicative activity in these patients. Tumorous and adjacent nontumorous liver tissues were obtained from 33 cryptogenic HCC patients and 28 HCC patients with identifiable causes (13 with chronic hepatitis B [CHB], six with chronic hepatitis C, and nine alcohol-related). OBI was identified by nested polymerase chain reaction (PCR). Intrahepatic HBV DNA, cova-lently closed circular DNA (cccDNA), and pregenomic RNA (pgRNA) were quantified by real-time PCR and reverse-transcription PCR (RT-PCR), respectively. OBI was identified in 24 (73%) cryptogenic HCC patients, one (17%) HCC patient with HCV, and five (56%) patients with alcohol-related HCC. In HCC patients with OBI, HBV DNA were detected in >2 HBV genomic regions more often in nontumorous tissues than in tumorous tissues (90% versus 57%, respectively; P = 0.007). Cryptogenic HCC patients with OBI had lower intrahepatic total HBV DNA levels than HCC patients with CHB (median: 0.010 versus 3.19 copies/cell, respectively; P< 0.0001). Only six (26%) cryptogenic HCC patients with OBI had detectable cccDNA (median: <0.0002 copies/cell), which was significantly lower than that of the CHB patients (median: 0.005 copies/cell; P < 0.0001). HBV pgRNA were detectable in 12 (52%) cryptogenic HCC patients with OBI (median: 0.0001 copies/cell), which was significantly lower than that of the CHB patients (median: 2.90 copies/cell; P < 0.001). Conclusion: 73% of patients with apparently unidentifiable causes for HCC were HBV-related. The detection rate was higher in nontumorous tissues than tumorous tissues. The low intrahepatic HBV DNA and pgRNA levels indicated that persistent viral replication and possibly HBV integration are the likely causes of HCC in OBI patients.
机译:我们旨在调查“隐源性”肝细胞癌(HCC)患者的隐匿性乙型肝炎感染(OBI)的发生率,并研究这些患者的HBV复制活性。从33例隐源性HCC患者和28例具有明确病因的HCC患者(13例慢性乙型肝炎[CHB],6例慢性丙型肝炎和9例与酒精有关的患者)中获得了肿瘤和相邻的非肿瘤肝组织。通过嵌套聚合酶链反应(PCR)鉴定OBI。分别通过实时PCR和逆转录PCR(RT-PCR)对肝内HBV DNA,胆囊闭合环状DNA(cccDNA)和前基因组RNA(pgRNA)进行定量。在24名(73%)隐源性HCC患者,1名(17%)HCV HCC患者和5名(56%)酒精相关HCC患者中发现了OBI。在患有OBI的HCC患者中,在非肿瘤组织中> 2 HBV基因组区域中检测到HBV DNA的频率要比在肿瘤组织中更高(分别为90%和57%; P = 0.007)。患有OBI的隐源性HCC患者的肝内总HBV DNA水平低于患有CHB的HCC患者(中位数分别为0.010对3.19拷贝/细胞; P <0.0001)。只有六名(26%)OBI隐源性HCC患者具有可检测的cccDNA(中位数:<0.0002拷贝/细胞),显着低于CHB患者(中位数:0.005拷贝/细胞; P <0.0001)。在12例(52%)OBI隐源性HCC患者中检测到HBV pgRNA(中位数:0.0001拷贝/细胞),显着低于CHB患者(中位数:2.90拷贝/细胞; P <0.001)。结论:73%的原因明确的HCC患者与HBV相关。非肿瘤组织中的检出率高于肿瘤组织。肝内HBV DNA和pgRNA的水平低表明,持续的病毒复制和可能的HBV整合是OBI患者HCC的可能原因。

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