Correlation of clinical characteristics with detection of hepatitis B virus X gene in liver tissue in HBsAg-negative,and HCV-negative hepatocellular carcinoma patients

Abstract: Purpose: We studied the clinical features and the etiology of hepatitis B virus surface antigen (HBsAg)-negative and antibody to hepatitis C virus (anti-HCV) negative patients with hepatocellular carcinoma. Methods: A total of 550 patients, hospitalized with an initial diagnosis of HCC were retrospectively studied. Eighty-one of these patients were HBsAg-positive (HB group), 404 patients were anti-HCV positive (HC group). The other 65 patients were negative for both HBsAg and for anti-HCV (NBNC group). We purified HBV-X gene from HCC or non-tumorous liver tissue of 23 NBNC patients using PCR. Results: Clinical features of NBNC as compared with HB and HC patients were as follows, respectively: non-cirrhosis rate (%): 57,37,15 (P = 0.02 for HB, P < 0.00001 for HC), the proportion of patients with normal ALT concentrations (%): 59,28,10 (P = 0.0002 for HB, P < 0.00001 for HC). Forty of 59 NBNC patients (68%) had anti-HBs and/or anti-HBc (healthy controls: 29%, P < 0.00001) and two of 56 had serum HBV DNA. Twelve of 23 NBNC patients had HBV-X gene in HCC and/or non-cancerous liver tissues (52%). None of 52 had serum HCV RNA. Conclusions: The NBNC patients with HCC had a higher frequency of non-cirrhotic liver without liver injury. The presence of the HBV-X gene in HCC suggests a possible role of past HBV infection in the development of HCC. About half of NBNC HCC is associated with seronegativity for HBsAg and positivity for the HBV-X gene in liver tissue.     

De novo hepatitis B virus infection in hepatocellular carcinoma following eradication of hepatitis C virus by interferon therapy

Epidemiological studies have revealed that hepatocellular carcinoma (HCC) is still observed in hepatitis C virus (HCV)‐positive patients with a sustained response to interferon (IFN) treatment, although a substantial decrease in the incidence of hepatocellular carcinoma (HCC) has been achieved in those patients. Why HCC develops in patients who have a complete clearance of HCV remains unclear. Here, we provided evidence of latent hepatitis B virus (HBV) infection in an initially HCV‐positive chronic hepatitis patient who developed HCC after the complete eradication of HCV by IFN therapy. Although he was initially negative for anti‐hepatitis B surface antigen (HBsAg) or circulating HBV DNA but positive for anti‐hepatitis B core antigen (anti‐HBc) in his sera, he developed HBsAg and HBV DNA during the course of the management of a series of cancers. HBV DNA was detectable in the liver tissues before HBV reactivation and the viral sequences derived from his anti‐HBc‐positive liver showed 100% homology to that from the serum after HBsAg appearance. These findings indicates that HCV‐positive individuals who are positive for anti‐HBc in the absence of HBsAg could have latent HBV infection in their liver tissues and intrahepatic HBV infection may play a pivotal role in the development of HCC after the IFN‐mediated eradication of HCV.     

乙型与丙型肝炎病毒感染对小肝癌患者预后的影响

目的 探讨HBV、HCV感染对小肝癌的外科治疗策略及其预后的影响.方法 回顾性分析1997年1月-2003年12月天津医科大学附属肿瘤医院413例手术根治切除治疗的小肝痛(≤3 cm)患者的临床资料,将其分为4组:HCV感染组75例、HBV感染组251例、HCV、HBV混合感染组33例和尢HCV、HBV感染组54例,对可能影响预后的因素采用Kaplan-Meier生存分析、log-rank时序检验.结果 413例患者术后1、3、5年尢瘤生存率分别为83%、66%和58%,术后共有168(40.8%)例患者出现肝内复发,5年复发率HCV感染组最高(64.2%),其次为HBV/HCV感染组(48.4%),HBV感染组(37.8%)及无感染组(32.3%).肝内复发肿瘤为多发者在HCV感染组发生率最高(占肝内复发肿瘤的66.0%),其次为HBV/HCV感染组(28.6%),HBV感染组(23.3%)及无感染组(17.6%).413例小肝癌患者术后1、3、5年总生存率分别为89%、70%和61%,HCV感染组预后最差.和其他组相比,HCV感染组肝硬化程度严重,肿瘤细胞分化低,更易发生血管侵犯.在随访过程中,HCV感染组肝内复发率高,且复发类型常为多结节型.结论 HCV感染相关肝癌的临床肝硬化症状更重,而且术后复发率较高,预后更差.     

Hepatitis B and C virus co-infections in human immunodeficiency virus positive North Indian patients

INTRODUCTION Diseases of the hepatobiliary system are a major problem in patients with human immunodeficiency virus (HIV) infection. An estimated one-third of deaths in HIV patients are directly or indirectly related to liver disease. Liver diseases in HI…     

Correlation of clinical characteristics with detection of hepatitis B virus X gene in liver tissue in HBsAg-negative,and HCV-negative hepatocellular carcinoma patients

PURPOSE: We studied the clinical features and the etiology of hepatitis B virus surface antigen (HBsAg)-negative and antibody to hepatitis C virus (anti-HCV) negative patients with hepatocellular carcinoma. METHODS: A total of 550 patients, hospitalized with an initial diagnosis of HCC were retrospectively studied. Eighty-one of these patients were HBsAg-positive (HB group), 404 patients were anti-HCV positive (HC group). The other 65 patients were negative for both HBsAg and for anti-HCV (NBNC group). We purified HBV-X gene from HCC or non-tumorous liver tissue of 23 NBNC patients using PCR. RESULTS: Clinical features of NBNC as compared with HB and HC patients were as follows, respectively: non-cirrhosis rate (%): 57,37,15 (P = 0.02 for HB, P < 0.00001 for HC), the proportion of patients with normal ALT concentrations (%): 59,28,10 (P = 0.0002 for HB, P < 0.00001 for HC). Forty of 59 NBNC patients (68%) had anti-HBs and/or anti-HBc (healthy controls: 29%, P < 0.00001) and two of 56 had serum HBV DNA. Twelve of 23 NBNC patients had HBV-X gene in HCC and/or non-cancerous liver tissues (52%). None of 52 had serum HCV RNA. CONCLUSIONS: The NBNC patients with HCC had a higher frequency of non-cirrhotic liver without liver injury. The presence of the HBV-X gene in HCC suggests a possible role of past HBV infection in the development of HCC. About half of NBNC HCC is associated with seronegativity for HBsAg and positivity for the HBV-X gene in liver tissue.     

Impact of occult hepatitis B virus infection and prior hepatitis B virus infection on development of hepatocellular carcinoma in patients with liver cirrhosis due to hepatitis C virus

Objective. Although hepatitis B virus (HBV) DNA can be detected in liver or sera of patients without serum hepatitis B surface antigen (HBsAg), its clinical relevance in hepatocarcinogenesis remains controversial. This observational cohort study was conducted to clarify the risk factors, including the presence of serum HBV DNA and hepatitis B core antibody (anti-HBc), for hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related liver cirrhosis (LC). Material and methods. The study comprised 123 patients with LC due to HCV, and negative for HBsAg. The risk factors for HCC development were analyzed by univariate and multivariate analysis. Serum samples were assayed for HBV DNA using real-time polymerase chain reaction. Results. Serum HBV DNA was detectable in 14 patients (11.4%) and serum anti-HBc in 96 (78.0%). During the follow-up period (mean 53.3 months), 80 patients (65.0%) developed HCC. The cumulative HCC development rate was significantly higher in the anti-HBc-positive group than in the anti-HBc-negative group (p=0.0039), but did not differ between the serum HBV DNA-positive and -negative groups (p=0.8570). The multivariate analysis indicated that male gender, alpha-fetoprotein (AFP) 20 ng/ml or greater, average serum alanine aminotransferase (ALAT) 80 IU/l or greater and the presence of anti-HBc were independent risk factors for development of HCC (p=0.038, p=0.013, p=0.020 and p=0.001, respectively). Conclusions. Serum anti-HBc, which indicates a previous HBV infection, has clinical significance in hepatocarcinogenesis in patients with HCV-related LC, but serum HBV DNA does not. Therefore, anti-HBc in serum is a significant predictor for HCC.     

慢性丙型肝炎患者混合或重叠感染其他病原体状况分析

目的了解丙型肝炎病毒（HCV）感染者混合或重叠感染乙型肝炎病毒（HBV）、人免疫缺陷病毒（HIV）和梅毒螺旋体（TP）的状况,为HCV感染的防治提供依据。方法采用ELISA法检测乙型肝炎病毒标志物、抗TP和抗HIV;采用化学发光法检测抗HCV;采用蛋白印迹法确认HIV感染。结果在169例HCV感染者中,重叠感染HBV 25例（14.8%）、HIV 4例（2.4%）、TP 9例（5.3%）,重叠感染HBV和TP 2例（1.2%）,重叠感染HBV和HIV 2例（1.2%）;静脉吸毒者重叠感染HIV（6.7%）和TP（11.1%）的比例均明显高于非静脉吸毒者（P〈0.05）;男性患者重叠感染HBV的比例（19.7%）明显高于女性患者（3.8%,P〈0.01）,女性患者重叠感染TP的比例（11.5%）明显高于男性患者（2.6%,P〈0.05）。结论随着感染方式的多元化,慢性丙型肝炎患者重叠感染其他病原体的情况更加常见。     

经血液(非静脉吸毒者)和性途径传播的HIV感染者合并HBV和HCV感染的现状

目的 探讨我国经血液(非静脉吸毒者)和性途径传播的HIV感染者合并乙型肝炎和丙型肝炎的状况.方法 回顾性分析2005年1至9月在全国13个研究中心就诊的362例HIV/AIDS患者(静脉吸毒者除外),应用酶联免疫试剂盒分别测定其HBsAg、抗-HBs,HBeAg、抗-Hbe、抗-HBc和抗-HCV.采用t检验和X2检验分别对计量和计数结果进行统计学分析.结果 315例检测血HBV和HCV的患者中,HBsAg阳性14例,占4.4%;抗-HCV阳性158例,占50.2%,抗-HCV阴性157例,占49.8%;HIV、HBV、HCV共感染2例,占0.6%.抗-HCV阳性组中经血液和性传播的比例分别占92%和4%,以血液传播为主;抗-HCV阴性组中经血液和性传播的比例分别占11%和66%,以性传播为主.抗-HCV阳性组的HIV确诊时间、CD4+T淋巴细胞绝对计数、ALT和AST均高于抗-HCV阴性组.两组患者的HBV标志物表达也存在差异,其中抗-HCV阳性组中HBsAg阳性2例,占1.3%,抗-HCV阴性组中HBsAg阳性12例,占7.6%,两组比较差异有统计学意义(X2=7.542,P<0.01).10例HBsAg阳性者进行HBV DNA检测,其中4例阳性,抗-HCV均为阴性.57例抗-HCV阳性患者进行HCV RNA检测,阳性者占63.2%.结论 我国输血和性传播途径的HIV感染合并HBV或HCV感染,以合并HCV感染为主,并多见于经输血感染者.合并HCV感染可加重HIV患者的肝脏损伤,同时也可能存在干扰HBV复制的情况.     

HBV/HCV重叠感染的抗病毒治疗

从全球范围看,乙型肝炎病毒(hepatitis B virus,HBV)和丙型肝炎病毒(hepatitis C virus,HCV)重叠感染估计约有700-2000万人口感染.重叠感染和单一HBV或HCV感染比较,更易发展为肝硬化、肝细胞癌甚至肝衰竭的比例也高,HBV和HCV重叠感染可有四种不同的临床模式,即HCV活动...     

Hepatocellular carcinoma, human immunodeficiency virus and viral hepatitis in the HAART era

The incidence of hepatocellular carcinoma （HCC） in patients with human immunodeficiency virus （HIV） is rising. HCC in HIV almost invariably occurs in the context of hepatitis C virus （HCV） or hepatitis B virus （HBV） co-infection and, on account of shared modes of transmission, this occurs in more than 33% and 10% of patients with HIV worldwide respectively. It has yet to be clearly established whether HIV directly accelerates HCC pathogenesis or whether the rising incidence is an epiphenomenon of the highly active antiretroviral therapy （HAART） era, wherein the increased longevity of patients with HIV allows long-term complications of viral hepatitis and cirrhosis to develop. Answering this question will have implications for HCC surveillance and the timing of HCV/HBV therapy, which in HIV co-infection presents unique challenges. Once HCC develops, there is growing evidence that HIV co-infection should not preclude conventional therapeutic strategies, including liver transplantation.     

Hepatocellular carcinoma, human immunodeficiency virus and viral hepatitis in the HAART era

The incidence of hepatocellular carcinoma (HCC) in patients with human immunodeficiency virus (HIV) is rising. HCC in HIV almost invariably occurs in the context of hepatitis C virus (HCV) or hepatitis B virus (HBV) co-infection and, on account of shared modes of transmission, this occurs in more than 33% and 10% of patients with HIV worldwide respectively. It has yet to be clearly established whether HIV directly accelerates HCC pathogenesis or whether the rising incidence is an epiphenomenon of the highly active antiretroviral therapy (HAART) era, wherein the increased longevity of patients with HIV allows long-term complications of viral hepatitis and cirrhosis to develop. Answering this question will have implications for HCC surveillance and the timing of HCV/HBV therapy, which in HIV co-infection presents unique challenges. Once HCC develops, there is growing evidence that HIV co-infection should not preclude conventional therapeutic strategies, including liver transplantation.     

Clinical features of HBsAg-negative but anti-HBc-positive hepatocellular carcinoma in a hepatitis B virus endemic area

BACKGROUND: The presence of antibody to the hepatitis B core antigen (anti-HBc) IgG in serum usually means a past infection of the hepatitis B virus (HBV). The clinical characteristics of patients with hepatocellular carcinoma (HCC), who have only a marker for past HBV infection, were investigated. METHODS: A total of 565 HCC patients were classified according to their markers for HBV and the hepatitis C virus (HCV). The clinical features and the survival rate of hepatitis B surface antigen (HBsAg)(-)/anti-HBc(+) patients were compared to those of HBsAg(+) patients. RESULTS: Four hundred and three patients were positive for HBsAg (B group, 71.3%), 64 were positive for anti-HCV (11.3%), and 90 were negative for both HBsAg and anti-HCV (N group, 15.9%). In the N group, 71 were positive for anti-HBc (PB group, 12.6% of total patients). The clinical characteristics of the PB group were different from those of the B group: age at diagnosis (60.6 +/- 9.6 vs 53.3 +/- 10.6 years, P < 0.001), habitual drinking (59.2% vs 23.6%, P < 0.001), family history of liver disease (9.9% vs 38.9%, P < 0.005), detection with periodic screening (28.2% vs 50.4%, P < 0.001), and elevated alpha-fetoprotein (53.5% vs 76.2%, P < 0.001). In both the PB group and the B group, liver cirrhosis was accompanied by a similar high prevalence (74.6% vs 89.1%). However, there was no significant difference in the cumulative survival rate. CONCLUSIONS: The prevalence of HBsAg(-)/anti-HBc(+) HCC is not rare or more common than that of anti-HCV(+) HCC in Korea, a high HBV endemic area. Although some differences in clinical characteristics may imply a different pathogenesis, chronic HBV infection or habitual drinking may be major contributing factors in the development of HCC in these patients.     

Coinfection of hepatitis B and hepatitis C virus in HIV-infected patients in south India

AIM To screen for the co-infection of hepatitis B (HBV)and hepatitis C virus (HCV) in human immunodeficiency virus (HIV) infected patients insouthern India.METHODS Five hundred consecutive HIV infected patients were screened for Hepatitis B Virus (HBsAg and HBV-DNA) and Hepatitis C virus (anti-HCV and HCV-RNA)using commercially available ELISA kits; HBsAg, HBeAg/anti-HBe (Biorad laboratories, USA) and anti-HCV (Murex Diagnostics, UK). The HBV-DNA PCR was performed to detect the surface antigen region (pre S-S). HCV-RNA was detected by RT-PCR for the detection of the constant 5' putative non-coding region of HCV.RESULTS HBV co-infection was detected in 45/500 (9%)patients and HCV co-infection in 11/500 (2.2%) subjects.Among the 45 co-infected patients only 40 patients could be studied, where the detection rates of HBe was 55%(22/40), antiHBe was 45% (18/40) and HBV-DNA was 56% (23/40). Among 11 HCV co-infected subjects, 6(54.5%) were anti-HCV and HCV RNA positive, while 3(27.2%) were positive for anti-HCV alone and 2 (18%)were positive for HCV RNA alone.CONCLUSION Since the principal routes for HIV transmission are similar to that followed by the hepatotropic viruses, as a consequence, infections with HBV and HCV are expected in HIV infected patients.Therefore, it would be advisable to screen for these viruses in all the HIV infected individuals and their sexual partners at the earliest.     

Updates on the treatment and outcomes of dual chronic hepatitis C and B virus infection

Dual hepatitis C virus(HCV)/hepatitis B virus(HBV)infection is found in HBV or HCV endemic areas,and in specific populations exhibiting a high risk of parenteral viral transmission.Clinical observations have revealed that HCV/HBV dually infected patients demonstrate a higher risk of liver disease progression compared with HBV or HCV monoinfected patients.The viral activity responsible for liver disease progression can be determined by examining the viral loads of HCV and HBV and by conducting liver biopsy examinations.Recent trials have confirmed that the combination therapy of peginterferon alpha-2a or 2b and ribavirin for dual hepatitis patients with HCV dominance appears to be as effective and safe as it is in patients with HCV monoinfections.Strikingly,approximately 60% of dually infected patients with inactive hepatitis B before treatment develop HBV reactivation after the clearance of the HCV.The clinical significance of this HBV reactivation and the strategy to prevent and treat this event should be determined.Furthermore,approximately 30%of dually infected patients lost hepatitis B surface antigen(HBsAg)within 5 years after the start of peginterferonbased therapy,and 40%of them harbored occult HBV infection.The underlying mechanisms of their accelerating HBsAg seroclearance and the development of occult HBV await further investigations.Moreover,the optimal treatment strategies for dually infected patients who are seropositive for the hepatitis B e antigen must be explored.Finally,the advent of new direct-acting antiviral-based anti-HCV therapy may change the optimal therapies for patients with dual hepatitis in the near future,which warrants further clinical trials.     

Occult hepatitis B virus infection is not associated with disease progression of chronic hepatitis C virus infection

AIM To clarify the prevalence of occult hepatitis B virus(HBV) infection(OBI) and the association between OBI and liver disease progression, defined as development of liver cirrhosis or hepatocellular carcinoma(HCC), worsening of Child-Pugh class, or mortality in cases of chronic hepatitis C virus(HCV) infection. METHODS This prospective cohort study enrolled 174 patients with chronic HCV infection(chronic hepatitis, n = 83; cirrhosis, n = 47; HCC, n = 44), and evaluated disease progression during a mean follow-up of 38.7 mo. OBI was defined as HBV DNA positivity in 2 or moredifferent viral genomic regions by nested polymerase chain reaction using 4 sets of primers in the S, C, P and X open reading frame of the HBV genome. RESULTS The overall OBI prevalence in chronic HCV patients at enrollment was 18.4%, with 16.9%, 25.5% and 13.6% in the chronic hepatitis C, liver cirrhosis and HCC groups, respectively(P = 0.845). During follow-up, 52 patients showed disease progression, which was independently associated with aspartate aminotransferase 40 IU/L, Child-Pugh score and sustained virologic response(SVR), but not with OBI positivity. In 136 patients who were not in the SVR state during the study period, OBI positivity was associated with neither disease progression, nor HCC development. CONCLUSION The prevalence of OBI in chronic HCV patients was 18.4%, and OBI was not associated with disease progression in South Koreans.     

Dual chronic hepatitis B virus and hepatitis C virus infection

Dual hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are common in HBV or HCV endemic areas. However, several clinical and pathogenetic issues remain unresolved. First, clinical and in vitro studies suggest the interactions between two viruses. The dynamics of the interaction in untreated setting versus treated setting and its influence on the long-term outcomes await further studies. A key issue regarding viral interactions is whether modulation of infection occurs in the same dually infected individual hepatocyte of the liver. Clarifying this issue may help to understand the reciprocal interference between HCV and HBV and provide clues for future immunopathogenetic studies. Second, the prevalence and clinical significance of coexisting occult HBV infection in patients with chronic HCV infection need further investigations. Third, combination therapy of peginterferon alfa-2a and ribavirin appears to be just as effective and safe for the treatment of hepatitis B surface antigen (HBsAg)-positive patients chronically infected with active chronic hepatitis C as it is in patients with HCV monoinfection. Nevertheless, one-third of dually infected patients with nondetectable serum HBV DNA-level pretreatment developed HBV reactivation posttreatment. How to prevent and treat this reactivation should be clarified. Furthermore, about 10% of the dually infected patients lost HBsAg. Underlying mechanisms await further investigations. Finally, the optimal treatment strategies for dually infected patients with hepatitis B e antigen-positive chronic hepatitis B should be identified in future clinical trials.     

Outcomes and management of viral hepatitis and human immunodeficiency virus co-infection in liver transplantation

Liver transplantation for human immunodeficiency virus(HIV)positive patients with viral hepatitis co-infection is increasingly offered in many North American and European liver transplant centers.Prior studies have demonstrated acceptable post-transplant outcomes and no increased risk of HIV complications in patients coinfected with hepatitis B virus(HBV).However,liver transplantation in HIV positive patients with hepatitis C virus(HCV)has poorer outcomes overall,requiring careful selection of candidates.This review aims to summarize the published literature on outcomes after transplant in HIV patients with HBV or HCV related end-stage liver disease and recommendations for management.In particular the pre-transplant factors impacting outcomes in HCV/HIV co-infected candidates and importance of multidisciplinary management will be discussed.     

Genomic mutations with amino acid substitutions of circulating hepatitis B virus found in non-B,non-C patients with hepatocellular carcinoma

OBJECTIVE: Most hepatocellular carcinoma (HCC) in Japan is caused by chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV). HBV DNA has been detected in the serum and liver tissue of some proportion of those patients who are HBs antigen-negative and HCV antibody-negative; i.e., non-B, non-C (NBNC) patients with HCC. We sought to detect HBV DNA in the serum from NBNC HCC cases and to investigate genomic mutations of HBV in seronegative cases. PATIENTS AND METHODS: The sera from 26 NBNC HCC patients were examined by polymerase chain reaction (PCR) followed by southern blotting for existence of HBV DNA. The precore/core and polymerase regions of the HBV genome in the sera from five seronegative cases were analyzed by direct sequence. RESULTS: HBV DNA was detected in 17 of 26 patients (65.4%). Demographic factors such as age, gender, anti-HBs positivity, anti-HBc positivity, complication with cirrhosis, and excessive alcohol intake did not affect circulating HBV positivity. Genomic mutations with amino acid substitutions were detected in the polymerase and the precore regions from one of the five cases, and in the core region from four of the five cases. CONCLUSIONS: PCR-based HBV screening is necessary in patients suffering from liver diseases of unknown etiology, although its etiological importance and benefit of viral elimination have not been established. Genomic mutations in the precore/core and the polymerase region detected in this study might be involved in the lack of HBsAg in NBNC HCC cases.     

Associations between antibody to hepatitis B core antigen positivity and outcomes in hepatocellular carcinoma patients undergoing hepatic resection

Aim

We aimed to evaluate the effect of antibody to hepatitis B core antigen (HBcAb) positivity on clinical outcomes after hepatic resection in hepatocellular carcinoma (HCC) patients with negative hepatitis B surface antigen (HBsAg) and hepatitis C virus antibody (HCVAb), termed non‐B, non‐C HCC (NBNC‐HCC), or with HCV‐related HCC.

Methods

Two hundred and sixty‐three patients who underwent hepatic resection for HCC and measurements of HBsAg, HCVAb, and HBcAb were enrolled in this study.

Results

The percentages of HBcAb positivity were 52.3% (n = 57) and 56.9% (n = 66) in patients with NBNC‐ and HCV‐related HCC, respectively. The proportion of multiple NBNC‐HCCs was significantly greater in patients with HBcAb positivity compared to HBcAb negativity (P = 0.028). There were no significant differences in the recurrence‐free and overall survival rates between NBNC‐HCC patients with HBcAb positivity versus negativity (P = 0.461 and P = 0.190, respectively). Furthermore, for HCV‐related HCC patients, there were no significant differences in the baseline factors between patients with positive versus negative HBcAb. The proportion of patients with HBcAb‐positive HCV‐related HCC who underwent anatomical resection of the liver was significantly greater than that of HBcAb‐negative patients, whereas the recurrence‐free and overall survival rates were not significantly different (P = 0.158 and P = 0.191, respectively).

Conclusion

In our study, the presence of HBcAb had no impact on surgical outcomes after hepatic resection in patients with NBNB‐ and HCV‐related HCC. Occult HBV infection might be associated with hepatocarcinogenesis in patients with NBNC‐related HCC.     

重叠乙型和丙型肝炎病毒感染的临床与病理分析

目的 观察HBV和HCV重叠感染的临床与病理,探讨HBV和HCV相互作用的特点.方法 收集226例慢性肝病患者的血清学指标,实时荧光定量PCR法测定HBV DNA和HCVRNA,ELISA检测HBV血清标志物、抗-HCV抗体.行肝穿刺活组织病理检查、免疫组织化学HBsAg、HBcAg和原位杂交HBV DNA、HCV RNA检测.计数资料比较采用X2检验或Fisher确切率检验.结果 HBV和HCV重叠感染的重度慢性肝炎患者比例为62.50%,高于HBV或HCV单独感染者的27.05%和30.56%(X2=14.70,P＜0.01).HBV感染组的血ALT、AST、TBil、DBil和Alb高于HBV和HCV重叠感染组和HCV感染组,差异均有统计学意义(X2=8.52,P＜0.05).重叠感染组和HBV感染组的血HBsAg与肝内HBsAg一致率比较,差异均有统计学意义(X2=15.60,P＜0.01).HBV和HCV重叠感染组血清HBV DNA阳性率为12.5%,低于HBV单独感染组的87.7%(X2=17.66,P＜0.01);而HBV和HCV重叠感染组HCV RNA阳性率为75.0%,低于HCV单独感染组的80.6%,差异无统计学意义(P＞0.05).结论 HBV和HCV重叠感染导致的肝损伤更明显.