60例孕妇HBV血清标志物水平与母婴传播的关系分析

目的 探讨孕妇乙型肝炎病毒（HBV）血清标志物水平与母婴传播的关系。方法 采取60例孕妇、脐带、新生儿血清用美国雅培试剂做HBV血清标志物（HBVM）包括：HBsAg、HBsAb、HBeAg、HBeAb、HBcAb定量分析,用荧光定量PCR法测HBV DNA。结果 HBsAg、HBeAg、HBcAb阳性母亲的新生儿脐血HBV M阳性率91．67％,新生儿血HBV M阳性率85％,母血HBsAg、HBeAg、HBcAb滴度显著高于脐血、新生儿血,且母血、脐血、新生儿血HBV M水平依次降低;HBV DNA阳性率也依次降低,分别为58、33％、10％、6、67％,滴度也依次降低。HBsAg、HBeAb、HBcAb阳性母亲,HBsAg、HBcAb阳性母亲和单项HBsAg阳性母亲的新生儿脐血、新生儿血HBV M阳性率较低。新生儿血以HBeAg阳性为主,滴度明显高于正常值,HBsAg滴度仅略高于正常值。结论 母婴垂直传播与母亲HBeAg高滴度有密切关系,与母亲HBV DNA阳性或阴性关系并不十分密切。检测脐血和新生儿血HBsAg、HBV DNA阴性并不能排除HBV感染,不如检测HBsAg、HBeAg更有意义,更经济。     

江苏启东地区不同背景HBsAg阳性者乙肝病毒感染状态对比分析

目的调查启东肝癌高发区不同背景HBsAg阳性者中乙肝病毒免疫状态和复制活跃程度。方法采用荧光定量PCR法对377例HBsAg阳性者进行血清HBV DNA载量检测,其中HBeAg阳性104例,原发性肝癌173例,有肝癌家族史129例。结果①肝癌患者抗-HBe转换率显著低于非肝癌患者,HBV DNA阳性率显著高于非肝癌患者（P〈0.05或〈0.01）。②HBeAg阳性者HBV DNA阳性率和平均水平均高于HBeAg阴性者,抗-HBe转换患者的HBV DNA平均水平显著低于未转换者（P均〈0.01）。③有肝癌家族史患者HBeAg阳性率显著低于无肝癌家族史患者,血清HBV DNA平均水平也显著低于后者（P〈0.05或〈0.01）。④HBV DNA与HBeAg呈正相关,与抗-HBe呈负相关;有肝癌家族史、抗-HBe阳性的男性患者HBV DNA水平较低。结论HBV活跃复制与肝癌发生密切相关;启东肝癌高发区HBV DNA水平与HBeAg呈正相关,与抗-HBe呈负相关;临床上应重视对HBsAg阳性者HBeAg模式和HBV DNA的联合检测,并根据不同背景正确判断病情及治疗效果。     

手术前和输血前血液传播性疾病感染因子检测及意义

目的：通过对手术前和输血前患者乙肝5项、HCV、HIV、TP等血液传播性疾病感染因子标记物及ALT检测,探讨其在医院感染控制、化解医疗风险和减少医疗纠纷中的作用。方法：采用ELISA法检测19 592例手术前和输血前患者乙肝5项指标、丙型肝炎病毒抗体（抗-HCV）、艾滋病病毒抗体（抗-HIV）、梅毒螺旋体抗体（抗-TP）,谷丙转氨酶（ALT）采用速率法。结果：单项HBsAg阳性率为16.09%,HBsAg加HBeAg阳性率1.62%,HBsAg加HBeAg加HBcAb阳性率7.16%,HBsAg加HBeAb加HBcAb阳性率8.49%,HBsAg加HBcAb阳性率0.51%,单项HBeAb阳性率0.59%,单项HBcAb阳性率4.76%;HBV总阳性率为38.92%。抗-HIV阳性率0.087%;抗-TP阳性率0.74%;抗-HCV阳性率1.27%;4898例ALT〉40 U/L,阳性率25%。17例抗-HIV阳性病例中HIV重叠感染HBV 7例（41.18%）;HIV重叠感染HCV 3例（17.65%）;HIV同时感染HCV和HBV三重感染2例（11.76%）。结论：①手术前和输血前进行相关感染疾病标记物的检测对防范手术和输血风险是十分必要的。②要加大经费和技术投入,最大限度的选用灵敏度高、重复性好的试剂和仪器,尽可能的采用能缩短＂窗口期＂的试剂,进一步提高检出率,才能有效地减少输血和手术医疗风险和纠纷的发生。     

HBsAg阳性孕妇免疫接种阻断HBV宫内感染疗效的Meta分析

目的评价HBsAg阳性孕妇产前应用乙肝免疫球蛋白（HBIG）或联用乙肝疫苗阻断胎儿HBV宫内感染的有效性及安全性。方法计算机检索6个数据库,手检9种期刊,并追查参考文献,纳入国内外符合纳入标准的随机对照试验和半随机对照试验,由两名评价员独立筛查文献,评价质量和提取资料。用Revman 4.2.10软件分析数据。采用χ2检验鉴定研究间异质性,使用固定效应或随机效应模型合并结果。结果HBsAg阳性/HBsAg和HBeAg均阳性孕妇孕期应用HBIG总剂量600 IU,胎儿HBV宫内感染率〈空白对照组（RR=0.42,95%CI=0.21-0.83,P=0.01）,新生儿HBV DNA阳性率低于空白对照组（RR=0.30,95%CI=0.10-0.85,P=0.02）,新生儿HBeAg阳性率Anti-HBs阳性率与空白组比较差异无统计学意义;总剂量大于600 IU时,宫内感染率〈空白对照组（RR=0.39,95%CI=0.26-0.58,P〈0.000 01）,新生儿Anti-HBs阳性率与对照组比较差异无统计学意义。HBsAg和HBeAg均阳性孕妇孕期应用HBIG总剂量〉600 IU,胎儿HBV宫内感染率、新生儿HBeAg阳性率、新生儿HBV DNA阳性率、新生儿Anti-HBs阳性率与对照组比较差异均无统计学意义;总剂量600 IU组新生儿HBeAg阳性率和新生儿HBV DNA阳性率与对照组比较差异有统计学意义。结论HBsAg阳性/HBsAg和HBeAg均阳性孕妇孕期应用HBIG可降低胎儿HBV宫内感染率;HBsAg和HBeAg均阳性孕妇孕期应用HBIG阻断宫内感染的疗效尚不清楚。     

慢性肝病患者乙肝病毒血清学标志物转换规律及其意义

目的探讨乙肝病毒血清学标志物（HBVM）在慢性肝病患者中的转换规律及临床意义。方法选择慢性肝病患者包括慢性病毒性乙型肝炎、慢性重型乙型肝炎、肝炎肝硬化和原发性肝癌患者183例,采用ELISA方法对HBVM（HBsAg、HBsAb、HBeAg、HBeAb和HBcAb）进行检测,采用荧光定量聚酶链反应法进行HBV DNA检测,将HBV DNA检测值进行对数转换行统计学分析。结果慢性肝病患者的HBVM共有3种模式：大三阳（L3PP：HB-sAg、HBeAg和HBcAb）、小三阳（S3PP：HBsAg、HBeAb和HBcAb）和小二阳（S2PP：HBsAg和HBcAb）。L3PP HBVDNA水平高于S3PP和S2PP（P〈0.01）。随着慢性肝病病情发展,L3PP阳性率呈下降趋势,S3PP和S2PP阳性率呈上升趋势（P均〈0.01）;不同临床类型的慢性肝病患者3种HBVM模式的分布存在统计学差异（P〈0.01）。结论 L3PP慢性肝病患者HBV DNA复制水平高于S3PP或S2PP模式。随着慢性肝病病情的进展,HBVM的模式可发生转换,HBeAg阴转,L2PP转为S3PP或S2PP。     

原发性肝癌患者血清HBV标志物和HBV DNA测定的临床意义

目的观察原发性肝癌患者血清HBV标志物模式及HBV DNA水平。方法采用化学发光法检测151例PHC、132例慢性乙型肝炎和140例乙型肝炎肝硬化患者血清乙型肝炎病毒标记物;采用聚合酶链反应检测血清HBV DNA水平。结果在151例原发性肝癌患者中,HBV感染率达97.4%（147/151）,HBV DNA阳性率为74.8%（113/151）,平均水平为5.6±1.1 lgcopies/ml;HBsAg（＋）、HBeAb（＋）、HBcAb（＋）90例（59.6%）,其血清HBVDNA检出率为76.7%,平均水平为5.1±0.9lgcopies/ml;HBsAg（＋）、HBeAg（＋）、HBcAb（＋）38例（25.2%）,血清HBVDNA检出率100.0%,平均水平为6.4±0.9 lgcopies/ml。结论 PHC患者HBV感染率高,HBV与PHC发生有十分密切的关系。随着慢性乙型肝炎和乙型肝炎肝硬化病情的进展,血清HBeAg自发性发生血清学转换和HBV DNA载量下降,要警防原发性肝癌的发生。     

前S1抗原在乙肝病毒感染与复制中的作用

目的 传统乙肝血清标志物是目前我国用于乙肝检测与筛查较普及的指标,但传统乙肝HBV-M检测在病毒复制等一些方面尚有不足.本研究分析前S1（Pre-S1）抗原在判断乙肝病毒的感染与复制中的作用.方法 HBV-M和Pre-S1抗原检测采用ELISA法;HBV DNA检测采用实时荧光定量PCR技术.结果 （1）Pre-S1抗原在乙肝病毒早期感染中的作用：787例ALT正常血清中,Pre-S1抗原阳性34例,HBV-M检测HBsAg（＋）2例,HBsAg（＋）、HBeAg（＋）1例,HBsAg（＋）、HBeAg（＋）、HBcAb（＋）7例,HBsAg（＋）、HBeAb（＋）、HBcAb（＋）18例,HBsAg（＋）、HBcAb（＋）4例,HBV DNA阳性35例,三者检出结果高度符合,无显著差异（P＞0.05）.（2）Pre-S1抗原在乙肝病毒复制中的作用：816例慢性乙肝患者中,HBeAg（＋）/HBeAb（-）396例,Pre-S1抗原阳性357例,HBV DNA阳性371例,阳性检出率分别为90.1%和93.6%.HBeAg（-）/HBeAb（＋）285例,Pre-S1抗原阳性223例,HBV DNA阳性247例,阳性检出率分别为78.2%和86.7%.HBeAg（-）/HBeAb（-）135例,Pre-S1抗原阳性85例,HBV DNA阳性105例,阳性检出率分别为62.9%和77.7%,若以HBV DNA≥103copy/ml为判断乙肝病毒存在复制的标准,则Pre-S1抗原的检出率为79%（414/525）,HBeAg（＋）的检出率为32.7%（172/525）;Pre-S1抗原、HBeAg（＋）与HBV DNA的总符合率分别为78.8%（615/723）、45.5%（327/723）,HBV DNA与Pre-S1抗原检出率差异无显著性（P＞0.05）,HBeAg（＋）与HBV DNA检出率差异有显著性（P＜0.05）.结论 Pre-S1抗原是乙肝病毒早期诊断与病毒复制的重要标志.     

丙型肝炎病毒/乙型肝炎病毒重叠感染对维持性血液透析患者HBV DNA水平及肝功能的影响

目的探讨HCV重叠感染对HBV感染的维持性血液透析（MHD）患者HBV DNA水平的影响。方法选取HBV感染血清标志物阳性的MHD患者178名,将其分为HBV合并HCV感染组（HBV＋HCV＋组,n=86）和单纯HBV感染组（HBV＋HCV-组,n=92）,同时检测两组HBV DNA水平及主要血生化指标。结果两组ALT、AST水平无明显差异（P〉0.05）,HBV＋HCV＋组HBVDNA水平较HBV＋HCV-组明显降低[（0.42±0.10）log scale/ml vs（1.25±0.28）log scale/ml,P〈0.01]。多元Logistic回归分析显示HCV感染与低HBV DNA水平独立相关（OR=0.316,95%CI：0.124～0.703,P〈0.01）。结论在HBV感染的MHD患者中,合并HCV感染能显著降低患者的HBV DNA水平,而不引起明显的肝功能损害加重。     

乙型肝炎病毒丹氏颗粒抗原在慢性乙型肝炎病毒检测中应用的研究

目的分析乙肝病毒五项检测方法和乙肝病毒丹氏颗粒抗原检测试剂在检测慢性乙型肝炎感染中的一致性,探讨丹氏颗粒抗原检测试剂在检测慢性乙肝感染的经济性和可靠性。方法ELISA方法检测134例慢性乙肝患者的血清标志物和丹氏颗粒抗原,荧光定量PCR方法检测HBV DNA。比较各组丹氏颗粒抗原水平及HBVDNA定量水平和乙肝五项的相互关系。结果慢性乙肝患者HBsAg、HBeAg、HBcAb阳性组、HBsAg、HBcAb阳性组、HBsAg、HBeAb、HBcAb阳性组和HBsAb、HBeAb、HBcAb阳性组丹氏颗粒抗原阳性率分别为100.0(、100.0(、94.3(和0。结论丹氏颗粒抗原试剂在检测慢性乙肝感染中与乙肝五项指标及HBV DNA定量之间具有一致性。丹氏颗粒抗原是一个能较好的反应乙肝病毒复制的指标,对乙肝的诊断、预后及抗病毒疗效观察有较好的实用价值。     

前S1抗原诊断乙型肝炎病毒复制的临床探讨

目的分析前S1抗原与乙型肝炎病毒血清复制指标之间的关系。方法对651例乙型肝炎病毒标志物阳性血清,检测其HBV DNA、HBeAg和前-S1,分析检出率及相关性。结果HBV DNA、前-S1在HBsAg、HBeAg、HB-cAb阳性组中的检出率分别达98.5%、97.0%,HBsAg、HBeAb、HBcAb阳性组中为63.0%、62.4%,HBsAg、HBcAb阳性组中为49.1%、45.4%。HBV DNA≥103拷贝/ml的399例中HBeAg和前-S1的阳性率分别为34.1%、95.7%;HBV DNA<103拷贝/ml的252例中HBeAg和前-S1的阳性率分别为0.9%、2.4%。HBV DNA与HBeAg的检出率差异有显著性,与前-S1的检出率差异无显著性。结论前-S1抗原较HBeAg更敏感地反映HBV复制的情况。     

血清乙型肝炎病毒DNA阳性与原发性肝癌危险性关系的前瞻性队列研究

目的 探讨血清HBV DNA阳性与原发性肝癌的关系.方法 以分层抽样方法 对广西隆安县12个乡镇30～55岁农村居民抽样,采静脉血,酶联免疫吸附试验检测ItBsAg,套式聚合酶链反应检测HBV DNA.根据tiBsAg和DNA检测结果,将研究对象分为HBsAg(+)/HBV DNA (+)组(A组)和HBsAg(+)/HBV DNA(-)组(B组);根据1:1匹配原则,从本村电HBsAg(-)者中为前两组观察对象挑选对照,组成HBsAg阴性对照组(C组),对这3组人群进行4年的前瞻性跟踪随访.卡方检验对各组及各因素的发病率进行统计分析,然后用Cox比例风险模型分析与PLC有关的危险因素,用后退法对数值进行迭代分析. 结果30～55岁人群HBsAg阳性率为14.52%(3975/27 379),HBsAg阳性者HBV DNA阳性率为40.35%(1604/3975).A、B两组总的肝癌发病率为672.45/10万人年,明显高于C组的17.19/10万人年(P<0.01),相对危险度为39.123,95%可信区间为9.018～159.146.A组肝癌发病率为984.03/10万人年,显明高于C组的324.38/10万人年(P<0.01),相对危险度为3.034,95%可信区间为1.795～5.125.对A、B两组进行肝癌危险因素的多因素Cox模型分析,结果表明性别、年龄、血清HBV DNA阳性、肝癌家族史和以玉米为主食均为肝痛的危险因素. 结论 血清HBV DNA阳性可增加HBsAg阳性者的肝癌危险性.     

TACE术后接受恩替卡韦治疗血清HBV DNA阴性的中晚期原发性肝癌患者生存率研究

目的 观察抗病毒治疗对血清HBV DNA阴性的中晚期肝癌患者中远期生存率的影响。方法 82例血清HBV DNA阴性的中晚期肝癌患者,采用随机数字表法分为观察组41例和对照组41例。在对照组,行经肝动脉栓塞化疗（TACE）治疗,观察组在TACE术基础上联合恩替卡韦进行抗病毒治疗。比较两组客观缓解率、疾病控制率、治疗48周和96周肝功能指标、2 a和3 a疾病无进展生存（PFS）和总生存（OS）时间。结果 术后8周,观察组和对照组客观缓解率分别为53.6%和50.3%,疾病控制率分别为82.9%和85.5% （均P>0.05）;两组治疗前后血清TBIL、ALT、INR、AFP水平差异均无统计学意义（P>0.05）;观察组3 a DFS和OS分别为61.0%和73.2%,显著高于对照组的36.6%和51.2% （P<0.05）;观察组血清HBV DNA转阳率为2.4%,显著低于对照组的19.5%（P<0.05）。结论 血清HBV DNA阴性的中晚期肝癌患者在TACE术后应用恩替卡韦进行抗病毒治疗可提高生存率,避免HBV DNA转阳,使患者远期获益。     

Prevalence of occult hepatitis B & C in HIV patients infected through sexual transmission.

BACKGROUND: Prevalence of Hepatitis B virus (HBV) and Hepatitis C virus (HCV) markers including active and occult infection has not been described in diverse cohorts among HIV-infected patients in India. Earlier studies have explained the role of HBV/HCV co-infection in cohorts of injection drug users (IDUs) but the sexual co-transmission of HBV/ HCV is not completely understood. OBJECTIVE: The objective of this study was to assess the prevalence of occult HBV & HCV infection in HIV positive sexually acquired transmission risk group. MATERIALS AND METHODS: 58 sexually acquired HIV positive patients were taken up for the study of occult HBV/HCV co-infection. Data on demographics, sexual behaviour, sexually transmitted diseases (STD), medical history, laboratory tests viz., serum ALT and CD4 count were recorded. HBV serology included HBsAg, anti HBs, IgG anti HBc and HBV DNA (PCR). HCV serology included anti HCV & HCV RNA (RT-PCR). RESULTS: Occult HBV infection (HBV DNA) was observed in 12.2% (7/58 with HBsAg -ve and IgG anti HBc +ve subjects) while an overall prevalence of HBV DNA was 13.7% (12% occult & 1.7% in HBsAg+ve patients). Out of 58 HIV positive patients 29.3% demonstrated reactivity for any marker of past or current HBV infection. (HBsAg 1.7%, anti HBs 10.3% anti HBc IgG 17.2%). 4/58 (6.8%) revealed anti HCV positivity along with HCV RNA positivity by RT-PCR while 6/58 (10.3%) individuals revealed an occult HCV infection (anti HCV negative). The overall HCV RNA prevalence was 17.2%. 2 out of 58 (3.4%) individuals were positive for occult infection of both HBV DNA & HCV RNA (Triple infection HIV/HBV/ HCV). The HBV/HCV co-infected group (n = 18) showed a significantly high ALT (114.3 + 12.3 U/I) & low CD4 count (202.5 + 33.7 cells/mm3). The percent prevalence of HBV/ HCV co-infection was higher in the illiterate group, in men less than 30 years of age, and in those who were married and exhibited polygamous activity. CONCLUSIONS: The study demonstrated that in HIV infected patients testing only serological viral markers like HBsAg, antiHBcIgG & anti HCV, fails to identify the true prevalence of co-infection with HBV & HCV. Qualitative PCR for HBV DNA & HCV RNA detects co-infection in patients who are negative for serological markers. Also, in subjects who had only a sexual risk factor for parenterally transmitted infections, HIV may enhance the sexual transmission of HBV and HCV.     

自体与异体LAK细胞治疗慢性肝炎130例

目的对ＬＡＫ细胞治疗慢性肝炎作客观估价．方法治疗与对照组均口服维生素，肌注肝炎灵．治疗Ａ组加回输自体ＬＡＫ细胞，每周２次，６周为１个疗程；Ｂ组每周输注异体ＬＡＫ细胞悬液１次，５次为１疗程．结果ＬＡＫ细胞治疗慢性肝炎能使部分患者ＨＢｅＡｇ及ＨＢＶＤＮＡ阴转．治疗结束时ＨＢｅＡｇ阴转率Ａ组为４７５％，Ｂ组为５８０％；而对照组Ｃ为１５０％（Ｐ＜００５）．ＨＢＶＤＮＡ阴转率Ａ组为４５０％，Ｂ组为６６０％，而对照组Ｃ为１１８％，（Ｐ＜００５％）．结论ＬＡＫ细胞治疗对ＨＢＶ复制有明显抑制作用．异体ＬＡＫ组的ＨＢｅＡｇ及ＨＢＶＤＮＡ阴转率高于自体ＬＡＫ组．     

Risk of hepatitis B exacerbation is low after transcatheter arterial chemoembolization therapy for patients with HBV-related hepatocellular carcinoma: report of a prospective study

OBJECTIVES: Systemic chemotherapy may lead to immune suppression and possible reactivation of hepatitis B virus (HBV), suggesting prophylactic antiviral therapy in cancer patients with HBV. Transcatheter arterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) is not a systemic chemotherapy, but has been partially associated with HBV reactivation. The aim of this study was to evaluate whether TACE aggravates HBV hepatitis in patients with HBV-related HCC. METHODS: Eighty-nine patients with HBV-related HCC were studied prospectively. Patients treated with TACE were enrolled in the case group (n = 69), and patients in follow-up or awaiting treatment were enrolled in the control group (n = 20). TACE was performed with doxorubicin (20-60 mg) and lipiodol (2-20 mL). RESULTS: Three (4.3%) patients in the TACE group and 2 (10%) patients in the control group showed HBV reactivation (p= 0.334). A twofold or more increase in serum HBV DNA was detected in 21 (30.4%) patients in the TACE group and 4 (20%) patients in the control group (p= 0.361). Exacerbation of viral hepatitis B was found in 4 (5.8%) patients in the TACE group and no patients in the control group, but the difference between the two rates was not statistically significant (p= 0.271). Three of the four reactivated patients showed spontaneous recovery within 1 month, and one showed tumor-progression-related exacerbation. CONCLUSIONS: One session of TACE using doxorubicin and lipiodol does not significantly aggravate HBV hepatitis in patients with HBV-related HCC.     

人类免疫缺陷病毒感染者合并隐匿性乙型肝炎病毒感染的现状调查

目的 调查分析上海地区HIV感染者中隐匿性HBV感染的流行现状.方法 对上海市公共卫生临床中心就诊的HIV感染者在尚未接受抗病毒治疗前采集血标本,检测HBsAg、抗-HBs、HBeAg、抗-HBe、抗-HBc,抗-HCV,CD4+T细胞计数,使用巢式PCR法检测HBV S区.结果 105例(男92例,女13例)HBsAg阴性的HIV感染者中32例(男27例,女5例)HBV DNA阳性;16～30岁年龄组22例,其中5例HBV DNA阳性,31～49岁年龄组44例,其中15例HBV DNA阳性,50～75岁年龄组39例,其中12例HBV DNA阳性;32例中有27例至少一项HBV血清学标志物阳性,5例均阴性.47例合并HCV感染者中有14例HBV DNA阳性,阳性率29.8%;58例未合并HCV感染的HIV感染者中18例HBV DNA阳性,阳性率为31.0%.CD4+T细胞计数平均值145.1个/μ(4～623个/μ1),75例CD4+T细胞<200个/μ1的患者中有26例HBV DNA阳性,约占34.7%,30例CD4+T细胞>200/μ1患者中有6例HBV DNA阳性,阳性率为20.0%.以上各项之间两两相比差异均无统计学意义.结论 HIV感染者中存在隐匿性HBV感染,且与HIV感染者性别、年龄、HBV标志物、是否合并HCV感染及CD4+T细胞计数无明显相关.     

乙型肝炎病毒基因型、BCP及PC区变异与拉米夫定治疗后HBV DNA反弹的关系

目的:探讨HBV基因型、C区基本核心启动子(BcP)及前C(PC)区变异与拉米夫定抗病毒治疗后HBV DNA反弹的关系.方法:应用多引物对巢式PCR法,PCR-序列分析法,检测拉米夫定治疗27例乙型肝炎患者(治疗组),以及19例从未用过抗病毒治疗患者(对照组)的HBV基因型PC区,BCP的突变位点.结果:27例HBV DNA反弹的患者9例检出G1896A变异率高于对照组(33.33% vs 5.26%,P<0.05),4例检出C1856T变异(14.81%).治疗组4份治疗前标本未检出G1896A、C1856T和BCP变异.与对照组比较,治疗组PC(G1896A)及BCP(A1762T G1764A)双变异的患者中B基因型的构成比增高,分别为75%和50%,C基因型的构成比下降,分别为25%和50%.其中在BCP(A1762T G1764A)变异患者中B、C基因型构成比与对照组比较有显著性差异(P<0.05).4例HBV DNA反弹患者治疗前未检出有基因变异,治疗后有2例检出变异,BCP变异1例,BCP PC变异1例.27例HBV DNA反弹患者BCP变异4例,PC变异2例,BCP PC变异8例.结论:BCP(T1762/A1764)变异、PC区(G1896A)变异可能与拉米夫定治疗后HBV DNA反弹有关.病毒变异导致的HBV DNA反弹可以是单基因变异引起,也可以是多个基因联合变异引起,拉米夫定治疗后B基因型患者更易发生A1762T G1764A变异.     

人乙型肝炎病毒感染与原发性肝癌──—在树忽的实验研究

用人乙肝病毒（ＨＢＶ）接种树的，建立ＨＢＶ感染动物模型，实现连续传代感染，并用乙肝疫苗预防其感染。以此模型研究ＨＢＶ及（或）黄曲霉毒素Ｂ１（ＡＦＢ１）在诱发肝癌中的作用。结果肝癌诱发率在同时接受两种因子者显著高于单一因子者，癌前病变的发生与肝癌诱发率相关，被感染树的肝组织及（或）肝癌中检出ＨＢＶＤＮＡ可整合于宿主肝ＤＮＡ。提示ＨＢＶ和ＡＦＢ１起协同致癌作用并支持ＨＢＶ与肝癌的病因学关系。     

The effects of nucleoside analogue prophylactic treatment on HBV activation in HBcAb+ patients undergoing immunosuppressive therapy

We investigated the effects of prophylactic nucleoside analogue treatment on HBV activation in patients with antibodies against core antigen (HBcAb+) patients undergoing immunosuppressive therapy. Patients (113), who were HBcAb+, with various autoimmune diseases, undergoing immunosuppressive therapy, were divided into two groups. The control group, not treated with antivirals, and the prophylactic group, treated with antiviral drugs. The two groups were evaluated for changes in serum biochemical marker (alanine aminotransferase ALT), virological marker (HBV DNA) and for seroconversion. In the control group, the number of patients with an increase in ALT in patients with isolated HBcAb and HBcAb and antibodies against HBsAg (HBsAb +) were five (20.0%) and one (2.8%), respectively (P < 0.05). There were six cases (24.0%) with an increase in HBV DNA in the isolated HBcAb+ subgroup and one case (2.8%) in HBsAb+/HBcAb+ subgroup (P < 0.05). In the HBcAb+ only population, six patients (24.0%) in the control group had an increase in HBV DNA compared with none in the antiviral prophylactic group (P < 0.05). One patient (4.0%) with HBcAb+ in the control group underwent an HBsAg seroconversion when receiving immunosuppressive therapy for 18 months, while none in the antiviral prophylactic group underwent reversion to HBsAg positivity (P = 0.4949). Under immunosuppressive condition, the risk of HBV activation was much higher in patients with HBcAb than in patients with both HBcAb and antibodies to HBsAb group. Antiviral prophylactic therapy could significantly reduce the risk of HBV reactivation.     

Chronic hepatitis B serum promotes apoptotic damage in human renal tubular cells

AIM: To investigate the effect of the serum of patients with chronic hepatitis B (CHB) on apoptosis of renal tubular epithelial cells in vitro and to study the role of hepatitis B virus (HBV) and transforming growth factor-β1 (TGF-β1) in the pathogenesis of hepatitis B virus associated glomerulonephritis (HBV-GN). METHODS: The levels of serum TGF-β1 were measured by specific enzyme linked immunosorbent assay (ELISA) and HBV DNA was tested by polymerase chain reaction (PCR) in 44 patients with CHB ,and 20 healthy persons as the control. The normal human kidney proximal tubular cell (HK-2) was cultured together with the sera of healthy persons, CHB patients with HBV-DNA nega-tive(20 cases) and HBV-DNA positive (24 cases) for up to 72 h. Apoptosis and Fas expression of the HK-2 were detected by flow cytometer. RESULTS: The apoptosis rate and Fas expression of HK-2 cells were significantly higher in HBV DNA positive serum group 19.01±5.85% and 17.58±8.35%, HBV DNA negative serum group 8.12±2.80% and 6.96±2.76% than those in control group 4.25±0.65% and 2.33±1.09%, respectively (P < 0.01). The apoptosis rate and Fas expression of HK-2 in HBV DNA positive serum group was significantly higher than those in HBV DNA negative serum (P < 0.01). Apoptosis rate of HK-2 cells in HBV DNA positive serum group was positively correlated with the level of HBV-DNA (r = 0.657). The level of serum TGF-β1 in CHB group was 163.05±91.35μg/L, significantly higher as compared with 81.40±40.75μg/L in the control group (P < 0.01). CONCLUSION: The serum of patients with chronic hepatitis B promotes apoptotic damage in human renal tubular cells by triggering a pathway of Fas up-regula-tion. HBV and TGF-β1 may play important roles in the mechanism of hepatitis B virus associated glomerulone-phritis.