小鼠感染日本血吸虫肝脏损害的动态观察

目的动态观察和探讨小鼠感染日本血吸虫肝脏虫卵肉芽肿病变及纤维化与血清学改变的相关性。方法小鼠经腹部皮肤感染日本血吸虫尾蚴,定期剖杀小鼠,观察肝脏大体变化并测定肝脏系数;HE染色及Masson胶原纤维染色观察肝虫卵肉芽肿面积及纤维化程度;ELISA检测血清谷草转氨酶(AST),谷丙转氨酶(ALT)含量。放免法检测血清透明质酸(HA),层粘连蛋白(LN),Ⅳ型胶原(Ⅳ-C)含量。结果肉眼观察感染后24d肝脏表面开始出现出血点,29d开始出现粟白色肉芽肿;HE染色发现感染后21d肝脏可见灶性炎症,28d始见虫卵,但无肉芽肿反应,29d可见肉芽肿反应并于42d达到高峰;血清ALT/AST在28d明显升高,39d达到高峰,42d开始下降,70d接近正常水平;统计学分析血清转氨酶水平与肉芽肿面积具有相关性。Masson染色表明肝脏纤维化42d开始出现,以后逐渐加重;血清HA、LN随着纤维化的出现而升高,Ⅳ-C水平无明显改变,但统计分析胶原染色面积与血清纤维化指标无相关性。结论肝脏虫卵肉芽肿和纤维化均是导致小鼠血吸虫病肝脏损害的主要原因,血清转氨酶变化与肝脏的肉芽肿病变动态相一致,并呈显著正相关;血清纤维化指标与肝脏早期纤维化病变无相关性。     

慢性病毒性肝炎血瘀证患者肝功能及肝纤维化血清学指标的临床研究

目的:探讨慢性病毒性肝炎血瘀证患者的血清肝功能及肝纤维化指标变化.方法:根据临床症状将患者分为血瘀证组和非血瘀证组,观察两组患者的血清丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、白蛋白(Alb)、球蛋白(Glb)、A/G、肝纤4项(HA、LN、ⅣC、PCⅢ)水平,并进行对照.结果:血瘀证患者的HA、LN、Ⅳ-C值的平均秩(MEAN RANK)分别为31.52、31.96、32.06,高于非血瘀证组,P＜0.05.而ALT、Alb、Glb、A/G及PCⅢ经检验P＞0.05,提示血瘀证组与非血瘀证组差异无显著性意义.结论:病毒性肝炎血瘀证患者肝组织内存在活动性肝纤维化,提示肝病的慢性化趋势.     

白花丹水煎液对四氯化碳诱导肝纤维化大鼠的干预作用

目的:观察白花丹水煎液对四氯化碳(carbon tetrachloride,CCl4)诱导肝纤维化大鼠的干预作用.方法:采用CCl4花生油溶液皮下注射诱导SD大鼠肝纤维化造模,随机分成6组,分别为空白对照组,模型对照组,秋水仙碱阳性对照组(0.25 mg/kg),白花丹水煎液高、中、低剂量组(8、4、2 g/kg).用紫外-乳酸脱氢酶法及紫外-苹果酸脱氢酶法分别测定血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,A S T)的含量,用钒酸盐氧化法测定血清总胆红素(total bilirubin,TBIL)、直接胆红素(direct bilirubin,DBIL)、间接胆红素(indirect bilirubin,IBIL)的含量;用放射免疫法观察血清透明质酸(hyaluronic acid,HA)、层黏蛋白(laminin,LN)、Ⅲ型前胶原(procollagen typeⅢ,P3NP)、Ⅳ型胶原(typeⅣcollagen,CⅣ)的含量.H E染色法检测肝组织纤维化程度.用免疫组织化学法染色观察肝组织Ⅰ型和Ⅲ型胶原蛋白、α-肌动蛋白(α-smooth muscle actin,α-SMA)的表达.结果:与模型组比较,白花丹水煎液能显著降低血清ALT、AST、TBIL、DBIL及IBIL含量,同时也能显著降低血清HA、P3NP、L N、CⅣ的含量;H E染色病理结果显示白花丹水煎液能显著减轻大鼠肝纤维化程度;免疫组织化学结果显示白花丹水煎液能明显降低大鼠肝脏内Ⅰ型、Ⅲ型胶原蛋白和α-SMA的含量.结论:白花丹水煎液具有很好的抗肝纤维化作用,其机制可能与改善肝功能,抑制肝细胞变性坏死、促进肝细胞再生以及抑制胶原合成与沉积,减少细胞外基质(extracellular matrix,ECM)的沉积和促进ECM的降解有关.     

抗纤软肝冲剂预防大鼠肝纤维化的实验研究

目的:观察抗纤软肝冲剂对肝纤维化的预防作用并探讨其机理。方法:采用四氯化碳、高脂、高胆固醇、低蛋白等复合因素制造肝纤维化模型,同时用抗纤软肝冲剂治疗,观察其对肝纤维化指标的影响,以秋水仙碱作为对照,结果:抗纤软肝冲剂对肝纤维化大鼠有升高白蛋白(Alb),降低谷丙转氨酶(ALT)和球蛋白(G)的作用;可调整机体免疫功能,降低血清免疫复合物(IC);具有显著降低血清透明质酸(HA)、层粘蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)、肝脏羟脯氨酸(Hyp)的作用;可以改善肝脏病理,抑制纤维化形成。结论:抗纤软肝冲剂具有确切的预防肝纤维化的作用。     

慢性乙型肝炎患者血清透明质酸、层粘蛋白和Ⅳ型胶原水平与肝脏病理对照研究

目的 了解血清透明质酸(HA)、层粘蛋白(LN)和Ⅳ型胶原(CⅣ)与肝脏炎症活动度及纤维化程度的关系。方法 对比分折慢性乙型肝炎患者血清HA、LN、CⅣ水平与肝脏病理诊断。结果血清HA、IN、CⅣ由G0—G4、S0—S4依次升高，但在各级及各期间升幅不全一致，以HA上升最早，级间升幅较大，LN在S2期后开始大幅升高，而CⅣ于S2期前即有大幅升高；血清HA、LN、CⅣ水平与肝病分级及分期均呈正相关。结论 HA对慢性肝炎病情严重程度判断价值较大，HA和CⅣ似有诊断早期肝纤维化的价值，LN可协助诊断中晚期肝纤维化。肝脏炎症活动度与纤维化程度有重叠现象，单一血清指标的特异性较差。     

透明质酸、层粘连蛋白、Ⅲ型前胶原和Ⅳ型胶原血清学指标对肝硬化诊断的价值

目的:评价血清纤维化指标对于诊断肝硬化的应用价值。方法:52例经肝穿刺确诊为慢性乙型肝炎及肝硬化患者,应用放射免疫法检测血清HA(透明质酸)、LN(层粘连蛋白)、PCⅢ(Ⅲ型前胶原)、CⅣ(Ⅳ型胶原)水平。结果:肝脏病理炎症及纤维化分级与血清HA、LN、PCⅢ、CⅣ水平有显著相关性,组间对比部分有统计学意义,炎症分级组较为明显。结论:检测血清HA、LN、PCⅢ、CⅣ水平对于判断肝脏炎症及纤维化程度有一定价值和意义。     

一氧化氮及一氧化氮合酶抑制剂对小鼠血吸虫病肝纤维化程度的影响

目的研究一氧化氮(NO)对小鼠日本血吸虫病肝纤维化程度的影响。方法昆明小鼠经腹部皮肤感染日本血吸虫,于感染后第4周末治疗组和抑制剂组分别给予NO前体-L-精氨酸(L-Arg)及一氧化氮合酶(NOS)抑制剂-NG-左旋-硝基精氨酸甲基乙酯(L-NAME),于第10周末处死小鼠,取血,分离血清,剖取肝脏。应用病理组织学方法及生物化学方法,观察各组小鼠血吸虫病肝纤维化程度,同时测定血清NO、层粘连蛋白(LN)、透明质酸(HA)、谷-草转氨酶(AST)及谷-丙转氨酶(ALT)活性和肝组织羟脯氨酸(Hyp)含量。结果小鼠感染血吸虫后,感染组肝脏有明显的纤维化,血清中HA、LN、AST、ALT等指标显著升高,肝组织内Hyp含量也明显增加。与感染组相比:L-Arg高、中剂量组肝纤维化程度评分降低显著,低剂量组虽有减轻但无统计学意义,同时,L-Arg高、中剂量组血清LN、HA、AST、ALT的水平和肝组织Hyp的含量有所降低;低剂量组HA、LN、AST、ALT的水平虽然降低,但无统计学意义,Hyp水平降低明显;抑制剂组血清LN、HA、AST、ALT含量和肝组织Hyp的水平均明显升高。血清NO的水平随着精氨酸剂量的增加而显著增加,而精氨酸抑制剂组NO的水平降低明显。结论NO能明显降低血吸虫病肝纤维化的程度和减轻肝纤维化所造成的损伤作用。     

B型超声"明亮肝”100例实验室肝功能检验分析

目的论证B型超声"明亮肝”并非是弥漫型脂肪肝的特异性声象图.方法使用日本产EUB-420型超声仪,探头3.5MHz经腹壁扫查肝脏,声象图显示"明亮肝”诊断脂肪肝.对其100例患者,进行了实验室肝功能检验.结果肝功能正常47例,异常53例.其中谷丙转氨酶增高7例,谷草转氨酶增高4例,两项转氨酶增高9例,碱性磷酸酶增高2例,两项转氯酶并碱性磷酸酶增高2例;总胆红素增高11例,总胆红素合并谷丙转氨酶增高5例,合并草转氨酶增高2例,合并两项转氨酶增高8例,合并碱性磷酸酶增高3例.结论肝细胞膜结构及细胞内质网损伤导致了肝脏功能异常.肝细胞膜完整性被破坏,细胞内容物外溢,血中肝细胞酶增高.肝细胞膜受损影响载体蛋白摄取胆红素,运往胞质内质网的胆红素减少及内质网受损胆红素外出,均可使血中总胆红素增高.     

扩张型心肌病心肌纤维化血清指标观察

目的 :观察原发性扩张型心肌病 (DCM )患者心肌纤维化血清学指标变化及血浆血管紧张素Ⅱ (AngⅡ )和醛固酮 (ALD)浓度 ,探讨心肌纤维化机制。方法 :采用放射免疫方法测定 35例原发性DCM和 2 4例正常对照者血清中Ⅲ型前胶原 (PCⅢ )、层粘连蛋白 (LN)、透明质酸 (HA)及血浆AngⅡ和ALD含量 ,将AngⅡ、ALD分别与PCⅢ、LN、HA进行相关分析。 结果 :原发性DCM血清PCⅢ、LN、HA及血浆AngⅡ、ALD浓度明显增高 ,AngⅡ、ALD分别与PCⅢ、LN、HA密切相关。结论 :原发性DCM存在不同程度心肌纤维化 ,血清中PCⅢ、LN、HA含量可间接反应心肌纤维化程度 ,AngⅡ、ALD在心肌纤维化过程中起着重要作用。     

乙型肝炎核心抗原阳性患者的血清ALT和AST异常分析

乙型肝炎核心抗原(HBcAg)是Dane氏颗粒的核心部分,由于乙型肝炎病毒在肝细胞内的直接复制,可导致谷丙转氨酶(ALT)和谷草转氨酶(AST)的增高。我们对346例血清HBcAg阳性患者同时检测了ALT和AST,其结果报告如下。     

温阳活血退黄方对阴黄证大鼠肝细胞凋亡及bcl-2和bax蛋白表达的影响

目的：观察温阳活血退黄方对阴黄证大鼠肝细胞凋亡，相关调控基因bcl—2、bax蛋白表达的影响。方法：72只大鼠随机分为6组：正常对照组，阴黄证模型组，阳黄对照组，阴黄证模型加温阳活血退黄方高、低剂量组，菌陈术附汤组。采用TUNEL和免疫组化法检测大鼠肝细胞凋亡和bcl—2、bax蛋白表达。结果：阴黄模型组大鼠肝细胞凋亡程度明显高于阳黄模型组及正常对照组(P＜0．01)，温阳活血退黄方高剂量组肝细胞凋亡程度明显低于阴黄模型组(P＜0．05)。温阳活血退黄方高、低剂量组肝组织bcl—2蛋白表达明显高于阴黄模型组(P＜0．0l，＜0．05)，且其bax蛋白表达明显低于阴黄模型组(P＜0．01，＜0．05)，体现较好量效关系。结论：温阳活血退黄方可能通过促进bcl—2蛋白表达抑制bax蛋白表达阻断阴黄证大鼠肝细胞凋亡，可能是其治疗阴黄证的机制之一。     

Serum Vpr regulates productive infection and latency of human immunodeficiency virus type 1.

In human immunodeficiency virus (HIV)-positive individuals, the vast majority of infected peripheral blood cells and lymph node cells may be latently or nonproductively infected. The vpr open reading frame of HIV-1 encodes a 15-kDa virion-associated protein, Vpr. The vpr gene has been shown to increase virus replication in T cells and monocyte/macrophages in vitro. We have previously reported that vpr expression in various tumor lines leads to growth inhibition and differentiation, indicating that Vpr may function as a regulator of cellular permissiveness to HIV replication. Here we show that Vpr protein is present in significant amounts in the serum of AIDS patients. Purified serum Vpr activated virus expression from five latently infected cell lines, U1, OM.10.1, ACH-2, J1.1, and LL58. Serum Vpr also activated virus expression from resting peripheral blood mononuclear cells of HIV-infected individuals. Together, these findings implicate serum Vpr in the activation of HIV replication in vivo and in the control of latency. Anti-Vpr antibodies inhibited Vpr activity, suggesting that humoral immunity modulates Vpr activity in vivo. These results have broad implications for the virus life cycle and for the prospective control of HIV replication and pathogenesis.     

肝癌和癌旁组织中乙型肝炎表面抗原及丙型肝炎抗原表达与肝纤维化标志物的相关性

目的研究肝癌组织、癌旁组织中乙型肝炎表面抗原(HBsAg)、丙型肝炎抗原表达与血清肝纤维化标志物的相关性。方法采用免疫组织化学法对肝癌组织及癌旁组织中的HBsAg、丙型肝炎抗原表达进行了标记和分析,同时检测其血清肝纤维化标志物水平,并研究它们的相关性。结果肝癌血清肝纤维化标志物水平在乙型、丙型肝炎病毒混合感染组中最高,单独乙型、丙型肝炎病毒感染组次之,无病毒感染组最低,肝癌组织、癌旁组织中HBsAg、丙型肝炎抗原表达与透明质酸、层黏连蛋白、Ⅳ型胶原蛋白呈正相关,相关系数分别为0.60、0.45、0.46,P值均<0.01。结论肝癌遵循慢性病毒性肝炎、肝硬化、肝癌的发展趋势,有病毒感染的肝癌组织,其血清肝纤维化水平明显高于无病毒感染者。一方面病毒的感染是肝癌发生的原因,另一方面长期的病毒血症会加重肝脏组织病变,所以病毒性肝炎的抗病毒干预治疗对肝癌的预后有着积极的意义。     

非酒精性脂肪性肝病患者甲状腺激素水平变化及其临床意义

目的探讨非酒精性脂肪性肝病（NAFLD）患者血清甲状腺激素水平变化及其临床意义。方法采用放射免疫法检测123例NAFLD患者及56例对照组的血清甲状腺激素（TT3、TT4、TSH）及透明质酸（HA）、层粘连蛋白（LN）、Ⅲ型前胶原氨基末端肽（PⅢNP）、Ⅳ型胶原（CⅣ）等反映肝纤维化的血清学指标。结果 非酒精性脂肪性肝炎（NASH）组血清TT3浓度低于对照组及非酒精性单纯性脂肪肝（NASFL）组（P〈0.05）;三组间血清TT4、TSH浓度比较无显著差异（P〉0.05）;NASFL组患者血清HA、PⅢNP浓度高于对照组（P〈0.05）,CⅣ、LN浓度与对照组比较无显著差异（P〉0.05）;NASH组血清HA、PⅢNP、CⅣ、LN浓度均高于对照组及NASFL组（P〈0.05）;中、重脂肪肝组TT3浓度低于对照组（P〈0.05）,HA、PⅢNP、CⅣ、LN浓度高于对照组（P〈0.05）;轻度脂肪肝组TT3、HA、PⅢNP、CⅣ、LN浓度与对照组比较无显著差异（P〉0.05）。NASFL患者血清TT3水平与HA、PⅢNP呈负相关（P〈0.05）;NASH组患者血清TT3水平与HA、PⅢNP、CⅣ、LN均呈负相关（P〈0.05）。结论 NAFLD患者存在血清TT3水平降低,且下降程度与临床分型、超声分度及肝纤维化严重程度一致,检测NAFLD患者血清TT3浓度变化对判断病情及预后有一定的临床意义。     

Yin Zhi Huang and other plant-derived preparations: where herbal and molecular medicine meet

A traditional herbal medicine enhances bilirubin clearance by activating the nuclear receptor CAR. Yin Zhi Huang, a decoction of Yin Chin (Artemisia capillaris) and three other herbs, is widely used in Asia to prevent and treat neonatal jaundice. We recently identified the constitutive androstane receptor (CAR, NR1I3) as a key regulator of bilirubin clearance in the liver. Here we show that treatment of WT and humanized CAR transgenic mice with Yin Zhi Huang for 3 days accelerates the clearance of intravenously infused bilirubin. This effect is absent in CAR knockout animals. Expression of bilirubin glucuronyl transferase and other components of the bilirubin metabolism pathway is induced by Yin Zhi Huang treatment of WT mice or mice expressing only human CAR, but not CAR knockout animals. 6,7-Dimethylesculetin, a compound present in Yin Chin, activates CAR in primary hepatocytes from both WT and humanized CAR mice and accelerates bilirubin clearance in vivo. We conclude that CAR mediates the effects of Yin Zhi Huang on bilirubin clearance and that 6,7-dimethylesculetin is an active component of this herbal medicine. CAR is a potential target for the development of new drugs to treat neonatal, genetic, or acquired forms of jaundice. [Abstract reproduced by permission of J Clin Invest 2004;113:137-143].     

Human parvovirus B19: relevance in internal medicine.

Infection by the human parvovirus B19 can lead to several clinical manifestations which are relevant in internal medicine. These include aplastic crisis in chronic haemolytic anaemias, exanthemathous disease and arthropathy, mainly in women, and chronic anaemia in the immunocompromised host. After initial replication, probably in the respiratory tract, the virus enters its target cells in the bone marrow, erythroid precursor cells, through its receptor, the blood group P antigen. Viral replication in these cells leads to an arrest in erythropoiesis, normally lasting approximately 1 week. In this stage, an aplastic crisis can be produced in all patients under 'erythropoietic stress'. The viraemia disappears as specific antibodies to the virus become detectable in serum, which may give rise to a rash or arthralgia, symptoms that are probably immune-mediated. In immunologically normal individuals the infection is cleared by the humoral immune system within several weeks, whereafter detectable specific IgG confers lifelong immunity to reinfection. In patients with absent or dysfunctional humoral immunity to this virus, however, persistent infection can occur, which results in chronic suppression of erythropoiesis with chronic anaemia. Passive immunization, by means of normal immunoglobulin preparations has been reported to be effective in treating this condition. Diagnosis of parvovirus infection is usually possible by the detection of specific antibodies of IgM class in cases of recent infection. In patients with aplastic crisis and patients with chronic anaemia diagnosis rests upon the detection of parvovirus B19 DNA in serum by polymerase chain reaction. Parvovirus B19 is a ubiquitous virus. By the age of 15, about 50% of individuals have serologic evidence of a past infection, which may present as the common childhood disease erythema infectiosum. At the age of 70, seroprevalence reaches 80 to 100%. A vaccine against this virus is currently being developed.     

Resistance to adefovir dipivoxil therapy associated with the selection of a novel mutation in the HBV polymerase

BACKGROUND & AIMS: Adefovir dipivoxil effectively inhibits both hepatitis B virus (HBV) replication and disease activity in patients with chronic hepatitis B. Resistance to treatment was not observed in 2 recent large placebo-controlled 48-week studies with this drug. The aim of this study was to characterize adefovir resistance in a patient who developed clinical and virologic evidence of breakthrough during a 96-week course of treatment. METHODS: HBV DNA was PCR amplified and sequenced. Phenotypic studies used patient-derived HBV as well as specific mutations created by site-directed mutagenesis of a HBV/baculovirus recombinant. RESULTS: Following the commencement of treatment with adefovir dipivoxil, the patient initially responded with a 2.4 log(10) decrease in serum HBV DNA and normalization of alanine aminotransaminase levels by week 16. During the second year of treatment, however, serum HBV DNA rose progressively, eventually returning to near-pretreatment levels. This increase in viral replication was associated with a marked increase in alanine aminotransferase and mild changes in bilirubin, albumin, and prothrombin time. Comparison of pretreatment and posttreatment HBV DNA by polymerase chain reaction sequencing identified a novel asparagine to threonine mutation at residue rt236 in domain D of the HBV polymerase. In vitro testing of a laboratory strain encoding the rtN236T mutation and testing of patient-derived virus confirmed that the rtN236T substitution caused a marked reduction in susceptibility to adefovir. CONCLUSIONS: The development of this novel mutation in the HBV polymerase confers resistance to adefovir dipivoxil. The patient responded to subsequent lamivudine therapy, achieving normalization of alanine aminotransferase and a significant decrease in serum HBV DNA.     

Serum endothelin-1 and hepatocyte growth factor levels in patients with obstructive jaundice.

BACKGROUND/AIMS: Endothelin-1, a potent vasoconstrictive peptide, is known to modulate changes in local circulation. Additionally, hepatocyte growth factor, a potent mitogen for hepatocytes, is increased in various liver diseases. The present study examined changes in serum endothelin-1 and hepatocyte growth factor levels in patients with obstructive jaundice before and after percutaneous transhepatic cholangio drainage. METHODOLOGY: Endothelin-1 and hepatocyte growth factor levels were measured by enzyme-linked immunosorbent assay using sera from 16 patients with obstructive jaundice before and after percutaneous transhepatic cholangio drainage. RESULTS: Serum endothelin-1 levels decreased rapidly in the good bilirubin decrease group after biliary drainage. Endothelin-1 levels decreased 1 week after drainage but then increased gradually in the worse bilirubin decrease group. Serum hepatocyte growth factor levels decreased gradually after biliary drainage, and were higher in the worse bilirubin decrease group than in the good bilirubin decrease group throughout the study. CONCLUSIONS: These results suggest that endothelin-1 may be associated with the microcirculatory disturbance in obstructive jaundice and prolonged cholestasis. Measurement of hepatocyte growth factor levels in patients with obstructive jaundice before percutaneous transhepatic cholangio drainage may be an early clinical predictor of the subsequent rate of decrease of the serum bilirubin concentration.     

Clinical observation of salvianolic acid B in treatment of liver fibrosis in chronic hepatitis B

AIM：To evaluate the clinical efficacy of salvianolic acid B(SA-B)on liver fibrosis in chronic hepatitsB.METHODS:Sixty patients with definite diagnosis of liver fibrosis with hepatits Bwere included in the trial.Interferon-γ（IFN-γ）was used as control drug.The patients took orally SA-Btablets or received muscular injection of INF-γin the double blind randomized test.The complets course lasted 6months.The histological changes of liver biopsy specimen before and after the treatment were the main evidence in evaluation.in combination with the results of contents of serumHA,LN,IV-C,P-Ⅲ-P,liver ultrasound imaping,and symptoms and signs.RESULTS:Reverse rate of fibrotic stage was 36.67%in SA-Bgroup and30.0%in IFN-γgroup.Inflammatory alleviating rate was 40.0%in SA-Bgroup and 36.67%inIFN-γgroup.The average content of HAandIV-C was significantly lower than that before treatment.The abnormal rate also decreased remarkably.Overall analysis of 4serological fibrotic markers showed significant improvement in SA-Bgroup as compared with the IFN-γgroup.Score of liver ultrasound imagin g was lower in SA-Bgroup than in IFN-γgroup(HA36.7%vs80%,IV-C3.3%vs23.2%).Before the treatment,ALTASTactivity and total bilirubin content of patients who had regression of fibrosis after oral administration of SA-B,were significantly lower than those of patients who had aggravation of fibrosis after oral administration of SA-B,IFN-γshowed certain side effects(fever and transient decrease of leukocytes,occurrence rates were 50%and 3.23%),but SA-Bshowed no side effects.CONCLUSION:SA-Bcould effectively reverse liver fibrosis in chronic hepatitisB.SA-Bwas better than IFN-γin reduction of serumHAcontert,overall decrease of 4serum fibrotic markers,and decrease of ultrasound imaging score.Liver fibrosis in chronic hepatitis Bwith slight liver injury was more suitable to SA-Bin anti-fibrotic treatment,SA-Bshowed no ovbious side effects.     

Lamivudine treatment for reverse seroconversion of hepatitis B 4 years after allogeneic bone marrow transplantation

Reverse seroconversion of hepatitis B virus (HBV) after allogeneic BMT is rare. We present a case of HBV reactivation late after allogeneic BMT which responded well to lamivudine therapy. A 35-year-old woman with CML received an allogeneic BMT. Before BMT, the patient had immunity to HBV, with serum antibodies against hepatitis B surface antigen (HBsAb), and the donor was completely negative for HBV. Four years after BMT, acute hepatitis occurred with a detectable level of HBV-DNA. Lamivudine rapidly reduced transaminase and bilirubin levels, and serum HBV-DNA decreased to negative. Retrospective analysis revealed that there had been a gradual decrease in serum HBsAb titers after BMT. Administration of lamivudine immediately after HBV replication may be more effective than vaccination of hepatitis B surface antigen-negative donors before BMT.