末治脾肾,能起沉疴--单纯中药治疗乙肝相关性肝癌1例

探讨中药审因论治对乙肝相关性肝癌的治疗作用。应用调补脾肾、搜邪泄浊法 ,对一例乙肝相关性肝癌患者进行单纯中药治疗。结果 :经过 12个月治疗 ,AFP由最高 10 0 0 0 μg/L降至正常 (<2 0 μg/L) ,AFP异质体同步转阴 ,B超、MRI显示肝部实质性肿块消散 ,肝功能好转。提示本治法对肝癌具有较好的治疗作用。     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.     

基于“伏邪”说的肝复安治疗慢性乙型病毒性肝炎患者铁代谢异常临床观察

目的观察基于"伏邪"说的肝复安治疗慢性乙型病毒性肝炎(简称慢乙肝)患者铁代谢异常的临床疗效。方法将102例铁代谢异常相关性肝病(慢乙肝及肝硬化)患者分为治疗组(48例)与对照组(54例)。治疗组予中药"肝复安"辨证治疗,对照组予西医常规药物(抗病毒、保肝药)治疗。两组疗程均为36个月,观察肝脏铁质沉积疗效,比较血清铁代谢指标、肝功能、病毒及相关免疫指标等的变化情况。结果 1组间肝脏铁沉积疗效比较,第24个月、第36个月差异均有统计学意义,治疗组优于对照组(P0.05)。2组间治疗后比较,血清铁(SI)、血清铁蛋白(SF)浓度及异常率差异有统计学意义,治疗组较对照组降低程度更显著、指标异常率更低(P0.05)。组间治疗后比较,转铁蛋白(TRF)浓度及异常率差异有统计学意义,治疗组较对照组升高程度更显著、指标异常率更低(P0.05)。3组间治疗后比较,治疗组丙氨酸氨基转移酶(ALT)水平较对照组降低更为明显,差异有统计学意义(P0.05);乙肝表面抗原(HBs Ag)浓度差异有统计学意义,治疗组较对照组降低程度更显著(P0.05);CD3~+水平及异常率差异有统计学意义,治疗组较对照组升高程度更显著、指标异常率更低(P0.05);CD4~+/CD8~+异常率差异有统计学意义(P0.05)。结论基于"伏邪"说的肝复安治疗慢乙肝患者铁代谢异常,能有效纠正铁代谢异常,恢复免疫功能,抑制病毒复制,减轻肝脏损伤。     

快速检测乙型肝炎病毒前核心区基因变异株方法的建立与初步应用

用聚合酶链反应（ＰＯＲ）选择性地扩增血清标本中乙型肝炎病毒（ＨＢＶ）基因前Ｃ区（Ｐｒｅ－Ｃ）后，以三种寡核苷酸探针Ｍ０（野毒株基因序列）、Ｍ１（ｎｔ．１８９８位点突变株基因序列）、Ｍ２（ｎｔ．１９９８位及ｎｔ．１９０１位上双点突变株基因序列）在极其严谨的条件下分别杂交，检测ＥＢＶＰｒｅ－Ｃ的最常见变异，结果本法具有根高的特异性。应用上述方法检测了３１份乙肝病人的血清标本，结果７份ＨＢｅＡｇ阳性标本中，有４份ＰＣＲ阳性，均与Ｍ０探针杂交，未出现变异；２４份抗－ＨＢｅ阳性标本中，有１０份ＰＣＲ阳性，其中８份表现为Ｍ０伴Ｍ１和（或）Ｍ２阳性，一份为野毒株，另一份与三种探针均不杂交。     

消化道印片细胞学镜下背景对诊断恶性肿瘤的临床意义

[目的]探讨消化道印片细胞学镜下背景对恶性肿瘤诊断的临床意义。[方法]电子胃镜检查并取黏膜组织印片，作细胞学检查。[结果]消化道恶性肿瘤黏膜组织印片镜下背景可见癌性坏死，与炎性疾病时背景不同。[结论]消化道印片细胞学检查背景的分析判断有助于提高消化道恶性肿瘤的检查准确率，可以作为细胞学检查判断的一个指标。     

肝癌中乙型肝炎病毒整合位点的分离鉴定

乙型肝炎病毒（HBV）慢性感染是导致肝癌发生的重要原因，HBV整合是致癌的可能机制之一。传统上，HBV整合位点的鉴定主要通过反复的筛选肝细胞癌（HCC）基因文库获得。现报道一种快速分离鉴定HBV整合位点的新方法，为探讨肝癌发生的分子机制提供新的研究手段。     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.     

乙肝患者血清抗－HBe效价与HBeAg阴性变异株出现频率关系的研究

利用多聚酶链反应（ＰＣＲ）结合寡核苷酸探针杂交的方法，对７７例抗－ＨＢｅ阳性的乙肝病人血清进行了乙肝病毒（ＨＢＶ）ＨＢｅＡｇ阴性变异的分析，同时研究了血清抗－ＨＢｅ滴度与ＨＢｅＡｇ阴性变异出现频率的关系。结果１４例单独野毒株感染的病人，抗－ＨＢｅ平均效价为４．７９±１４．４５；１９例野毒株与变异株混合感染的病人，抗－ＨＢｅ平均效价为１２８．８３±２３．４４；１８例单独变异株感染的病人，抗－ＨＢｅ平均效价为２８．１８±３７．１５；２６例无ＨＢＶ复制的病人，抗－ＨＢｅ平均效价为８１．２８±２２．９１。单独野毒株感染组抗－ＨＢｅ效价显著低于混合感染组（Ｐ＜０．０１）及无ＨＢＶ复制组（Ｐ＜０．０５）。结果提示：高效价的抗－ＨＢｅ可能是选择ＨＢｅＡｇ阴性变异株的重要条件。在抗－ＨＢｅ效价高而ＨＢＶＤＮＡ仍为阳性的病人中，可能存在ＨＢｅＡｇ阴性变异株感染。     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.