慢性病毒性肝炎相关血小板减少症研究进展

血小板减少为公认的与感染相关的疾病。许多研究表明血小板减少与慢性肝炎病毒感染相关。慢性病毒性肝炎相关血小板减少症具有多重发病机制。本文目的在于评估该病的流行病学特征、探究其发病机制、总结相关文献提出的治疗方法。     

慢性病毒性肝炎患者肝功能、脾脏指数与血小板数量的关系分析

为了探讨慢性病毒性肝炎患者肝功能与血小板数量的关系,从2000年1月起对我院住院患者进行前瞻性观察研究,以探讨慢性病毒性肝炎患者血小板减少的发病机制,为血小板减少症的治疗提供依据.     

病毒性肝炎血小板减少机制探讨

病毒性肝炎患者血小板减少十分常见，在各型慢性肝炎和肝硬化中发生率约为37％～77％，在重症肝炎和暴发性肝衰竭患者中也有约50％的患者发生。长期以来，人们始终很自然的认为脾大及脾功能亢进是肝病血小板减少的主要原因。近年来，随着有关血小板生成素及免疫研究的不断深入，对病毒性肝炎血小板减少的原因有了一些新的认识，其机制较为复杂，为多种因素综合作用的结果。为合理治疗病毒性肝炎血小板减少，本文就其发病机制做一些探讨。     

病毒性肝炎

RNA干扰在肝病研究中的进展(综述)——周伟等(重庆重庆医科大学附属第二医院消化内科400010)；《国外医学-消化系疾病分册》，2004，24(5)：296-298[RNA干扰是利用双链RNA(dsRNA)所诱导的生物体内同源rnRNA转录后的基因沉默，这种作用有高度特异性，但目前其作用机制尚不清楚。RNA干扰技术目前不断完善，并广泛应用于许多领域。     

肝素相关血小板减少症

本文综述了肝素相关血小板减少症的发病率、临床特征、诊断、发病机理以及处理原则。     

肝素引起的血小板减少症

肝素引起的血小板减少症 ( HIT)曾有多个名称 ,包括 型 HIT、HIT/血栓栓塞综合征( HITTS)、肝素相关的血小板减少 ( HAT)以及白色血栓综合征。对于非免疫机制的肝素相关性血小板减少则称为非免疫性肝素相关性血小板减少症。1　发病机制HIT由肝素依赖性抗体 (常为 Ig G1 ,或 Ig G、Ig M共有或 Ig M型 )通过其 Fcγ a受体激活血小板。血小板 Fc受体的单克隆抗体可抑制血小板的激活 ,这就使 HIT与其他 Ig G介导的、药物诱发的免疫性血小板减少性紫癜区分开来 (如奎宁、磺胺类抗生素 )。后者起因于 Ig G Fab和药物 /血小板膜糖…     

脾淤血所致的血小板减少症

各种原因所致的脾肿大均可引起血小板减少。     

肝素诱导的血小板减少症研究进展

肝素诱导的血小板减少症是一种特异性自身免疫性疾病,是由于抗体对肝素-血小板因子4复合物的识别,损伤了血小板以及内皮细胞而导致,以血小板减少及血栓形成为主要表现,通过4T评分以及实验室检查可有助于诊断,治疗上需要立即停用肝素及其相关制剂并开始替代抗凝治疗。     

Adefovir dipivoxil-associated thrombocytopenia in a patient with chronic hepatitis B

A 56-year-old male patient received adefovir dipivoxil (10 mg/day) for chronic hepatitis B resistant to lamivudine. On the fifth week of treatment, the platelet count dropped to 26 x 10(3) mm(-3); anti-platelet antibodies were detectable in serum. The drug was discontinued and the platelet count improved spontaneously. A re-challenge with adefovir caused a new episode of thrombocytopenia, again after a five-week treatment period. To date, thrombocytopenia has not been described after adefovir therapy for chronic hepatitis B and seems to be a rare event.     

重型病毒性肝炎并发低血糖临床分析

目的 探讨重型病毒性肝炎患者血糖低于正常值的临床特点及防治对策。方法 回顾性分析2002年6月至2004年4月住院重型病毒性肝炎患者空腹血糖,对其在治疗过程中的变化做动态分析。结果 92例重型病毒性肝炎患者,空腹血糖低于正常67例(72．8％),其中死亡56例(68．7％),与其他并发症并存的发生率较高。动态分析空腹血糖降低患者治疗过程中血糖变化有三种形式,空腹血糖持续多次减低患者死亡率亦较高。空腹血糖减低患者中,仅部分呈典型低血糖症表现,死亡率最高。结论 重型病毒性肝炎常并发空腹血糖减低者的死亡率高。在积极综合治疗后,持续多次空腹血糖减低患者死亡率较高。呈低血糖症患者死亡率最高。血糖减低的治疗需要采取综合措施,个体化原则。     

饮酒对病毒性肝炎病程及转归影响的临床调查

目的　探讨饮酒因素对病毒性肝炎病情、病程及转归的影响。方法　对 2 0 3 8例病毒性肝炎患者依饮酒程度分为三组 :不饮酒组、饮酒组和酗酒组。观察不同临床类型在各组中分布、病情演变及预后。结果　饮酒因素与感染肝炎病毒类型无关 ,但各组患者中急性肝炎、重型肝炎、慢性肝炎、肝硬变等发生率 ,病情及预后则有显著性差异 (P <0 0 5 )。结论　饮酒可加重病情 ,延长病程 ,加速不良预后。     

2014年慢性病毒性肝炎临床诊疗进展

<正>病毒性肝炎(Viral hepatitis)是一个严重的全球公共卫生问题,每年超过100万人死于病毒性肝炎[1]。根据病原学分型,目前已被公认的有甲、乙、丙、丁、戊五种肝炎病毒,其中乙型、丙型和丁型肝炎病毒感染可发展为慢性化,全球超过半数的肝硬化和肝细胞癌(Hepatocellular carcinoma,HCC)由乙型肝炎病毒(Hepatitis B virus,HBV)或丙型肝炎病毒(Hepatitis C     

Regulatory T cells in viral hepatitis

The pathogenesis and outcome of viral infections are significantly influenced by the host immune response. The immune system is able to eliminate many viruses in the acute phase of infection. However, some viruses, like hepatitis C virus (HCV) and hepatitis B virus (HBV), can evade the host immune responses and establish a persistent infection. HCV and HBV persistence is caused by various mechanisms, like subversion of innate immune responses by viral factors, the emergence of T cell escape mutations, or T cell dysfunction and suppression. Recently, it has become evident that regulatory T cells may contribute to the pathogenesis and outcome of viral infections by suppressing antiviral immune responses. Indeed, the control of HCV and HBV specific immune responses mediated by regulatory T cells may be one mechanism that favors viral persistence, but it may also prevent the host from overwhelming T cell activity and liver damage. This review will focus on the role of regulatory T cells in viral hepatitis.     

Fibrosis in chronic viral hepatitis

In the last years, several studies have been performed with the aim to evaluate the real impact of antiviral treatments on fibrosis progression in patients with chronic viral hepatitis. The main goal of therapy in patients with chronic hepatitis B is viral suppression. This outcome leads to an important improvement in both hepatic inflammation and fibrosis and reduces the HCC occurrence. An histological improvement has been largely demonstrated in patient treated with oral nucleoside and nucleotide analogs achieving the rate of 72% with entecavir and tenofovir. Similarly, in patients with chronic hepatitis C, sustained virologic response to interferon therapy is associated with regression of fibrosis and lower liver decompensation and HCC occurrence. In the next future further studies will assess the real impact of the new directly anti-viral agents on liver necroinflammation and fibrosis in chronic hepatitis C.     

门冬氨酸-鸟氨酸治疗黄疸型慢性病毒性肝炎的临床疗效观察

目的评价门冬氨酸-鸟氨酸治疗黄疸型慢性病毒性肝炎的临床疗效。方法将108例黄疸型慢性病毒性肝炎患者随机分为3组,分别接受4周的门冬氨酸-鸟氨酸、腺苷蛋氨酸和门冬氨酸钾镁等治疗,并检测患者治疗前后的血清总胆红素。结果门冬氨酸-鸟氨酸和腺苷蛋氨酸组在4周治疗结束时降低血清总胆红素的有效率分别为75.0%和72.2%,显著高于门冬氨酸钾镁组（30.6%）,P〈0.01;门冬氨酸-鸟氨酸与腺苷蛋氨酸组患者血清总胆红素每日降幅分别为4.3μmol/L±5.1μmol/L和4.3μmol/L±5.6μmol/L,显著高于门冬氨酸钾镁对照组（2.1μmol/L±8.3μmol/L）,P〈0.01。结论注射用门冬氨酸-鸟氨酸粉针剂能有效降低黄疸型慢性病毒性肝炎患者的血清总胆红素水平。     

小剂量多巴胺和肝素联合治疗急、慢性病毒性肝炎疗效观察

本文采用多巴胺２０ｍｇ和肝素５０ｍｇ加入１００％葡萄糖液２５０ｍｌ中缓慢静脉滴注，每日１次，疗程３￣４周，治疗急、慢性病毒性肝炎６１例。结果显示在缓解症状、降ＡＬＴ和ＳＢ，以及临床疗效方面优于对照组（Ｐ〈０．０５，Ｐ〈０．０１）。该治疗简便价廉，无明显不良反应。     

病毒性肝炎患者血中一氧化碳的测定及临床意义

目的了解不同程度病毒性肝炎患者静脉血中碳氧血红蛋白(COHb)的变化并分析其临床意义,探讨一氧化碳(CO)在肝脏疾病中的作用。方法采用双波长分光光度法测量不同程度病毒性肝炎患者血中COHb的浓度,并与正常对照组进行比较,对各组间COHb水平进行统计学分析。结果病毒性肝炎患者组血中COHb水平较正常对照组有显著性差异,病毒性肝炎重度组COHb水平与血中丙氨酸氨基转移酶(ALT)统计分析显示具有正相关性。结论不同程度病毒性肝炎患者血中COHb水平的改变提示CO在肝脏炎性疾病中发挥一定的作用。     

Overview of the microbiota in the gut-liver axis in viral B and C hepatitis

Viral B and C hepatitis are a major current health issue, both diseases having a chronic damaging effect on the liver and its functions. Chronic liver disease can lead to even more severe and life-threatening conditions, such as liver cirrhosis and hepatocellular carcinoma. Recent years have uncovered an important interplay between the liver and the gut microbiome: the gut-liver axis. Hepatitis B and C infections often cause alterations in the gut microbiota by lowering the levels of ‘protective’ gut microorganisms and, by doing so, hinder the microbiota ability to boost the immune response. Treatments aimed at restoring the gut microbiota balance may provide a valuable addition to current practice therapies and may help limit the chronic changes observed in the liver of hepatitis B and C patients. This review aims to summarize the current knowledge on the anato-functional axis between the gut and liver and to highlight the influence that hepatitis B and C viruses have on the microbiota balance, as well as the influence of treatments aimed at restoring the gut microbiota on infected livers and disease progression.