Hemostatic abnormalities in cirrhosis and tumor-related portal vein thrombosis

In order to investigate the relationship between hemostatic abnormalities and portal vein thrombosis (PVT) in hepatocellular carcinoma (HCC), platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time, fibrinogen, d-dimer, fibrinogen degradation products (FDPs), protein C, protein S, antithrombin, plasminogen, antiplasmin, coagulation factors (CFs) V, VII, VIII, IX, XI, and XIII, von Willebrand factor (vWF), prothrombin fragment 1 + 2 (PF 1 + 2), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor 1 (PAI-1) were studied in patients with HCC, cholangiocarcinoma, and metastatic liver tumors and in cirrhosis patients with or without PVT. Platelet, antithrombin, protein C, plasminogen, and CFs V, VII, IX, XI, and XIII levels of HCC group were found lower and PT, aPTT, thrombin time, vWF, FDPs, PF 1 + 2, tPA, and PAI-1 levels were higher than the control group. Our findings suggested that the abnormalities of coagulation and fibrinolysis systems have some role in provoking thrombosis of portal veins in HCC, in addition to the invasion of portal veins by hepatoma cells.     

肝硬化并发门静脉血栓研究进展

肝硬化并发门静脉血栓（Portal vein thrombosis,PVT）将增加肝硬化并发症的发生率。由于PVT可与上消化道出血同时发生,增加了治疗的难度。PVT形成的主要原因是门静脉血流速度降低。目前,治疗PVT仍以药物为主,研究表明抗凝治疗并不增加消化道出血的风险,因此对于有适应症的患者,在食管胃静脉曲张经治疗消失后,应及时针对PVT进行治疗。部分脾动脉栓塞患者,在治疗后常规给予抗凝处理可减少门静脉血栓的发生。在治疗过程中,早期诊断、抗凝治疗的监测指标、肝素用量、预防复发方面仍有较多问题等待解决。     

肝硬化合并门静脉血栓的研究现状

肝硬化是门静脉血栓(PVT)患者常见病因之一,肝硬化合并PVT易出现顽固性腹水、上消化道出血、肠坏死等并发症。可导致严重的后果而危及患者生命。在对PVT的概述基础上,论述了肝硬化阶段PVT形成的原因、机制,PVT的诊断、治疗及目前仍然存在争议的问题。     

乙肝肝硬化患者门静脉宽度与门静脉血栓形成的关系

背景门静脉血栓(portal vein thrombosis,PVT)的早期诊断仍是临床上一个难题,急需要发现可早期预测诊断的无创指标.目的探讨门静脉宽度与PVT形成之间的关系.方法收集418例乙肝肝硬化患者.根据是否发生PVT分为PVT组(n=66)和非PVT组(n=352)组.比较两组患者的一般资料差异,使用多因素Logistic回顾分析影响PVT发生的危险因素.通过受试者工作特征(receiver operating characteristic,ROC)曲线评估不同危险因素预测PVT的效能.结果与非PVT组患者相比,PVT组患者的Child-Pugh评分更高、Child-Pugh A级比例更低、血小板水平更高、D-二聚体水平更高、门静脉宽度更宽、门静脉血流更慢,上述差异均存在统计学意义(P<0.05).Logistic回归显示门静脉宽度(OR=3.941,P=0.001)、门静脉血流(OR=0.841,P=0.007)、血小板水平(OR=1.024,P=0.008)和D-二聚体水平(OR=2.383,P=0.000)是肝硬化患者发生PVT的独立危险因素.门静脉宽度诊断PVT的ROC曲线下面积最大为0.874,最佳诊断值为>12.5 mm,此时的预测敏感性和特异性分别为78%和82%.结论门静脉直径增加是肝硬化患者PVT发生的危险因素,对PVT诊断具有一定价值.     

肝硬化合并门静脉血栓致门静脉高压症治疗现状

肝硬化合并门静脉血栓(PVT)并不少见,PVT会进一步加重门静脉高压症,此时针对PVT的治疗可改善肝硬化患者的预后。目前的治疗方式包括抗凝治疗及经颈静脉肝内门体支架分流术(TIPS)。本文就此类患者的治疗现状作一综述。     

肝硬化后门静脉血栓形成的临床特点研究

目的研究肝硬化(liver cirrhosis,LC)后门静脉血栓(portal vein thrombosis,PVT)形成的临床特点。方法对9678例LC患者进行回顾性分析,采用腹部B超/腹部增强CT及腹部增强MRI检查门脉主干或左右分支,筛选出LC伴PVT形成者(PVT组),同时将LC后无PVT患者纳为对照组,比较2组的Child-Pugh分级、门静脉及脾静脉宽度、脾脏面积及厚度、腹水、上消化道出血、肝性脑病和肝肾综合征等并发症。结果 LC患者中有396例(4.09%)PVT形成。PVT组中LC的病因主要有乙型肝炎、酒精性及丙型肝炎LC,PVT主要分布在门静脉主干、门静脉右支、肠系膜上静脉、门静脉左支和脾静脉。按Child-Pugh进行分级,PVT组与对照组比较,肝损伤较重(P<0.01)。PVT组合并腹水、上消化道出血、肝性脑病及肝肾综合征等并发症的发病率均较对照组高(P<0.01)。PVT组门静脉和脾静脉宽度分别为(1.50±0.23)cm和(1.25±0.34)cm,对照组为(1.38±0.23)cm和(1.06±0.29)cm。PVT组脾脏面积为(97.48±32.90)cm2,脾脏厚度为(6.09±1.21)cm;对照组分别为(81.19±29.10)cm2和(5.26±0.99)cm。PVT组门静脉及脾静脉宽度和脾脏厚度均大于对照组,差异有统计学意义(P<0.05)。PVT组有侧支循环开放的患者占96.21%,对照组为78.25%,2组比较差异有统计学意义(P<0.05)。结论 LC后PVT形成对LC患者的临床转归有重要影响。     

肝硬化患者门静脉血栓形成的相关危险因素

目的:研究肝硬化患者门静脉血栓(portal veinthrombosis,PVT)形成的相关危险因素.方法:2006-2007年我院确诊的肝炎和酒精性肝硬化患者90例,其中23例肝硬化PVT患者作为血栓组,67例肝硬化非血栓患者作为对照组.采用凝固法检测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)和纤维蛋白原(Fib),发色底物法检测抗凝血酶-Ⅲ(AT-Ⅲ),酶联免疫吸附双抗体夹心法检测蛋白-C(PC)、蛋白-S(PS)、D-二聚体(d-dimer)、组织纤溶酶原激活物剂(t-PA)和组织纤溶酶原激活物抑制剂-I(PAI-1).将门静脉血栓形成的相关因素纳入研究,进行统计学分析.结果:d-dimer升高是肝硬化PVT形成的危险因素(OR=13.236,95%CI:2.345-74.721),PC和AT-Ⅲ升高是肝硬化PVT形成的保护因素(OR=0.242,95%CI:0.08-0.727;OR=0.917,95%CI:0.841-0.999).研究未能提示性别、肝功能Child-Pugh分级和APTT等止凝血指标是PVT形成的危险因素.结论:d-dimer升高是肝硬化PVT形成的危险因素,PC和AT-Ⅲ升高是肝硬化PVT形成的保护因素.     

肝硬化门静脉血栓形成的临床分析

目的　探讨肝硬化 (LC)门静脉血栓 (PVT)形成对LC病程发展的影响。方法　检索我院自 1 995至 2 0 0 2年肝硬化PVT形成患者 ,血栓诊断依据彩色多普勒和 (或 )CT。 4 8例肝硬化PVT形成患者入选血栓组 ;同阶段LC门脉高压症的非血栓病例中选择 5 2例作为对照组。对两组患者的肝功能Child Pugh分级、凝血功能、门静脉、脾静脉宽度及脾脏面积、厚度进行比较。行t检验 ,χ2 检验 ,Logistic回归分析。结果　肝硬化PVT形成除继发于脾切除等手术后 ,75 .0 %隐匿发病 ,85 .4 %的血栓发生于门静脉主干 ,脾脏增大与门静脉增宽是PVT形成的危险因素 (P =0 .0 0 3、0 .0 1 0 )。血栓组门静脉及脾静脉宽度分别为 (1 .4 8± 0 .2 6 )cm ,(1 .2 3± 0 .38)cm ,与对照组比较差异有显著性 [(1 .37± 0 .2 2 )cm ,(1 .0 5± 0 .30 )cm ,P =0 .0 37,0 .0 31 ]。血栓组脾面积平均值为 (96 .6 4± 33.4 )cm2 ,脾厚径为 (6 .0 7± 1 .2 0 )cm ,分别大于对照组的 (80 .81± 2 8.9)cm2 ,(5 .2 3± 1 .0 8)cm(P =0 .0 36 ,0 .0 0 1 )。血栓组食管胃底静脉曲张程度重于非血栓组 ,大出血、大量腹水比例高 (P <0 .0 5 )。血栓形成后 1年内死亡率为1 6 .6 % ,较非血栓组增高 (P =0 .0 2 3)。两组肝功能Child Pugh分级、凝血功能、血小板计     

肝硬化患者门静脉系统血栓形成29例分析

目的提高对肝硬化患者门静脉系统血栓（PVT）形成的认识及诊治水平。方法收集我院2007年3月至2009年8月收治的肝硬化合并PVT患者29例进行回顾性分析。结果肝硬化合并PVT临床表现多样且缺乏特异性;D-二聚体及血小板水平的升高或相对升高是肝硬化患者发生PVT的独立危险因素;PVT诊断主要依赖影像学检查;在患者条件允许的前提下,及时、合理地选择各种方法进行抗凝、溶栓是治疗的关键。结论提高对肝硬化合并PVT的认识,及时诊断、合理选择治疗方案是决定本病预后的关键。     

Therapeutic and clinical aspects of portal vein thrombosis in patients with cirrhosis

Portal vein thrombosis(PVT) is a frequent complication in cirrhosis, particularly in advanced stages of the disease. As for general venous thromboembolism, risk factors for PVT are slow blood flow, vessel wall damage and hypercoagulability, all features of advanced cirrhosis. Actually, the old dogma of a hemorrhagic tendency in cirrhosis has been challenged by new laboratory tools and the clinical evidence that venous thrombosis also occurs in cirrhosis. The impaired hepatic synthesis of both pro- and anticoagulants leads to a rebalanced hemostasis, more liable to be tipped towards thrombosis or even bleeding. Conventional anticoagulant drugs(low molecular weight heparin or vitamin K antagonists) may be used in cirrhosis patients with PVT, particularly in those eligible for liver transplantation, to prevent thrombosis progression thus permitting/facilitating liver transplant. However, several doubts exist on the level of anticoagulation achieved as estimated by coagulation tests, on the efficacy of treatment monitoring and on the correct timing for discontinuation in non-transplant candidates, while in transplant candidates there is expert consensus on continuing anticoagulation until transplantation. The recent introduction of direct acting oral anticoagulant drugs(DOACs) in other clinical settings generates much interest on their possible application in patients with cirrhosis and PVT. However, DOACs were not evaluated yet in patients with liver disease and cannot be recommended for the present time.     

肝硬化并发门静脉血栓的研究进展

门静脉血栓在肝硬化中常见。肝硬化患者出现门静脉血栓,但并未引起临床医生重视,相关研究信息也较少。到目前为止,肝硬化基础上门静脉血栓的诊治仍未达成共识。近年来,随着临床诊疗技术的提高及对该疾病认识的深入,其对肝硬化患者的病程影响越来越被临床医生所重视。详细探讨了肝硬化患者门静脉血栓形成的发生发展机制、诊断、预防及相关治疗。     

肝硬化合并门静脉血栓的研究进展

门静脉血栓(PVT)是肝硬化常见并发症之一,回顾了近几年肝硬化合并PVT的研究进展,认为PVT是多种因素共同作用的结果,血流动力学紊乱是PVT发生的重要基础,PVT的分类可根据血栓栓塞程度及受累门静脉分支分为不同种类,药物抗凝和介入治疗是目前常用的治疗手段,而PVT的发生不会加重肝硬化患者病程的进展,但可能影响肝硬化患者行肝移植术的预后。     

肝硬化脾切除术后门静脉系统血栓形成的危险因素分析*

目的 分析影响肝硬化患者脾切除术后门静脉系统血栓形成（PVT）的危险因素。方法 2015年1月~2018年6月我院收治的肝硬化患者94例,接受脾切除联合食管下段周围曲张血管离断术,使用彩色多普勒超声检查门静脉系统。采用多因素Logistic回归分析影响术后PVT形成的危险因素。结果 术后1个月随访,经彩色多普勒超声检查,发现PVT形成30例,未发生PVT患者64例;PVT组有腹水者为56.7%,显著高于无PVT组的32.8%（P<0.05）,脾脏厚度为（75.8±9.4） mm,显著大于无PVT组【（69.1±8.8） mm,P<0.05】,脾脏体积为（141.7±18.1） mm2,显著大于无PVT组【（126.8±17.2） mm2,P<0.05】,门静脉内径为（16.2±2.1） mm,显著大于无PVT组【（14.1±1.9） mm,P<0.05】,门静脉血流流速为（12.2±1.5） cm/s,显著慢于无PVT组【（14.6±1.6） cm/s,P<0.05】;应用低分子右旋糖苷或低分子肝素抗凝干预患者所占比例显著低于无PVT组（P<0.05）;Logistic回归分析显示,未应用抗凝治疗（OR=0.503,P=0.023）、门静脉流速减慢（OR=0.491,P=0.014）、脾脏体积增加（OR=1.872,P=0.044）和门静脉内径增宽（OR=1.982,P=0.021）是肝硬化脾切除术患者术后PVT形成的独立危险因素。结论 肝硬化脾切除术患者术后可能存在PVT形成,了解一些危险因素并给予积极的干预可能减少PVT形成的发生,使患者获益。     

Antiphospholipid antibodies are related to portal vein thrombosis in patients with liver cirrhosis

The pathogenesis of portal vein thrombosis (PVT) in cirrhotic liver patients is not known. PVT has been related to liver dysfunction, neoplasm, hemodynamic factors, and hypercoagulability states. PVT has been reported in patients with antiphospholipid syndrome without liver cirrhosis. Our aim was to find the role of antiphospholipid antibodies (APAs) and coagulation inhibitors in PVT in patients with liver cirrhosis. We present a case-controlled study, matched by age, liver function, and etiology, to discover the role of APAs and anticoagulant protein activity in PVT in cirrhotic patients. We studied 30 cirrhotic patients: 6 of 10 (60%) patients with PVT were APA-positive, whereas only 2 of 20 (10%) in the cirrhotic control group were APA-positive (p < 0.005). Low serum levels of protein C, protein S antithrombin III, and plasminogen were found in cirrhotic patients; and, no differences were found between patients with and without PVT. Significantly lower protein S and antithrombin III levels were found in patients with Child-Pugh class C. Therefore, APAs were related to PVT in cirrhotic patients; but, a lower concentration of coagulation inhibitors was associated with liver dysfunction alone.