肝硬化并发食管胃底静脉曲张破裂出血与门静脉血栓形成的危险因素

目的:探讨肝硬化并发食管胃底静脉曲张破裂出血与门静脉血栓(portal vein thrombosis,PVT)形成的危险因素,并分析出血与血栓形成患者影响预后的相关因素,为临床治疗提供参考.方法:采用病例对照研究,严格按照病例和对照的纳入和排除标准.选取2010-01/2016-01在华北理工大学附属医院和唐山市传染病医院收住院的肝硬化并发食管胃底静脉曲张破裂出血与PVT的患者74例为病例组;选择同期住院的肝硬化并发食管胃底静脉曲张破裂出血的患者110例、肝硬化并发PVT的患者76例、单纯肝硬化患者(无出血和PVT形成)112例为对照组.对4组患者的临床资料和实验室检查结果进行比较,分析肝硬化并发食管胃底静脉曲张破裂出血与门静脉血栓形成的危险因素.结果:肝硬化并发食管胃底静脉曲张破裂出血与PVT形成的患者与对照组相比,在性别、年龄、肝硬化病因、白细胞、HB、食管胃底静脉曲张等方面,差异无统计学意义(P0.05);在门静脉内径、肝功能Child-Pugh分级、血小板计数及肝硬化并发症之间存在明显差异(P0.05).结论:门静脉内径、肝功能Child-Pugh分级、血小板计数及肝硬化并发症是影响肝硬化并发食管胃底静脉曲张破裂出血与PVT形成的危险因素.     

肝硬化患者门静脉血栓形成危险因素的Logistic回归分析

目的研究肝硬化患者门静脉血栓（PVT）形成的相关危险因素。方法回顾性分析我院消化内科2007—2008年确诊的肝硬化患者80例,其中19例肝硬化PVT患者作为血栓组,61例肝硬化非血栓患者作为对照组,收集相关临床资料,对可能影响PVT形成的因素进行单因素分析和Logistic回归模型分析。结果Logistic回归模型分析结果显示,血浆D-二聚体、门静脉宽度（MPV）、血小板（PLT）是肝硬化患者PVT形成的独立危险因素（P值分别为0.003、0.012、0.036）。结论肝硬化患者应注意监测血浆D-二聚体、门静脉宽度、血小板等指标,以便早期预防和发现PVT的形成。     

肝硬化并发门静脉血栓患者临床特征及其危险因素分析

目的 总结肝硬化并发门静脉血栓(PVT)患者的临床特征并分析PVT形成的危险因素。方法 回顾性分析2015年2月～2019年2月我院肝胆包虫科治疗的160例肝硬化患者,分析比较PVT组与未发生PVT组患者临床资料的差异,采用多因素分析发生PVT的危险因素。结果 80例PVT患者腹痛、腹水和消化道出血发生率、血小板(PLT)和白细胞(WBC)计数显著高于80例未发生PVT组(P<0.05);经多因素分析,发现PLT计数、糖尿病史和脾切除史为肝硬化并发门静脉血栓形成的独立危险因素(P<0.05)。结论 肝硬化并发PVT患者以HGB、PLT、WBC为主要实验室表现,以腹水、下消化道出血、肝功异常为主要临床症状。PLT、糖尿病史和脾切除史为肝硬化并发门静脉血栓的独立危险因素。     

基于倾向性评分匹配分析门静脉血栓对肝硬化患者预后的影响

目的分析门静脉血栓(PVT)对肝硬化患者短期预后的影响并探讨肝硬化患者预后的危险因素。方法回顾性分析西南医科大学附属医院2018年9月—2020年3月的肝硬化住院患者临床资料,其中合并PVT患者58例为PVT组,随机选取同期无PVT患者116例为非PVT组,通过1∶1倾向性评分匹配(PSM)均衡组间协变量获取PVT组及非PVT组各44例。满足正态性计量资料2组间比较采用t检验,非正态性计量资料2组间比较采用Mann-Whitney U秩和检验;计数资料2组间比较采用χ~2检验和Fisher确切概率法。利用Kaplan-Meier法及log-rank法分析PSM前后2组患者的生存情况及出血情况,并使用Cox风险模型分析PSM前后影响肝硬化患者预后的危险因素。结果 PSM前非PVT组患者总体生存率明显高于PVT组(P=0.008),而PSM后2组患者总体生存率无明显差异(P=0.076)。PSM前非PVT组上消化道出血或再出血率明显低于PVT组(P 0.001),PSM后结果与PSM前一致(P=0.028)。PSM前肝硬化患者预后多因素分析显示,PVT(HR=2.944, 95%CI:1.364～6.441,P=0.007)和MELD评分≥15(HR=3.531,95%CI:1.630～7.650,P=0.001)是肝硬化患者短期死亡的危险因素。PSM后肝硬化患者预后多因素分析显示,MELD评分≥15是肝硬化患者短期死亡的危险因素(HR=3.312, 95%CI:1.049～10.457,P=0.041)。结论肝硬化合并PVT增加上消化道出血或再出血风险,但其不是肝硬化患者短期死亡的独立危险因素,MELD评分≥15是肝硬化患者短期死亡的独立危险因素。     

门静脉血栓形成对肝硬化病程发展影响

目的探讨门静脉血栓（PVT）形成对肝硬化病程的影响。方法回顾我院2003年～2011年肝硬化伴PVT形成的患者资料。18例肝硬化伴PVT形成患者人选血栓组;随机选择同阶段肝硬化门静脉高压症的无门静脉血栓形成患者19例作为对照组,比较两组患者的门静脉宽度、脾脏厚度、食管胃底静脉曲张、腹水及上消化道大出血发生等情况。结果血栓组的门静脉宽度及脾脏厚度大于对照组,差异有统计学意义（P〈0．05）。血栓组食管胃底重度静脉曲张、上消化道大出血和大量腹水比例两组比较,差异有统计学意义（P〈0．05）。结论脾肿大和门静脉增宽是PVT形成的主要危险因素,PVT形成加重门静脉高压的程度,从而增加上消化道出血几率,使腹水难以消退,增加相关并发症发生率并使相关症状加重,预防门静脉血栓形成有助于延缓肝硬化病情发展。     

肝硬化门静脉血栓形成相关危险因素的研究进展

肝硬化是消化系统常见疾病,门静脉血栓(PVT)可增加肝硬化患者死亡率。研究发现,D-二聚体升高、脾脏厚度增加、高Child-Pugh评分是肝硬化PVT的独立危险因素。此外,门静脉直径增宽、门静脉血流速度减慢、P-选择素水平升高对肝硬化门静脉高压术后PVT的发生具有较高的预测价值。本文就肝硬化PVT形成相关危险因素的研究进展作一综述。     

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.     

肝硬化患者门静脉血栓形成的临床表现和危险因素

目的研究肝硬化患者门静脉血栓(PVT)形成的临床表现及危险因素。方法收集2008年4月-2015年4月宁夏医科大学总医院收治的肝硬化患者资料541例。其中76例肝硬化合并PVT的患者为研究组,同阶段通过匹配患者的性别、年龄及肝功能Child-Pugh分级,76例肝硬化不合并PVT为对照组。对比分析两组患者的临床资料及相关检查指标。计量资料组间比较采用t检验,计数资料组间比较采用χ2检验,并应用非条件Logistic回归模型筛选肝硬化PVT形成的独立危险因素。结果肝硬化PVT患者中,42.1%(32/76)隐匿起病,57.9%(44/76)有明显临床表现。大部分患者肝功能分级为Child-Pugh B和C级。血小板、血糖、中性粒细胞百分比、重度食管胃底静脉曲张、血浆D-二聚体、门静脉宽度、脾脏厚度在两组患者中差异有统计学意义(P值均0.05)。进一步非条件Logistic回归模型分析显示中性粒细胞百分比[比值比(OR)=1.044,P=0.040]、血浆D-二聚体(OR=0.091,P0.001)、门静脉宽度(OR=0.030,P=0.008)、脾脏厚度(OR=0.427,P=0.003)为PVT形成的危险因素。结论肝硬化PVT可隐匿起病,也可伴有不同的临床表现。肝硬化PVT常发生在晚期肝硬化患者中,血浆D-二聚体、门静脉宽度、脾脏厚度、中性粒细胞百分比为肝硬化PVT形成的独立危险因素。     

肝硬化合并门静脉血栓形成的危险因素分析

目的探讨肝硬化合并门静脉血栓(portal vein thrombosis,PVT)形成的危险因素。方法收集2014年8月至2016年8月郑州大学第一附属医院收治的肝硬化合并PVT患者57例的临床资料,设为PVT组,同时期肝硬化无PVT患者63例作为对照组,分析PVT形成的危险因素。对可能影响PVT形成的因素进行单因素和Logistic回归模型分析。结果单因素分析显示,糖尿病史、Child-Pugh分级、血红蛋白、血小板计数、D-二聚体、门静脉主干直径、脾脏厚度、门静脉血流速度在两组之间比较,差异有统计学意义(P0.05)。进一步进行非条件性Logistic回归分析显示,糖尿病史、Child-Pugh分级、D-二聚体、门静脉血流速度为PVT形成的独立危险因素。结论对于肝硬化患者应定期监测肝脏功能、门静脉血流速度和D-二聚体,尽早发现和治疗PVT,预防病情加重。     

从Virchow三要素分析肝硬化患者发生门静脉血栓危险因素

肝硬化患者门静脉血栓(PVT)的发生率明显高于健康人群。门静脉血栓形成会影响患者预后。Virchow三要素(血液高凝状态、血管内皮损伤、血流速度减慢)是经典的血栓形成理论。肝硬化患者脾功能亢进、肝功能下降导致与出凝血相关的血液成分发生变化,肝纤维化压迫肝内血管,硬化剂治疗、腹部手术、感染、内毒素血症等损伤血管内皮,压迫或药物原因导致门静脉血流受阻等均可以是门静脉血栓形成的危险因素。本文主要从Virchow三要素角度入手,描述与肝硬化患者PVT形成相关的危险因素,为制定准确预测PVT发生的方法,预防和治疗PVT提供理论依据。     

Obesity is an independent risk factor for pre-transplant portal vein thrombosis in liver recipients

ABSTRACT: BACKGROUND: Portal vein thrombosis is a frequent complication in end-stage cirrhosis with a considerable peri-operative risk for liver transplant candidates. We aimed to characterize the pre-transplant portal vein thrombosis in a cohort of liver transplant recipients, and to identify independent risk factors for this complication. METHODS: 380 consecutive primary orthotopic liver transplants were performed in the Digestive Surgery Department of "12 de Octubre" Hospital (Madrid, Spain), between January 2001 and December 2006. The main risk factors considered were smoking, obesity, metabolic disorders, previous immobility, surgery or trauma, nephrotic syndrome, associated tumor, inflammatory disease, neoplasm myeloprolipherative. Furthermore we have reported genetic thrombophilia results for 271 recipients. RESULTS: Sixty-two (16.3%) patients developed pre-transplant portal vein thrombosis and its presence had no impact in the overall survival of liver recipients. Obesity was the only independent risk factor for pre-transplant portal vein thrombosis. CONCLUSION: We recommend close control of cardiovascular factors in patients with liver cirrhosis in order to avoid associated thrombosis.     

肝硬化食管静脉曲张出血内镜治疗后早期再出血的危险因素分析

目的探讨内镜治疗肝硬化食管静脉曲张破裂出血(EVB)后早期再出血的危险因素。 方法回顾分析2016年8月至2018年8月因肝硬化食管静脉曲张(EV)首次出血就诊于包头医学院二附院并采用内镜下治疗的患者资料,依据术后6周内是否再出血分再出血组和未出血组,对两组患者的一般资料、肝功能、血常规、凝血、门静脉血栓、门静脉异常分流等情况进行单因素分析,探讨内镜治疗EV术后早期再出血的危险因素。 结果(1)入组患者共450例,治疗后6周内出血27例,止血成功率94%;(2)单因素分析AST、GGT、TBIL、ALB、PTA、TG、肝功能、Child-Pugh分级、EV程度、门静脉血栓、门静脉异常分流在出血和未出血组之间的差异具有统计学意义;(3)多因素Logistic回归分析结果显示AST等是影响EV术后再出血的危险因素;ALB、门静脉异常分流是影响EV术后再出血的保护因素(P<0.05)。 结论AST、GGT、PTA、TG、肝功能Child-Pugh分级、EV程度、门静脉血栓是影响EV术再出血的危险因素;ALB、门静脉异常分流是影响EV术后早期再出血的保护因素。     

ARFI评估肝硬化并发食管胃底静脉曲张患者出血和门静脉血栓的价值分析*

目的 探讨采用声脉冲辐射力弹性成像（ARFI）评估肝硬化并发食管胃底静脉曲张（EGV）患者出血或发生门静脉血栓的价值。方法 2015年4月~2017年6月我院收治的87例肝硬化并发EGV患者,采用AEFI测量肝实质剪切波速度（LSWV）和脾脏剪切波速度（SSWV）。采用二元Logistic回归分析影响患者发生门静脉血栓的危险因素。应用受试者工作特征曲线（ROC）下面积（AUC）分析LSWV和SSWV诊断患者出血或发生门静脉血栓的效能。结果 在随访的3个月内,发生消化道出血34例,未出血53例;EGV出血组LSWV和SSWV分别为（2.6±0.5） m/s和（3.3±0.5） m/s,显著高于EGV未出血组[分别为（1.9±0.4） m/s和（2.5±0.3） m/s,P<0.05];在87例患者中25例（28.7%）并发门静脉血栓,单因素和多因素分析显示,Child分级、门静脉内径、血小板计数、感染、腹水、肝性脑病、LSWV、SSWV、EGV分级和EGV出血为EGV患者发生门静脉血栓的危险因素;联合检测LSWV和SSWV诊断EGV患者并发门静脉血栓的AUC为0.893（0.829~0.946）,诊断效能较高。结论 采用ARFI测量LSWV和SSWV可以帮助判断肝硬化并发EGV患者门静脉血栓的发生,对临床具有一定的指导意义。     

Splanchnic and Extrasplanchnic Thrombosis in Cirrhosis: Prophylaxis vs Treatment

Venous thromboembolism (deep vein thrombosis and pulmonary embolism) and portal vein thrombosis (PVT) occur in up to 6.3 % and 15.9 % of patients with cirrhosis, respectively. There is recent evidence that a procoagulable prothrombotic state is related to cirrhosis despite the reduced levels of many coagulation factors, and decreased platelet counts. Indeed, (i) the combination of high levels of factor VIII, with low levels of protein C and antithrombin induces a procoagulant state in vitro; while (ii) increased levels of von Willebrand factor and decreased ADAMTS 13 activity can compensate for decreased platelet counts. PVT is partial in a majority of patients in whom it develops and may spontaneously resolve in some of them. Although PVT is associated with features of more severe liver disease, it is uncertain whether it plays a causal role in the decompensation of cirrhosis. In patients listed for liver transplantation, PVT may make the procedure difficult or impossible. Pre-transplant PVT is associated with increased post-transplant mortality rates. Studies evaluating clinical outcome of anticoagulation therapy for splanchnic or extrasplanchnic venous thrombosis are scarce. Anticoagulation therapy, given to patients with cirrhosis of intermediate severity before PVT occurrence, in prophylactic doses, appears to decrease decompensation and mortality rate. Interestingly, this improvement is out of proportion of the prophylaxis of extrahepatic portal vein thrombosis. The risk of bleeding does not seem to be increased in patients with cirrhosis receiving anticoagulation therapy, once prophylaxis for bleeding related to portal hypertension has been implemented. Overall, the room for anticoagulation therapy is probably larger than previously recognized, and may be of particular benefit in patients without portal vein thrombosis. However, clinical trials remain to be done before the benefit risk ratio of anticoagulation therapy is properly evaluated.     

Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis

BACKGROUND/AIMS: Portal vein thrombosis in patients with liver cirrhosis is usually associated to hepatocellular carcinoma. Clinical presentation of non-neoplastic portal vein thrombosis (PVT) in cirrhotic patients has not been specifically studied and risk factors of PVT in this group of patients are still poorly understood. METHODS: We studied all patients with PVT and liver cirrhosis admitted to our Unit from January 1998 to December 2002. They were paired (by gender, age and Child-Pugh score) to a group of cirrhotic patients without PVT and screened for acquired and inherited thrombophilic risk factors. These factors together with the site of thrombosis and the severity of the liver disease were correlated to the clinical presentation of PVT. RESULTS: Out of a total of 701 cirrhotic patients admitted to our hospital and routinely screened with Doppler ultrasound, 79 (11.2%) were found to have PVT. Of these, 34 (43%) were asymptomatic and 45 (57%) were symptomatic (31 presented with portal hypertensive bleed and 14 with abdominal pain, 10 of whom had intestinal infarction). Mesenteric vein involvement was never asymptomatic and lead to intestinal ischemia or infarction. Most patients were in class Child-Pugh B and C. Among thrombophilic risk factors studied only the mutation 20210 of the prothrombin gene resulted independently associated to PVT. CONCLUSIONS: Portal vein thrombosis may be completely asymptomatic in patients with liver cirrhosis; however in more than half of cases presents with life-threatening complications such as gastrointestinal haemorrhage and intestinal infarction. Cirrhotic patients with PVT usually have an advanced liver disease and the presence of the mutation 20210 of the prothrombin gene increases more than fivefold the risk of PVT.     

肝硬化并发门静脉血栓危险因素的Logistic回归分析

目的 探讨肝硬化并发门静脉血栓(PVT)形成的危险因素。方法 2012年3月~2016年12月收治444例肝硬化患者,其中并发PVT者44例,无PVT者400例。收集并对比两组患者的临床资料。采用t检验或x²检验进行危险因素的单因素分析,采用非条件多因素Logistic回归模型进行独立危险因素分析。结果 单因素分析显示,PVT组与无PVT组患者在Child-Pugh评分（7.65±2.01对6.90±1.85）、血红蛋白（HB）、血小板（PLT）、D-二聚体、纤维蛋白原降解产物（FDP）、白蛋白、门静脉内径、脾脏长径、脾脏厚径、门静脉流速和糖尿病发生率方面比较差异均具有统计学意义（均P<0.05）;多因素Logistic回归分析结果显示:门静脉内径（OR=1.258,95%CI 1.035~1.616,P=0.009）、D-二聚体（OR=3.915,95%CI 2.243~5.796,P=0.000）和糖尿病（OR=4.189,95%CI 2.067~6.231,P=0.000）是肝硬化并发PVT形成的独立危险因素。结论 影响肝硬化并发PVT发生的因素众多,其中血D-二聚体水平升高、门静脉内径增宽和伴有糖尿病是其独立危险因素,应给予充分的重视。     

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.     

Direct oral anticoagulant administration in cirrhotic patients with portal vein thrombosis: What is the evidence?

In recent years, the traditional concept that cirrhosis-related coagulopathy is an acquired bleeding disorder has evolved. Currently, it is known that in cirrhotic patients, the hemostatic system is rebalanced, which involves coagulation factors, fibrinolysis and platelets. These alterations disrupt homeostasis, skewing it toward a procoagulant state, which can lead to thromboembolic manifestations, especially when hemodynamic and endothelial factors co-occur, such as in the portal vein system in cirrhosis. Portal vein thrombosis is a common complication of advanced liver cirrhosis that negatively affects the course of liver disease, prognosis of cirrhotic patients and success of liver transplantation. It is still debated whether portal vein thrombosis is the cause or the consequence of worsening liver function. Anticoagulant therapy is the mainstay treatment for acute symptomatic portal vein thrombosis. In chronic portal vein thrombosis, the role of anticoagulant therapy is still unclear. Traditional anticoagulants, vitamin K antagonists and low-molecular-weight heparin are standard-of-care treatments for portal vein thrombosis. In the last ten years, direct oral anticoagulants have been approved for the prophylaxis and treatment of many thromboembolic-related diseases, but evidence on their use in cirrhotic patients is very limited. The aim of this review was to summarize the evidence about the safety and effectiveness of direct oral anticoagulants for treating portal vein thrombosis in cirrhotic patients.