Endoscopic treatment of esophagogastric variceal bleeding in patients with noncirrhotic extrahepatic portal vein thrombosis: a long-term follow-up study

BACKGROUND: Esophagogastric variceal bleeding is the most important complication of extrahepatic portal vein thrombosis (EPVT) and is usually treated endoscopically. Little is known about the prognosis of these patients. OBJECTIVES: To investigate the long-term clinical outcome and efficacy of endoscopic treatment in patients with esophagogastric variceal bleeding secondary to EPVT. DESIGN: Retrospective observational study. SETTINGS: Single university center. PATIENTS: Twenty-seven consecutive patients with esophagogastric variceal bleeding, secondary to noncirrhotic, nonmalignant EPVT, who underwent endoscopic treatment between 1982 and 2005. INTERVENTIONS: Endoscopic band ligation and/or endoscopic sclerotherapy. MAIN OUTCOME MEASUREMENTS: The overall rebleeding risk, overall survival, complications of the endoscopic procedures, and predictive values of rebleeding. Analyses were performed by the Kaplan-Meier method and univariate Cox regression. RESULTS: All patients were followed-up after the first endoscopically treated variceal bleeding. A total of 241 endoscopic procedures were performed. In all patients, initial control of bleeding was obtained. The overall rebleeding risk was 23% (95% CI, 0%-24%) at 1 year and 37% (95% CI, 43%-83%) at 5 years. Extension of thrombosis into the splenic vein and the presence of fundal varices were significant predictors of rebleeding, with a nearly 5-fold increased risk for patients with EPVT and fundal varices at the time of the first variceal hemorrhage (hazard ratio 5.07, P = .01). A portosystemic shunt procedure was performed in 5 patients: 4 for variceal bleeding and in one patient for refractory ascites. Seven patients died, none from variceal bleeding. Overall 5-year and 10-year survivals were 100% and 62% (95% CI, 38%-96%), respectively. LIMITATIONS: Retrospective design. CONCLUSIONS: In patients with variceal bleeding secondary to EPVT endoscopic treatment, in particular, band ligation appears safe and effective. EPVT-related mortality is primarily determined by other causes than variceal bleeding.     

门静脉血栓介入治疗研究进展

正门静脉血栓是指门静脉主干及其分支血栓形成,可导致门静脉部分或完全性梗阻,部分门静脉血栓可以延伸至脾静脉或肠系膜上静脉。门静脉血栓的形成原因有多种,主要包括肝硬化、肿瘤、免疫系统疾病、感染、凝血功能障碍和口服避孕药物等~([1])。在肝硬化进展期或合并肿瘤患者,门静脉血栓的发生率更高~([2,3])。据统计,肝硬化并发门静脉高压患者门静脉血栓发生率约为0.6%～15.8%~([4])。伴有门静脉血栓的肝硬化患者发生消化道出血的风险更高~([5])。门静脉血栓形成所导致的临床表现差异较大,轻症患者可无任何临床症状,常常在随访过程中被发现。     

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。     

Thrombophilic gene mutations in cirrhotic patients with portal vein thrombosis

OBJECTIVE: Thrombophilic gene mutations have been reported to be associated with the formation of portal vein thrombosis (PVT). This study aimed to investigate the role of thrombophilic gene mutations in cirrhotic patients with PVT. PATIENTS AND METHODS: A total of 74 cirrhotic patients (17 with PVT, 57 without PVT), and 19 non-cirrhotic patients with PVT and 80 healthy controls were included. Factor V Leiden G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase C677T mutations were analysed by restriction fragment length polymorphism. RESULTS: Aetiologies and Child-Pugh distribution of cirrhotic patients with and without PVT were similar. Five of 17 (29%) of cirrhotic patients with PVT but only two of 57 (3.5%) of cirrhotics without PVT, five of 80 (6%) of controls and none of the 19 non-cirrhotic patients with PVT had factor V Leiden G1691A mutation (P<0.05). Prothrombin G20210A mutation was found in five (29%) cirrhotic patients with PVT while only two (3.5%) cirrhotic patients without PVT, one (5%) non-cirrhotic patient with PVT and two (2.5%) controls had this mutation (P<0.05). The frequency of the homozygote methylenetetrahydrofolate reductase 677C-T mutation was similar in all four groups. CONCLUSIONS: Inherited thrombophilic gene mutations appear to increase the risk of PVT formation in cirrhotic patients but not in patients without liver disease in a cohort of Turkish patients.     

Deficiency of protein C in patients with portal vein thrombosis

Portal vein thrombosis has been considered idiopathic in 50% of cases reported in adults. Protein C deficiency is a recently described disorder characterized by a predisposition to develop thromboembolic disease. We report the findings in two patients with portal hypertension and bleeding varices due to portal vein thrombosis in whom a deficiency of protein C was present. Both cases were very similar, with a history of recurrent episodes of systemic thromboembolic disease, mesenteric venous thrombosis that required intestinal resection and upper gastrointestinal bleeding from gastroesophageal varices. Portal hypertension as well as portal vein thrombosis were demonstrated. The hematologic work-up revealed a deficiency of protein C. Both patients were subjected to the Sugiura procedure, and anticoagulation was instituted thereafter. At the time of surgery, a liver biopsy was performed, which was reported as "normal." Two years and 3 months, respectively, after surgery both patients are in good condition. We conclude that protein C deficiency should be investigated in all cases of portal vein thrombosis, especially in those with a history of thromboembolic disease elsewhere.     

Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis

The prevalence and pathogenesis of portal vein thrombosis (PVT) in patients with cirrhosis without hepatocellular carcinoma are not clearly defined. The role of thrombophilic genetic factors is well established in other venous thrombotic diseases, as well as in noncirrhotic portal thrombosis. Recently, new, inherited thrombophilic disorders (factor V Leiden [FVL], mutation G20210A of prothrombin [PTHR A(20210)], and mutation TT677 of methylenetetrahydrofolate reductase [MTHFR C677-->T]) have been identified and associated with increased risk of venous thrombosis. The aim of our study was to investigate the role of these thrombophilic disorders in the pathogenesis of PVT in cirrhotic patients. Twenty-three cirrhotic patients with PVT and 40 cirrhotics without PVT were included. A group of 184 patients with deep vein thrombosis (DVT) and 431 healthy persons served as controls. The FVL, PTHR A(20210), and MTHFR C(677)-->T genotypes were identified by a polymerase chain reaction and restriction analysis. The frequencies of FVL, PTHR A(20210) mutation, and homozygous MTHFR C(677)-->T were 13%, 34.8%, and 43.5% in cirrhotic patients with PVT and 7.5%, 2.5%, and 5% in cirrhotic patients without PVT, respectively. Five patients in the former group had associated defects. A thrombophilic genotype was detected in 69.5% of the patients with PVT. Identification of this high-risk group may have implications in patients who are candidates for major surgery or liver transplantation, and may influence the duration of oral anticoagulation.     

肝硬化合并门静脉血栓形成的临床特点

目的分析肝硬化患者合并门静脉血栓形成(PVT)的临床特点及危险因素,了解该类患者药物性预防措施是否有效.方法 2008年1月至2011年3月各种原因的肝硬化住院患者共339例,将其分为两组,分别为肝硬化合并有门静脉血栓形成组及未合并有门静脉血栓组.记录患者年龄、性别、凝血酶原时间(PT)、总胆红素、白蛋白、肝硬化的病因...     

Portal vein thrombosis with protein C-S deficiency in a noncirrhotic patient

There are several conditions that can lead to portal vein thrombosis(PVT), including including infection, malignancies, and coagulation disorders. Anew condition of interest is protein C and S deficiencies, associated with hypercoagulation and recurrent venous thromboembolism. We report the case of a non-cirrhotic 63-year-old male diagnosed with acute superior mesenteric vein thrombosis and PVT and combined deficiencies in proteins C and S, recanalized by short-term low molecular heparin plus oral warfarin therapy.     

Study of portal vein thrombosis in patients with idiopathic portal hypertension in Japan.

BACKGROUND/AIMS: The aim of this study was to elucidate the incidence and clinical manifestations of portal vein thrombosis (PVT) in patients with idiopathic portal hypertension (IPH) in Japan during long-term follow-up. PATIENTS AND METHODS: Twenty-two patients with IPH were examined for PVT by sonography during a follow-up of 12+/-6 years. Clinical manifestations and patient outcome related to PVT were studied. Seventy patients with liver cirrhosis were examined by sonography as an incidence control of thrombosis. RESULTS: Nine IPH patients had portal thrombosis (9/22, 41%), a higher incidence than in liver cirrhosis patients (7/70, 10%). Those with thrombosis showed ascites, marked hypersplenism, and low serum albumin. Four patients with thrombosis died. Patients without thrombosis showed less clinical problems after long-term follow-up. Plasma antithrombin III and protein C activity decreased in almost half of the patients. However, there were no differences in these parameters between patients with and without thrombosis. CONCLUSIONS: In Japan, IPH patients had a high incidence of portal thrombosis, a significant factor for poor prognosis. Whether the management of PVT contributes to an improvement of a clinical course of IPH or not should be clarified in further study.     

肝硬化门静脉高压脾切除术后门静脉血栓形成的研究进展

门静脉血栓形成(PVT)是指门静脉或其分支、脾静脉和肠系膜上静脉内形成的血栓。PVT是门静脉高压症脾切除术后的一种常见并发症,往往可能会导致肝损伤、上消化道出血、肝昏迷,甚至是缺血性肠坏死。因而,早期发现PVT并进行有效干预,对降低PVT患者的病死率有十分重要的意义。对肝硬化脾切除术后PVT危险因素和治疗进行了综述,指出PVT应及早进行有效干预。     

Transjugular intrahepatic portosystemic shunt is effective in patients with chronic portal vein thrombosis and variceal bleeding

Background: Studies about treatment of patients with chronic portal vein thrombosis(CPVT) are still limited, especially in different types of CPVT. This study aimed to evaluate the effect of transjugular intrahepatic portosystemic shunt(TIPS) in all types of CPVT with variceal bleeding. Methods: Patients with CPVT who received TIPS treatment between January 2011 and June 2019 were divided into four types according to the extent of thrombosis. All patients had a history of variceal bleeding. The characteristics and clinical parameters were collected and recorded. Data on procedure success rate, variation in portal vein pressure, rebleeding, hepatic encephalopathy(HE), stent stenosis, and overall mortality were analyzed. Results: A total of 189 patients were included in this study(39 in type 1, 84 in type 2, 48 in type 3, 18 in type 4). The TIPS procedure success rate was 86.2%. The success rate was significantly different among the four types(89.7% vs. 88.1% vs. 83.3% vs. 77.8%, P = 0.001). In the TIPS success group, portal vein pressure was significantly reduced from 27.15 ± 6.59 to 19.74 ± 6.73 mm Hg after the procedure( P 0.001) and the rebleeding rate was significantly lower than that of the fail group(14.7% vs. 30.8%, P = 0.017). In addition, there were no significant differences in HE rate(30.7% vs. 26.9%, P = 0.912) or overall mortality(12.9% vs. 19.2%, P = 0.403) between the TIPS success group and the fail group. In the TIPS success group, we found that the occurrence of HE was significantly different( P = 0.020) among the four types, while there were no significant differences in rebleeding rate( P = 0.669), stent stenosis rate( P = 0.056), or overall mortality( P = 0.690). Conclusions: TIPS was safe and effective in decreasing portal vein pressure and rebleeding rate in patients with CPVT.     

肝硬化门脉高压症并发血栓形成机制和治疗研究进展*

肝硬化门脉高压症并发血栓是临床研究实践过程中面临的难题。本文通过对其形成机制和治疗相关研究进展进行总结,重点介绍了近年来国内外关于肝硬化门脉高压并发门脉血栓发生机制和治疗进展。目前认识的主要发生机制包括肝星状细胞的活性、内皮细胞的功能、机体促凝血和凝血抑制失衡等,治疗措施包括低分子肝素等抗凝治疗、β受体阻滞剂和其他药物,如辛伐他汀、利福昔明和益生菌等联合应用以降低门脉压力治疗、提高一氧化氮合成酶磷酸化水平和针对线粒体的抗氧化治疗等措施。     

脾切除联合贲门周围血管离断术治疗肝硬化门脉高压症患者预防门静脉血栓形成研究

目的 探讨脾切除联合贲门周围血管离断术治疗肝硬化门脉高压症患者门静脉血栓(PVT)的预测措施。方法 2017年1月～2019年3月我院肝胆外科诊治的肝硬化并发门脉高压症患者60例,均接受脾切除联合贲门周围血管离断术。术后将患者分成A组和B组。在B组,当出现抗凝指针时给予低分子肝素短期抗凝治疗。使用彩超检查门脉指标和诊断PVT形成。结果 术后,在B组30例患者中有20例(66.7%)接受了短期抗凝治疗;在术后3 w末,超声检查发现PVT患者15例(25.0%),其中A组11例(36.7%),显著高于B组的4例【(13.3%),P<0.05】;血栓形成组门静脉直径为(1.5±0.3)cm,与无血栓形成组比,无显著性差异【(1.4±0.2)cm,P>0.05】,门静脉血流流速为(12.3±1.4)cm/s,显著低于无血栓形成组【(14.5±1.7)cm/s,P＜0.05】;血栓形成组血清D-二聚体水平显著高于无血栓形成组(P＜0.05);血栓形成组外周血血小板计数为(142.6±58.9)×10⁹/L,显著高于无血栓形成组【(91.4±52.4)×10⁹/L,P＜0.05】。结论 在采取脾切除联合贲门周围血管离断术治疗肝硬化并发门脉高压症患者时,需警惕术后PVT的形成。对术后血小板计数急剧升高、血清D-二聚体显著升高和门脉血流减慢的患者应该及时给予抗凝治疗。     

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.