肝硬化并发门静脉血栓防治研究进展

门静脉血栓（PVT）是肝硬化的常见并发症,也是患者预后不良的临床标志之一。肝硬化常并发食管胃底静脉曲张、凝血酶原时间延长和血小板降低,存在门脉高压所致出血的风险。临床上,对应用抗凝药物防治PVT存在较多的疑虑。目前,防治肝硬化并发PVT仍缺乏可以遵循的诊疗指南。然而,日益增加的证据显示,抗凝治疗不仅不会增加肝硬化患者出血的风险,而且可获得较高的血管再通率。预防性抗凝治疗可有效降低肝硬化患者PVT发病率,并可能改善肝硬化疾病进程。如抗凝治疗无效,经颈静脉肝内门体静脉支架分流术（TIPS）或溶栓治疗可作为肝硬化并发PVT的备选处理方案。TIPS可获较高的血管再通率,但技术难度较大,而溶栓治疗存在出血风险,需谨慎进行。     

肝硬化患者门静脉血栓形成的自然病程和抗凝治疗

门静脉血栓形成(PVT)是肝硬化的常见并发症之一,但其自然病程和治疗管理尚未得到国际指南和会议共识的明确建议。既往研究表明PVT可自发再通,而抗凝治疗明显有利于PVT的再通。由于肝硬化患者本身存在凝血功能受损和门静脉高压带来的出血风险,目前对于肝硬化患者PVT的抗凝治疗存在争议。然而,近年来许多研究表明抗凝治疗对肝硬化...     

肝硬化非肿瘤性门静脉血栓的治疗进展

门静脉血栓(portal vein thrombosis,PVT)在肝硬化患者中并不是一种罕见的并发症.PVT增加了消化系出血的风险,目前治疗PVT以药物为主,研究表明抗凝治疗并不增加消化系出血的风险,因此,对于有适应症的患者,应早期进行抗凝治疗.对于存在食管胃底静脉曲张的患者,采取预防措施后应及时对PVT进行治疗.抗凝治疗无效时可考虑介入及手术治疗.这篇综述的目的在于,总结近年来关于PVT的研究,探讨肝硬化非肿瘤性PVT的治疗进展.     

肝硬化合并门静脉血栓治疗进展

门静脉血栓(PVT)是肝硬化的常见并发症之一,由于肝硬化存在凝血功能障碍和出血风险,临床上对于肝硬化合并PVT的治疗存在诸多争议。PVT常用治疗方法包括抗凝、介入和溶栓,重点阐述了肝硬化合并PVT的治疗现状,以期为临床制订规范合理的治疗策略提供帮助。     

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。     

抗凝治疗对肝硬化上消化道出血的影响

<正>【据《Hepatology》2015年8月报道】题:抗凝治疗对肝硬化上消化道出血的影响:一项回顾性多中心研究(作者Cerini F等)近期研究显示肝硬化(LC)呈现为一种获得性高凝状态,其血栓形成风险增加,这是为什么这些患者现在经常使用抗凝治疗(AT)。静脉曲张破裂出血是肝硬化的一种严重并发症,尚不清楚抗凝治疗是否会影响这些出血患者的预后。本研究评估了52例抗凝治疗的上消化道出血(UGIB)患者,其中14例患者因门静脉血栓(PVT),38例患者因不同的心血管     

肝硬化患者门静脉血栓形成合并消化道出血的研究进展

肝硬化患者门静脉血栓形成(PVT)近年来逐渐被重视,可导致肝硬化患者门静脉压力升高,加重食管胃底静脉曲张,甚至破裂出血。本文回顾了国内外肝硬化患者PVT合并消化道出血的流行病学、机制及不同情况下的治疗进展。PVT合并消化道出血的具体治疗方法及抗凝药的使用剂量及疗程等方面国内外仍存在争议,未来仍需大量高证据级别研究来明确其详细治疗方法。     

抗凝治疗肝硬化门静脉血栓的临床效果及安全性

<正>【据《Am J Gastroenterol》2018年12月在线报道】题:抗凝治疗肝硬化门静脉血栓的临床效果及安全性(作者Pettinari I等)门静脉血栓形成(PVT)是肝硬化的常见并发症。抗凝治疗肝硬化PVT的获益、安全性及用药持续时间仍有争议。本研究旨在分析肝硬化PVT患者接受或未接受抗凝治疗的疾病病程。本研究对2008年1月-2016年3月期间的182例肝硬化合并PVT患者(首次发现PVT后至少随访3个月)的数     

合并门静脉血栓的乙型肝炎肝硬化患者,使用不同剂量依诺肝素抗凝治疗的安全性和有效性

<正>【据《Eur J Gastroenterol Hepatol》2015年4月报道】题:并发门静脉血栓的乙型肝炎肝硬化患者,使用不同剂量依诺肝素抗凝治疗的安全性和有效性(作者Cui SB等)肝硬化患者门静脉血栓(PVT)的发生率很高,而肝硬化患者PVT的最佳治疗方案尚不清楚,目前尚未有关于使用依诺肝素治疗肝硬化PVT最佳剂量的文献报道。为了评估乙型肝炎肝硬化合并PVT应用不同剂量依诺肝素进行抗凝治疗的安全性及疗效,来自山东大学附属省立医院的Cui SB等使用不同剂量依诺肝素治疗65例乙型肝炎相关肝硬化合并急性PVT患者,所有患者随机分为2组,给予一组患者1 mg/kg,每12 h皮下注射,给予对照组1.5 mg/kg,每24 h皮下注射。在治疗过程中,应用临床、生化、多     

抗凝作用对肝硬化患者上消化道出血的影响:一项回顾性多中心研究

正【据《Hepatology》2015年10月报道】题:抗凝作用对肝硬化患者上消化道出血的影响:一项回顾性多中心研究(作者Cerini F等)近期研究表明肝硬化表现为获得性高凝状态,血栓风险增高。这是肝硬化患者应用抗凝治疗的原因。静脉曲张破裂出血是肝硬化的严重并发症。抗凝是否会影响肝硬化患者消化道出血的结局尚不清楚。     

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.     

Changing perspectives in portal vein thrombosis

The aetiology of portal vein thrombosis (PVT) is heterogeneous. Important primary risk factors for PVT are cirrhosis, hepatobiliary malignancies and pancreatitis. Newly discovered thrombotic risk factors, such as latent myeloproliferative disorders and prothrombotic genetic defects, have also been identified as major risk factors for PVT. At least one-third of PVT patients demonstrate a combination of thrombotic risk factors. PVT, which does not have a detrimental effect on liver function, usually becomes manifest as a variceal haemorrhage in the oesophagus months to years after the development of thrombosis. Owing to intact coagulation variceal bleeding has a better prognosis among patients with PVT than cirrhotics. Endoscopic sclerotherapy or band ligation is the primary therapeutic option for variceal bleeding in patients with PVT. It is questionable whether anticoagulant therapy should be started, since it has not proven beneficial for most PVT patients. Therapy with anticoagulants is only recommended for those with acute PVT (especially in association with mesenteric vein thrombosis), those who recently underwent a portosystemic shunt procedure, and those with other thrombotic manifestations, particularly in case of proven hypercoagulability. Mortality of patients with PVT may be associated with concomitant medical conditions which lead to the PVT or with manifestations of portal hypertension, such as variceal haemorrhage. Multivariate analysis of a large Dutch PVT population has shown that age, malignancy, ascites and the presence of mesenteric vein thrombosis are independently related to survival. Death due to a variceal haemorrhage is rare. Poor outcome of PVT thus appears to be associated primarily with concomitant diseases which lead to PVT, and not the complications of portal hypertension. It is therefore uncertain whether surgical portosystemic shunting affects survival favourably.     

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT.     

Portal vein thrombosis: What is new?

Portal vein thrombosis (PVT) is one of the most common vascular disorders of the liver with significant morbidity and mortality. Large cohort studies have reported a global prevalence of 1%, but in some risk groups it can be up to 26%. Causes of PVT are cirrhosis, hepatobiliary malignancy, abdominal infectious or inflammatory diseases, and myeloproliferative disorders. Most patients with PVT have a general risk factor. The natural history of PVT results in portal hypertension leading to splenomegaly and the formation of portosystemic collateral blood vessels and esophageal, gastric, duodenal, and jejunal varices. Diagnosis of PVT is made by imaging, mainly Doppler ultrasonography. According to its time of development, localization, pathophysiology, and evolution, PVT should be classified in every patient. Some clinical features such as cirrhosis, hepatocellular carcinoma, and hepatic transplantation are areas of special interest and are discussed in this review. The goal of treatment of acute PVT is to reconstruct the blocked veins. Endoscopic variceal ligation is safe and highly effective in patients with variceal bleeding caused by chronic PVT. In conclusion, PVT is the most common cause of vascular disease of the liver and its prevalence has being increasing, especially among patients with an underlying liver disease. All patients should be investigated for thrombophilic conditions, and in those with cirrhosis, anticoagulation prophylaxis should be considered.     

Efficacy and safety of anticoagulation in non-malignant portal vein thrombosis in patients with liver cirrhosis

Background and aim

Treatment for portal vein thrombosis (PVT) is not well established. Nevertheless, anticoagulation therapy can seemingly be used as first-line therapy. However, there are limited data on the role of this treatment in patients with PVT and cirrhosis. We sought to assess the safety and efficacy of anticoagulation therapy in a series of patients with non-malignant PVT and liver cirrhosis.

Nontumoral Portal Vein Thrombosis: A Challenging Consequence of Liver Cirrhosis

Nontumoral portal vein thrombosis (PVT) is an increasingly recognized complication in patients with cirrhosis. Substantial evidence shows that portal flow stasis, complex thrombophilic disorders, and exogenous factors leading to endothelial dysfunction have emerged as key factors in the pathogenesis of PVT. The contribution of PVT to hepatic decompensation and mortality in cirrhosis is debatable; however, the presence of an advanced PVT increases operative complexity and decreases survival after transplantation. The therapeutic decision for PVT is often determined by the duration and extent of thrombosis, the presence of symptoms, and liver transplant eligibility. Evidence from several cohorts has demonstrated that anticoagulation treatment with vitamin K antagonist or low molecular weight heparin can achieve recanalization of the portal vein, which is associated with a reduction in portal hypertension-related events and improved survival in cirrhotic patients with PVT. Consequently, interest in direct oral anticoagulants for PVT is increasing, but clinical data in cirrhosis are limited. Although the most feared consequence of anticoagulation is bleeding, most studies indicate that anticoagulation therapy for PVT in cirrhosis appears relatively safe. Interestingly, the data showed that transjugular intrahepatic portosystemic shunt represents an effective adjunctive therapy for PVT in cirrhotic patients with symptomatic portal hypertension if anticoagulation is ineffective. Insufficient evidence regarding the optimal timing, modality, and duration of therapy makes nontumoral PVT a challenging consequence of cirrhosis. In this review, we summarize the current literature and provide a potential algorithm for the management of PVT in patients with cirrhosis.     

Portal vein thrombosis in liver cirrhosis简

Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.     

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis(PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to:(1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis;(2) describe the principal factors most frequently involved in PVT development; and(3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.