肝硬化合并房颤的抗凝治疗进展

近年来相关研究显示, 在肝硬化患者中, 房颤的发生率明显增高, 心房颤动是慢性、长期抗凝治疗最常见的适应证, 抗凝治疗对降低缺血性卒中的发生有明确作用。肝硬化合并房颤患者抗凝治疗时, 由于肝硬化凝血功能障碍, 其出血及栓塞风险明显增高。同时此类患者在使用目前批准的抗凝药物时, 均会经肝脏不同程度地代谢与消除。使得抗凝治疗更加复杂。现对肝硬化合并房颤患者抗凝治疗风险与获益的临床研究进行总结, 以期为此类患者抗凝治疗提供参考。     

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...     

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     

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。     

抗凝治疗肝硬化患者并发门静脉血栓的循证医学证据*

门静脉血栓（PVT）对肝硬化患者的预后有着不良的影响,因此需要给予恰当的处理。临床上常用的治疗策略为抗凝治疗,但是考虑到肝硬化伴有PVT患者食管胃底静脉曲张破裂出血的风险比无肝病的原发性PVT患者要高很多,抗凝治疗的选择十分困难。大多指南对于肝硬化并发PVT患者应当如何治疗并未作出明确的推荐。我们通过检索相关临床研究发现,在肝硬化PVT患者应用抗凝药物能获得较高的再通率,而不会显著增加出血的风险,但研究的证据级别普遍较低,需要更多的前瞻性、大样本研究以进一步论证,同时临床应用抗凝治疗时仍需根据患者的具体情况进行个体化的治疗。     

肝硬化合并心房颤动的病因及抗凝治疗

肝硬化是由于不同原因导致的肝脏疾病终末阶段。而肝硬化患者中可观察到各类心律失常,其中心房颤动已有数据报道。由于肝硬化通常会出现凝血功能紊乱,给心房颤动患者抗凝治疗带来挑战,致使如何平衡出血与抗凝治疗成为治疗的矛盾所在。目前关于肝硬化合并心房颤动相关知识论述报道不多,现结合资料做一综述,以飨从事相关实践的医师。     

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。     

肝硬化上消化道出血患者抗凝治疗的影响:一项多中心回顾性研究

<正>近期研究表明,肝硬化患者处于高凝状态,可增加血栓风险,不常应用抗凝治疗。静脉曲张破裂出血是肝硬化的严重并发症。目前尚不清楚抗凝是否会诱发这些患者出血。来自巴塞罗那大学的Cerini F等对52例上消化道出血患者行抗凝治疗进行了评估。研究中分别有14名和38名患者符合门静脉血栓和各种心血管疾病抗凝治疗的指征,104名未经抗凝治疗的肝硬化上消化道出血患者作为对照组,对纳入研究患者的肝硬化严重程度、年龄、性别、出血原因、SOFA评分等进行比较。结果显示,99名(63%)患者上消化道出血的原因为门静脉高压,57名(37%)患者上消化道出血的原因是溃疡/血管病变,26名(17%)患者5天后出现衰     

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。     

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.     

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.     

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。     

Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy

Characteristics and outcomes of recent portal or mesenteric venous thrombosis are ill-known. We intended to compare these features with those of patients with portal cavernoma, and also to assess the incidence of recanalization of recent thrombosis on anticoagulation therapy. All patients seen between 1983 and 1999 were enrolled into this retrospective study if recent portal or mesenteric venous thrombosis or portal cavernoma had been documented, and if cancer of the liver, pancreas, or bile duct, intrahepatic block including cirrhosis, and obstruction of the hepatic veins had been ruled out. The proportion of recent thrombosis was 7% in patients seen before 1990 and 56% after 1994 (P <.05). Patients with recent thrombosis (n = 33) or cavernoma (n = 108) did not differ with regard to age, sex ratio, or prevalence of prothrombotic states and of previous thrombotic events. In patients with recent thrombosis, septic pylephlebitis was more common and the incidence of gastrointestinal bleeding was lower (2.4 vs. 12.7/100 patient-years). Recanalization occurred in 25 of 27 patients given anticoagulation and 0 of 2 patients not given anticoagulation. The probability of recanalization was related to the extent of thrombosis (P =.003). In conclusion, mesenteric or portal venous thrombosis is increasingly recognized at an early stage. The features differentiating recent thrombosis and cavernoma are related to silent onset precluding early recognition and therapy in the latter. Frequent association with prothrombotic states and frequent recanalization on anticoagulation support the recommendation of early anticoagulation therapy in all patients with recent portal vein thrombosis.     

Portal Vein Thrombosis

Portal vein thrombosis is a condition not infrequently encountered by clinicians. It results from a combination of local and systemic prothrombotic risk factors. The presentation of acute thrombosis varies widely from an asymptomatic state to presence of life-threatening intestinal ischemia and infarction. In the chronic stage, patients typically present with variceal bleeding or other complications of portal hypertension. Abdominal ultrasound color Doppler imaging has a 98% negative predictive value, and is considered the imaging modality of choice in diagnosing portal vein thrombosis. Controlled clinical trials to assist with clinical decision-making are lacking in both acute and chronic portal vein thrombosis. Oral anticoagulant therapy is initiated if the risks of bleeding are low, but long-term anticoagulation is generally not recommended in patients with concomitant hepatic cirrhosis. The roles of invasive therapeutic approaches such as thrombolysis and transjugular intrahepatic portosystemic shunt continue to evolve. This review conflates dissenting views into a rational approach of managing patients with portal vein thrombosis for the general internist.     

Extrahepatic portal hypertension: spleno-portal thrombosis secondary to protein C deficiency

Portal vein thrombosis (PVT) is the most frequent cause of hypertension portal extrahepatic. It is a rare disorder an the main risk factors are cirrhosis, hepatobiliary malignancies and prothrombotic disorders, which have been identified as major risk. Therapy with anticoagulants must to be considered in acute portal thrombosis or chronic one and proven hypercoagulability. We present the case of a twenty-nine years old patient, with extrahepatic portal hypertension secondary to portal and splenic vein thrombosis, who was diagnosed because of splenomegaly and a coagulation disorder. A protein C deficiency were discovered and anticoagulation and beta-blocker therapy were initiated. One year later the patient had not presented complications concerning to the disease or to the treatment.     

Emergency anticoagulation treatment for cirrhosis patients with portal vein thrombosis and acute variceal bleeding

Abstract

Objective. To determine the safety and efficacy of anticoagulation treatment for portal vein thrombosis in cirrhosis patients with acute variceal bleeding, with patient eligibility determined by contrast ultrasonography findings. Materials and methods. This prospective study included 23 consecutive cirrhosis patients (63.8 ± 11.8 years old, 12 males and 11 females) with emergency admission for acute variceal bleeding with or without portal vein thrombus. Eligibility for anticoagulation treatment was determined by positive intra-thrombus enhancement on contrast ultrasonography (perflubutane microbubble agent, 0.0075 mL/kg) performed before endoscopy. Low-molecular-weight heparin was administered after hemostasis was achieved by band ligation. Repeated band ligation or injection sclerotherapy combined with argon plasma coagulation was performed for variceal disappearance. Results. Hemostasis was achieved in all 10 patients with active bleeding. Five of these patients had portal vein thrombus, and all showed positive intra-thrombus enhancement on contrast ultrasonography. Anticoagulation treatment of these five patients resulted in complete recanalization of the portal vein within 2–11 days. There were no significant differences in the number of endoscopic treatment sessions or the length of hospital stay between the groups with and without thrombosis, and no complications including rebleeding were reported. Long term, none of the patients who continued oral anticoagulation treatment had recurrence of thrombosis (4/5). Variceal recurrence occurred only in the non-thrombosis group (2/18) during the follow-up period (median: 351 days). Conclusions. Early anticoagulation treatment in cirrhosis patients with portal vein thrombosis and acute variceal bleeding may be safe, tolerated, and effective in cases with positive intra-thrombus enhancement on contrast ultrasonography.     

Should anticoagulants be administered for portal vein thrombosis associated with acute pancreatitis?

Venous complications in patients with acute pancreatitis typically occur as a form of splenic, portal, or superior mesenteric vein thrombosis and have been detected more frequently in recent reports. Although a well-organized protocol for the treatment of venous thrombosis has not been established, anticoagulation therapy is commonly recommended. A 73-year-old man was diagnosed with acute progressive portal vein thrombosis associated with acute pancreatitis. After one month of anticoagulation therapy, the patient developed severe hematemesis. With endoscopy and an abdominal computed tomography scan, hemorrhages in the pancreatic pseudocyst, which was ruptured into the duodenal bulb, were confirmed. After conservative treatment, the patient was stabilized. While the rupture of a pseudocyst into the surrounding viscera is a well-known phenomenon, spontaneous rupture into the duodenum is rare. Moreover, no reports of upper gastrointestinal bleeding caused by pseudocyst rupture in patients under anticoagulation therapy for venous thrombosis associated with acute pancreatitis have been published. Herein, we report a unique case of massive upper gastrointestinal bleeding due to pancreatic pseudocyst rupture into the duodenum, which developed during anticoagulation therapy for portal vein thrombosis associated with acute pancreatitis.     

A case of portal vein thrombosis associated with acute pancreatitis and cholangitis]

Portal vein thrombosis is a rare complication accompanied with acute pancreatitis or cholangitis/cholecystitis. The main pathogenesis of portal vein thrombosis in pancreatitis or cholangitis/cholecystitis are suggested to be venous compression by pseudocyst and an imbalance between the blood coagulation and fibrinolysis. In this case report, we experienced a 63 year old male who developed portal vein thrombosis later in the course of the treatment of acute gallstone pancreatitis with cholangitis/cholecystitis without any symptom or sign. The diagnosis of portal vein thrombosis was given on follow up CT scan and serum protein S activity was decreased to 27% in laboratory study. Immediate anticoagulation therapy with heparin and thrombolytic therapy with urokinase and balloon dilatation were performed. Despite the aggressive treatment, complete reperfusion could not be obtained. With oral warfarin anticoagulation, the patient showed no disease progression and was discharged. We report a case of portal vein thrombosis as a complication of acute pancreatitis and cholangitis/cholecystitis with a review of literatures.     

Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.