关键词: ACLA, anti-cardiolipin antibody AFP, alpha feto protein BCS, Budd-Chiari syndrome CDUS, color doppler ultrasonography CT, computed tomography CTP, Child Turcotte Pugh EHPVO, extra hepatic portal venous obstruction EST, endoscopic sclerotherapy HCC, hepatocellular carcinoma HVPG, hepatic venous pressure gradient IGF-1, insulin like growth factor-1 IGFBP-3, insulin like growth factor binding protein-3 INR, international normalized ratio JAK-2, Janus kinase 2 LA, lupus anticoagulant LMWH, low molecular weight heparin MELD, model for end stage liver disease MPD, myeloproliferative disorder MRI, magnetic resonance imaging MTHFR, methylenetetrahydrofolate reductase MVT, mesenteric vein thrombosis OCPs, oral contraceptive pills PAI-1 4G-4G, plasminogen activator inhibitor type 1- 4G/4G genotype PNH, paroxysmal nocturnal hemoglobinuria PV, portal vein PVT PVT, portal vein thrombosis PWUS, Pulsed Wave ultrasonography RFA, radio frequency ablation SMA, superior mesenteric artery SMV, superior mesenteric vein TAFI, thrombin activatable fibrinolysis inhibitor TARE, Trans arterial radioembolization TB, tuberculosis TIPS, transjugular intrahepatic portosystemic shunt UFH, unfractionated heparin acute and chronic anticoagulation imaging prothrombotic rtPA, recombinant tissue plasminogen activator

来  源:   DOI:10.1016/j.jceh.2014.12.008   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.
摘要:
门静脉血栓构成是门静脉高压症的重要病因。PVT与肝硬化相关,或由于肝细胞癌的恶性侵袭或甚至在没有相关肝病的情况下发生。根据目前对其起源的研究,大多数人现在有潜在的血栓前状态可检测到.内皮激活和停滞的门静脉血流也有助于血栓的形成。急性非肝硬化PVT,慢性PVT(EHPVO),肝硬化和门静脉血栓形成是门静脉血栓形成的三个主要变体,其病因和表现和管理差异不同。应积极调查促凝状态。抗凝治疗是急性非肝硬化PVT的主要治疗手段,并有证据支持其在肝硬化人群中的使用。另一方面,慢性PVT(EHPVO)需要门脉高压的治疗,并在潜在的血栓前状态下发挥抗凝作用。然而,没有潜在血栓前状态的患者仍在等待数据.即使在PVT的情况下,TIPS和肝移植也是可行的,但是需要适当选择候选人和手术类型。溶栓和取栓有一定的作用。TARE是肝癌门静脉侵犯的一种新的治疗方法。
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