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Chawla YK, Bodh V. Portal vein thrombosis. J Clin Exp Hepatol. 2015;5(1):22-40doi: 10.1016/j.jceh.2014.12.008.
Chawla, Y. K., & Bodh, V. (2015). Portal vein thrombosis. Journal of clinical and experimental hepatology, 5(1), 22-40. https://doi.org/10.1016/j.jceh.2014.12.008
Chawla, Yogesh K, and Bodh, Vijay. "Portal vein thrombosis." Journal of clinical and experimental hepatology vol. 5,1 (2015): 22-40. doi: https://doi.org/10.1016/j.jceh.2014.12.008
Chawla YK, Bodh V. Portal vein thrombosis. J Clin Exp Hepatol. 2015 Mar;5(1):22-40. doi: 10.1016/j.jceh.2014.12.008. Epub 2015 Jan 06. PMID: 25941431; PMCID: PMC4415192.
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J Clin Exp Hepatol. 2015 Mar;5(1):22-40. doi: 10.1016/j.jceh.2014.12.008. Epub 2015 Jan 06.

Portal vein thrombosis.

Journal of clinical and experimental hepatology

Yogesh K Chawla, Vijay Bodh

Affiliations

  1. Department of Hepatology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India.

PMID: 25941431 PMCID: PMC4415192 DOI: 10.1016/j.jceh.2014.12.008

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.

Keywords: 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

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