Portal Vein Thrombosis after Variceal Endoscopic Sclerotherapy in Cirrhotic Patients: Role of Genetic Thrombophilia

Amitrano, Lucio; Brancaccio, Vincenzo; Guardascione, Maria Anna; Margaglione, Maurizio; Sacco, Monica; Martino, Randall R. De; Nucci, C. De; Mosca, S; Iannaccone, Luigi; Ames, P. R. J.; Romano, L; Balzano, A.

doi:10.1055/s-2002-33210

Cited by 84 publications

(77 citation statements)

References 15 publications

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“…PVT has been described following endoscopic sclerotherapy in patients with cirrhosis in association with these thrombophilic conditions. 65 Endotoxemia in cirrhosis may increase the risk of PVT in cirrhosis.…”

Section: Vascular Endothelial Injurymentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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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. ( J CLIN EXP HEPATOL 2015;5:22-40)

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Section: Vascular Endothelial Injurymentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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“…Splenomegaly and a large splenic vein diameter are independent risk factors for PVT after splenectomy in patients with concomitant cirrhosis and portal hypertension [39,46,47] . The role of sclerotherapy as a potential trigger for PVT is controversial [48,49] . Some recent reports showed that thrombopoietin receptor agonists might be associated with an increased incidence of PVT in patients with cirrhosis [50,51] .…”

Section: Etiology Of Pvt In Cirrhosismentioning

confidence: 99%

Portal vein thrombosis in liver cirrhosis

Kinjo¹,

Kawanaka²,

Akahoshi³

et al. 2014

WJH

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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.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Portal vein thrombosis; Liver cirrhosis; Thrombophilic factors; Anticoagulation; Splenectomy Core tip: Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis; however, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions. The understanding and information on the management of PVT in cirrhosis are incomplete. 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.

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“…35,36 The role of sclerotherapy and cyanoacrylate glue injection as a potential trigger factor for PVT is controversial but has been reported in literature. [37][38][39] Such associations could be as a result of selection bias of patients with more severe portal hypertension.…”

Section: Pathophysiologymentioning

confidence: 99%

Portal Vein Thrombosis in Cirrhosis

Raja

Jacob

Asthana

2014

Journal of Clinical and Experimental Hepatology

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Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10-25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33-45% and 15-35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term. ( J CLIN EXP HEPATOL 2013;4:320-331)

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Portal Vein Thrombosis after Variceal Endoscopic Sclerotherapy in Cirrhotic Patients: Role of Genetic Thrombophilia

Abstract: Endoscopic sclerotherapy of esophageal varices may represent a trigger factor for portal vein thrombosis in cirrhotic patients with genetic thrombophilia.

Cited by 84 publications

References 15 publications

Portal Vein Thrombosis

Portal Vein Thrombosis

Portal vein thrombosis in liver cirrhosis

Portal Vein Thrombosis in Cirrhosis

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