High levels of factor VIII and risk of extra-hepatic portal vein obstruction

Martinelli, Ida; Primignani, Massimo; Aghemo, Alessio; Reati, R.; Bucciarelli, Paolo; Fabris, F; Battaglioli, Tullia; Dell’Era, Alessandra; Mannucci, Pier Mannuccio

doi:10.1016/j.jhep.2008.12.020

Cited by 67 publications

(55 citation statements)

References 34 publications

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“…29,30 A recent data on thrombophilia by D Amico et al showed that myeloproliferative disorders were the most common cause in PVT patients and thrombophilia work up in the PVT patients revealed PAI-1 4G-4G (plasminogen activator inhibitor type 1-4G/4G genotype) as the most common cause (55.5%) followed by MTHFR mutation (28.6%), factor V Leiden mutation (7.4%) and prothrombin gene mutation (7.4%). Atleast one thrombophilic state was present in 81.5% and more than one hypercoagulable state was present in 18.5%.…”

Section: Inherited Prothrombotic Disordersmentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

150

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: Inherited Prothrombotic Disordersmentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

150

147

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“…A recent meta-analysis questioned the utility of anti-thrombin, protein C, and protein S levels to predict PVT [34], while measurement of congenital deficiencies of anticoagulants may be informative in patients with cirrhosis and a personal or familial history of thrombosis. Carriers of polymorphisms of factor V or prothrombin gene were at increased risk of PVT [35], as were those with increased levels of factor VIII [36]. Anti-phospholipid syndrome also carries a risk for thrombosis in the population without cirrhosis; however, the laboratory diagnosis of this syndrome which is based on phospholipid-dependent coagulation tests, is unreliable in patients with cirrhosis, who have abnormal coagulation tests at baseline.…”

Section: Testing For Thrombophiliamentioning

confidence: 99%

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

Andriulli

Tripodi

Angeli

et al. 2016

Digestive and Liver Disease

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a b s t r a c tPatients with cirrhosis present with hemostatic alterations secondary to reduced availability of procoagulant and anti-coagulant factors. The net effect of these changes is a rebalanced hemostatic system. The Italian Association of the Study of the Liver (AISF) and the Italian Society of Internal Medicine (SIMI) promoted a consensus conference on the hemostatic balance in patients with cirrhosis. The consensus process started with the review of the literature by a scientific board of experts and ended with a formal consensus meeting in Rome in December 2014. The statements were graded according to quality of evidence and strength of recommendations, and approved by an independent jury. The statements presented here highlight strengths and weaknesses of current laboratory tests to assess bleeding and thrombotic risk in cirrhotic patients, the pathophysiology of hemostatic perturbations in this condition, and outline the optimal management of bleeding and thrombosis in patients with liver cirrhosis.

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“…16 A recent study reported that high levels of factor VIII were independently associated with cirrhotic PVT, with odds ratio for thrombosis being 6.0 if factor VIII levels were above 129 IU/dl. 28 While in non-cirrhotic patients, PVT is related to prothrombotic states (myeloproliferative diseases and/or inherited coagulation disorders) in a significant percentage of patients, in cirrhotic patients portal hemodynamics also plays an important role in the development of PVT. 29 Portal flow is reduced in cirrhotic livers due to increased intrahepatic vascular resistance and this phenomenon is further pronounced as liver disease progresses.…”

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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High levels of factor VIII and risk of extra-hepatic portal vein obstruction

Cited by 67 publications

References 34 publications

Portal Vein Thrombosis

Portal Vein Thrombosis

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

Portal Vein Thrombosis in Cirrhosis

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