Coagulation inhibitors in alcoholic liver cirrhosis

Raya-Sánchez, J.M.; González‐Reimers, Emilio; Rodriguez-Martin, Juan; Santolaria-Fernández, Francisco; Molina-Perez, M.; Rodríguez-Moreno, F.; Martı́nez-Riera, Antonio

doi:10.1016/s0741-8329(97)00082-7

Cited by 34 publications

(22 citation statements)

References 13 publications

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“…The results obtained in the present study confirm several earlier reports showing that haemostatic tests could be of great practical value in the assessment of hepatocyte function in liver disease [6,13,27,40,41]. Not surprisingly, our study showed that the reduction in the level of antithrombotic proteins is strongly related to the severity of liver cirrhosis according to the MELD scoring system.…”

Section: Factorsupporting

confidence: 91%

Thrombotic risk factors in patients with liver cirrhosis: Correlation with MELD scoring system and portal vein thrombosis development

Zocco

Stasio

Cristofaro

et al. 2009

Journal of Hepatology

415

353

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Section: Factorsupporting

confidence: 91%

Thrombotic risk factors in patients with liver cirrhosis: Correlation with MELD scoring system and portal vein thrombosis development

Zocco

Stasio

Cristofaro

et al. 2009

Journal of Hepatology

415

353

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“…However, even anticoagulants such as Proteins C and S as well as the levels of circulating protease inhibitors are reduced in hepatic insufficiency. 18,19 The physiologic effects of a deficiency of anticoagulants is not reflected in the PT or APTT, which measure only the procoagulant side of the hemostatic pathway. In vivo it is always the balance between the procoagulant and anticoagulant factors that ultimately determines whether bleeding, thrombosis, or appropriate hemostasis will occur in a particular setting.…”

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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“…cirrhosis; thus, elevated PT/INR values may not necessarily reflect the actual coagulative status of these patients. 1,2 All hospitalized cirrhosis patients should be assessed for VTE risk and, when appropriate, an individualized course of a prophylaxis anticoagulant should be initiated. Evaluation for portal or hepatic vein thrombosis might provide additional insight.…”

mentioning

confidence: 99%