81 a Role for Anticoagulation in Fibrogenesis: Suppression of Human Hepatic Stellate Cell Contractility and Liver Fibrosis in Vitro and Vivo

Dhar, Ameet; Anstee, Quentin M.; Sadiq, Fouzia; Levene, Adam P; Cobbold, Jeremy; Petts, Gemma; Taylor-Robinson, Simon D; Goldin, R.D.; Thursz, Mark

doi:10.1016/s0168-8278(12)60095-6

Cited by 3 publications

(1 citation statement)

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“…If prothrombotic states accelerate liver fibrosis and coagulation proteins activate hepatic stellate cells to promote fibrosis, then conversely, anticoagulation may reverse hepatic fibrosis. In fact, findings from several animal studies support this hypothesis; warfarin and thrombin antagonists have shown anti-fibrotic properties in a carbon tetrachloride mouse model of liver fibrosis [ 114 ]; Rivaroxaban, an oral direct-acting FXa inhibitor, has proven more effective than direct thrombin inhibition in suppressing fibrosis in a thioacetamide mouse model of liver fibrosis [ 115 ]; prolonged administration of enoxaparin in a rat model of cirrhosis (induced using carbon tetrachloride or thioacetamide) resulted in the improvement of both portal hypertension and liver fibrosis, presumably by potentiating fibrosis regression and ultimately decreasing portal pressure [ 116 ]. Alongside the clinical response to warfarin therapy in pulmonary fibrosis, these results provide a rationale for testing anticoagulants as a treatment for liver fibrosis wherein the cause of the underlying liver disease cannot be removed.…”

Section: From Bench-to-bed Side: Should We Consider Thromboprophylmentioning

confidence: 99%

Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma

Zanetto

Campello

Spiezia

et al. 2018

Cancers

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It is common knowledge that cancer patients are more prone to develop venous thromboembolic complications (VTE). It is therefore not surprising that patients with hepatocellular carcinoma (HCC) present with a significant risk of VTE, with the portal vein being the most frequent site (PVT). However, patients with HCC are peculiar as both cancer and liver cirrhosis are conditions that can perturb the hemostatic balance towards a prothrombotic state. Because HCC-related hypercoagulability is not clarified at all, the aim of the present review is to summarize the currently available knowledge on epidemiology and pathogenesis of non-malignant thrombotic complications in patients with liver cirrhosis and HCC. They are at increased risk to develop both PVT and non-splanchnic VTE, indicating that both local and systemic factors can foster the development of site-specific thrombosis. Recent studies have suggested multiple and often interrelated mechanisms through which HCC can tip the hemostatic balance of liver cirrhosis towards hypercoagulability. Described mechanisms include increased fibrinogen concentration/polymerization, thrombocytosis, and release of tissue factor-expressing extracellular vesicles. Currently, there are no specific guidelines on the use of thromboprophylaxis in this unique population. There is the urgent need of prospective studies assessing which patients have the highest prothrombotic profile and would therefore benefit from early thromboprophylaxis.

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Section: From Bench-to-bed Side: Should We Consider Thromboprophylmentioning

confidence: 99%

Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma

Zanetto

Campello

Spiezia

et al. 2018

Cancers

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Anticoagulation in chronic liver disease

Dhar

Mullish

Thursz

2017

Journal of Hepatology

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Anticoagulation in Patients with Liver Cirrhosis (Literature Review)

Енисеева

2019

Acta biomedica scientifica

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Liver cirrhosis is accompanied by complex hemostatic disorders with an increase in the risk of both hemorrhagic and thrombotic complications. Reduced coagulation protein synthesis, such as factors II, VII, IX, X and thrombocytopenia are associated with an increased risk of bleeding. Reducing the synthesis of such anticoagulants as protein C, protein S, antithrombin III is accompanied by increased generation of thrombin, which leads to procoagulant status, increased risk of venous thrombosis, pulmonary embolism, and portal vein thrombosis. Activation of the coagulation cascade increases the risk of thrombosis, and also plays an important role in liver damage, contributing to the progression of fibrosis. Cirrhosis increases the risk of thromboembolic complications of atrial fibrillation.Anticoagulants are necessary for the prevention of thrombosis and thromboembolic complications. However, there are no large prospective studies. There is insufficient data on the safety of anticoagulant therapy in cirrhosis. There are difficulties in monitoring anticoagulation in the application of vitamin K antagonists and low molecular weight heparins.The review presents the available data on the use of warfarin, unfractionated heparin, low molecular weight heparins and direct oral anticoagulants in patients with liver cirrhosis, indicating the need for prevention of venous thrombosis in patients with risk factors, the possibility of preventing decompensation of cirrhosis, reducing the frequency of cardioembolic strokes in patients with atrial fibrillation.

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81 a Role for Anticoagulation in Fibrogenesis: Suppression of Human Hepatic Stellate Cell Contractility and Liver Fibrosis in Vitro and Vivo

Cited by 3 publications

References 0 publications

Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma

Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma

Anticoagulation in chronic liver disease

Anticoagulation in Patients with Liver Cirrhosis (Literature Review)

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