New concepts of coagulation and bleeding in liver disease

Caldwell, Stephen H.

doi:10.1007/s11739-009-0345-1

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…However, in patients with liver cirrhosis and with > 50,000 platelets/mL, decreased synthesis of anticoagulant factors and normal generation of thrombin, resulting in a nearnormal hemostatic balance, has been reported. [14][15][16] In keeping with this, portal vein thrombosis and occlusion of small intrahepatic vein branches are common findings in these patients. 17 Autopsy and explantation studies have shown portal vein thrombosis in as many as 54% of cirrhotic patients.…”

Section: Thrombocytopenia In Liver Diseasesupporting

confidence: 72%

Prevention of Venous Thromboembolism in Medical Patients with Thrombocytopenia or with Platelet Dysfunction: A Review of the Literature

Tufano

Guida

Minno

et al. 2011

Semin Thromb Hemost

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Current guidelines for venous thromboembolism (VTE) primary prophylaxis are based on randomized clinical trials that exclude subjects at a potentially high bleeding risk. Thus no specific recommendation/algorithm for pharmacological prophylaxis in patients with thrombocytopenia and/or platelet dysfunction is available. Because at least 25% of subjects admitted to medical departments exhibit these conditions, information on this subject is provided here to optimize their VTE prophylaxis. Low platelet number/function and clotting abnormalities are common in patients with liver cirrhosis. However, these patients have a high incidence of portal and idiopathic venous thromboses, implying that cirrhotic coagulopathy does not protect against thrombosis. At variance with severe thrombocytopenia (< 50,000/mL), mild/moderate thrombocytopenia (> 50,000/mL) should not interfere with VTE prevention decisions. In severe thrombocytopenia, prophylaxis should be considered on an individual basis, however. In patients with antiphospholipid antibodies and thrombocytopenia, a thrombotic tendency is usually associated rather than a bleeding risk. VTE prophylaxis in high-risk conditions is thus suggested in these patients. Except in cases with contraindications to anticoagulation, antithrombotic prophylaxis should be always considered in hospitalized cancer patients with thrombocytopenia, especially in those with hematologic malignancies and multiple VTE risk factors. Aspirin treatment is not as effective as heparins in lowering the risk of VTE. Studies in stroke suggest that thromboprophylaxis with heparins is safe in patients with ischemic stroke undergoing aspirin treatment. The need for VTE prophylaxis in patients on chronic treatment with aspirin and/or clopidogrel should be evaluated after assessing the individual risk-benefit ratio.

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Section: Thrombocytopenia In Liver Diseasesupporting

confidence: 72%

Prevention of Venous Thromboembolism in Medical Patients with Thrombocytopenia or with Platelet Dysfunction: A Review of the Literature

Tufano

Guida

Minno

et al. 2011

Semin Thromb Hemost

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“…Because of the comparatively slow course of the disease, the prevalence of coronary disease, and the relative hypercoagulable state, NAFLD and NASH appear to be reasonable disease states to further explore this idea in human trials. Pitfalls will remain as there are no good laboratory tests clinically available to measure hypercoagulability in liver disease patients, 121 bleeding risk and tolerability are unproven, and noninvasive measures of fibrosis are still forthcoming in this population. As long as liver biopsy is the gold standard for fibrosis assessment, anticoagulation trials will be difficult logistically and poorly accepted by clinicians and patients.…”

Section: Microvascular Diseasementioning

confidence: 99%

Hypercoagulation and Thrombophilia in Nonalcoholic Fatty Liver Disease: Mechanisms, Human Evidence, Therapeutic Implications, and Preventive Implications

2012

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Nonalcoholic fatty liver disease (NAFLD) is a spectrum of disorders with a high prevalence in the industrialized world. Despite the high prevalence, the etiology and fundamental pathophysiology for the disease process is poorly understood. There is now a growing fund of knowledge suggesting that the ongoing inflammatory state associated with NAFLD leads to a low-level activation of the coagulation system. Although the data supporting this activation of the coagulation system are significant, the link with end-organ disease, mainly cardiovascular disease, is less firm and mostly epidemiological. In this review, we will explore the evidence for and against a hypercoagulable or thrombophilic state in NAFLD. We will examine possible pathophysiologic explanations and mechanisms, human epidemiologic and population-based data, and the possible therapeutic and preventative implications for treatment of thrombophilia in patients with this disease process.

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“…A complex balance between the pro‐ and anticoagulation systems exists in hepatobiliary disease . Classically, patients with liver disease were thought to be hypocoagulable, but recent evidence suggests hypercoaguable states may be present.…”

Section: Introductionmentioning

confidence: 99%