Primary Hemostasis in Chronic Liver Disease and Cirrhosis: What Did We Learn over the Past Decade?

Marie-Astrid Van Dievoet,Xavier Stephenne,Stéphane Eeckhoudt

doi:10.3390/ijms21093294

Abstract

Changes in primary hemostasis have been described in patients with chronic liver disease (CLD) and cirrhosis and are still subject to ongoing debate. Thrombocytopenia is common and multifactorial. Numerous studies also reported platelet dysfunction. In spite of these changes, primary hemostasis seems to be balanced. Patients with CLD and cirrhosis can suffer from both hemorrhagic and thrombotic complications. Variceal bleeding is the major hemorrhagic complication and is mainly determined by high portal pressure. Non portal hypertension-related bleeding due to hemostatic failure is uncommon. Thrombocytopenia can complicate management of invasive procedures in CLD patients. Recently, oral thrombopoietin agonists have been approved to raise platelets before invasive procedures. In this review we aim to bundle literature, published over the past decade, discussing primary hemostasis in CLD and cirrhosis including (1) platelet count and the role of thrombopoietin (TPO) agonists, (2) platelet function tests and markers of platelet activation, (3) von Willebrand factor and (4) global hemostasis tests.

Highlights

Chronic liver disease (CLD) was for a long time considered as a model of acquired hemorrhagic disease, reflected by, for example, prolonged prothrombin time
Variable thrombocytopenia is present in the majority of CLD patients [14]. This is in part counterbalanced by elevated von Willebrand factor (VWF) supporting enhanced platelets’ adhesion [15,16]
Eltrombopag is not recommended as an alternative for platelet transfusion for patients with CLD due to thrombotic complications during the ELEVATE clinical trial [43]

Summary

Introduction

Chronic liver disease (CLD) was for a long time considered as a model of acquired hemorrhagic disease, reflected by, for example, prolonged prothrombin time. Patients with CLD and cirrhosis can suffer from both hemorrhagic and thrombotic complications. A distinction is made between portal hypertension-related bleeding, spontaneous bleeding and provoked bleeding. The risk of variceal hemorrhage is mainly determined by portal hypertension (hepatic venous pressure gradient > 12 mmHg), severity of liver disease, the size of varices and presence of red signs [3,4]. Thrombotic complications encompass portal vein thrombosis (PVT) and venous thromboembolism. In a recent meta-analysis, an increased venous thromboembolic risk was confirmed in cirrhotic patients with a prevalence of 3.7% [6]. Cirrhotic subjects were more at risk of deep venous thrombosis and pulmonary embolism compared to controls. A lower incidence of PVT, hepatic decompensation and an improved survival were reported in patients with advanced cirrhosis, randomized to prophylaxis with low molecular weight heparin, compared to standard of care [7]. Liver transplantation without the need for blood products is feasible in this patient group [13]

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