Von Willebrand Factor as a Biomarker for Liver Disease - An Update.

The von Willebrand factor (vWF) is best known for its role in the hemostatic pathway, aiding platelet adhesion and aggregation, as well as circulating along with coagulation factor VIII, prolonging its half-life. However, vWF is more than a hemostatic protein and is a marker of endothelial dysfunction in patients with cirrhosis. The levels of vWF increase progressively as cirrhosis progresses. Despite its qualitative defects, it can support and carry out its hemostatic role and contribute to a pro-coagulant disbalance. Moreover, it has been shown to be a good noninvasive marker for predicting clinically significant portal hypertension (CSPH). The vWF has been shown to predict decompensation and mortality among cirrhosis patients independently of the stage of liver disease and severity of portal hypertension. Increased vWF levels in the setting of endothelial injury predict bacterial translocation and systemic inflammation. The vWF-to-thrombocyte ratio (VITRO) score adds to the diagnostic ability of vWF alone in detecting CSPH non-invasively. Not only have vWF levels been shown to help predict the risk of hepatocellular carcinoma (HCC) among cirrhosis patients, but they also predict the risk of complications post-resection for HCC and response to systemic therapies. vWF-induced portal microthrombi have been purported to contribute to the pathogenesis of acute liver failure progression as well as non-cirrhotic portal hypertension. The prospect of modulation of vWF levels using drugs such as non-selective beta-blockers, statins, anticoagulants, and non-absorbable antibiotics and its use as a predictive biomarker for the response to these drugs needs to be explored.