Thus, the recent Baveno V consensus conference on PH VX-765 nmr recommended to investigate and identify further noninvasive markers for PH.3 Hepatic decompensation is the most important predictor of prognosis and mortality in patients with liver cirrhosis, with several precipitating factors contributing to the first event of decompensation.5 Endothelial dysfunction is considered as an important determinant of the increased

intrahepatic vascular resistance in cirrhotic livers.6, 7 von Willebrand factor antigen (vWF-Ag) is released by activated endothelial cells (ECs) and therefore represents an indicator of EC activation8 and plays a crucial role in high shear stress, depending on primary hemostasis. Furthermore, in patients with liver cirrhosis, elevated levels of vWF-Ag are frequently observed.9 vWF-Ag levels were also shown to be an independent risk factor of myocardial infarction and mortality in patients with angina pectoris.10, 11 Although it is established that VWF-Ag is increased in patients with cirrhosis, no data on the association of vWF-Ag and portal pressure exist. One recent study describes a correlation

between vWF-Ag and HVPG in patients with CSPH, but patients without PH were not included, and thus the diagnostic power of vWF-Ag for CSPH could not be evaluated.12 Because vWF-Ag plays a phosphatase inhibitor library crucial role in primary hemostasis and is an indicator of endothelial selleck activation and development of thrombotic vascular obliteration, which are all discussed as possible mechanisms leading to PH,13 we hypothesized that patients with CSPH have increased vWF-Ag levels, compared to patients without CSPH. Thus, the aims of our study were (1) to evaluate the diagnostic performance of vWF-Ag to detect clinically significant PH defined by HVPG, compared to TE in patients with compensated liver cirrhosis (i.e., when CSPH is not clinically evident), and (2) to evaluate vWF-Ag levels in the prediction of mortality

and decompensation in patients with liver cirrhosis. Ag, antigen; AUC, area under the curve; CI, confidence interval; CPS, Child Pugh score; CSPH, clinically significant portal hypertension; ECs, endothelial cells; HCC, hepatocellular carcinoma; HR, hazard ratio; HVPG, hepatic venous pressure gradient; IFN, interferon; IQR, interquartile range; ITD, intention to diagnose; LT, liver transplantation; MELD, Model for End-Stage Liver Disease; NPV, negative predictive value; OR, odds ratio; PH, portal hypertension; PPV, positive predictive value; ROC, receiver operator characteristic TE, transient elastography; TIPS, transjugular intrahepatic portosystemic shunt; vWF, von Willebrand factor. Patients referred to the hepatic hemodynamic laboratory at the Department of Internal Medicine III, Division of Gastroenterology, Medical University of Vienna (Vienna, Austria) were included between September 2006 and December 2009.