Association between plasma fibrinogen levels and mortality in acute-on-chronic hepatitis B liver failure.

Zhexin Shao,Jie Zhang,Guofang Feng,Ying Zhao,Limin Feng,Juanwen Zhang

doi:10.1155/2015/468596

Abstract

Acute-on-chronic liver failure (AoCLF) is the most common type of liver failure and is associated with high mortality. Fibrinogen is critical in maintaining primary and secondary hemostasis. Therefore, we prospectively analyzed the association between fibrinogen and outcomes in AoCLF patients. Plasma fibrinogen was measured in 169 AoCLF, 173 chronic hepatitis B (CHB), and 171 healthy patients using a coagulation method. The predictive ability of fibrinogen for 3-month mortality in AoCLF patients was assessed using receiver operating characteristic (ROC) curve and multivariable logistic regression analyses. Plasma fibrinogen was significantly lower in nonsurvivor AoCLF patients compared with survivor AoCLF, CHB, and control patients. The sensitivity, specificity, and area under the ROC curve of 1/fibrinogen predicting mortality in AoCLF patients were 66.7%, 72.5%, and 0.746 (95% confidence interval (CI): 0.672–0.820, P < 0.001), and the fibrinogen cutoff value was 0.90 g/L. On multivariate logistic regression analysis, low fibrinogen was an independent factor predicting mortality (odds ratio: 0.304; 95% CI: 0.094–0.983; P = 0.047). Nonsurvivor AoCLF patients had significantly decreased fibrinogen levels, suggesting that low plasma fibrinogen may be a useful predictor of poor prognosis in AoCLF patients.

Highlights

Hepatitis B virus (HBV) infection is a global health threat with approximately 1% of HBV-infected patients developing liver failure, a prevalence that primarily reflects the HBV virulence combined with spontaneous or induced factors [1]
The fibrinogen level was 1.39 ± 0.58 g/L in the acute-on-chronic liver failure (AoCLF) group, which was significantly lower than the levels in the healthy control and chronic hepatitis B (CHB) groups
During the first phase of clot formation, fibrinogen serves as a molecular link mediating platelet aggregation, and during the second phase, fibrinogen initiates fibrin polymerization and converts to a fibrin matrix that gives the clot shape, strength, flexibility, and stability [16,17,18]

Summary

Introduction

Hepatitis B virus (HBV) infection is a global health threat with approximately 1% of HBV-infected patients developing liver failure, a prevalence that primarily reflects the HBV virulence combined with spontaneous or induced factors [1]. The liver plays a key role in hemostasis regulation [4]. In patients with liver disease, hemostasis tests may be required to evaluate the severity of hepatocellular failure [6]. Fibrinogen (coagulation factor I) is a 300 kDa soluble plasma glycoprotein comprising two identical subunits, each containing three polypeptide chains (Aα, Bβ, and γ) and synthesized in the liver [7]. Fibrinogen plays several key roles in maintaining both primary and secondary hemostasis and is converted by thrombin into an insoluble fibrin network that, together with platelet aggregates, induces hemostasis in response to rupture of the endothelium [8]. Cong et al observed that the plasma fibrinogen concentration in liver cirrhosis patients progressively decreased as liver cirrhosis

Methods

Results

Conclusion