Alpha-Fetoprotein as a Predictive Marker for Patients with Hepatitis B-Related Acute-on-Chronic Liver Failure

Background and Aims. The value of alpha-fetoprotein (AFP) in hepatitis B-related acute-on-chronic liver failure (HBACLF) is not fully understood. The present study aimed to evaluate the prognostic effect of AFP on the prediction of HBACLF outcomes. Methods. We investigated a cohort of patients with HBACLF admitted from January 2013 to May 2017. The endpoint of followup was 180 days, death, or liver transplantation. AFP concentrations were estimated on admission. To make statistical comparisons, we used chi-squared test, receiver operating characteristic (ROC) curve analysis, survivorship curve analysis, and Cox proportional-hazards model. Results. A total of 92 patients (81.5% male, median age of 46 years) were included. Overall survival rate within 180 days was 43.48%, and the value of log10AFP⁡  ≥ 2.04 indicated a better prognosis with 76.9% specificity and 62.5% sensitivity for patients with HBACLF. Age (HR 1.041), total bilirubin (HR 1.004), log10AFP⁡  (HR 2.155), and INR (HR 1.446) were found to be risk factors of survival. Conclusion. AFP could be a useful marker to predict outcomes of acute-on-chronic liver failure

Deoxycholic acid (DCA) confers an intestinal phenotype on esophageal squamous epithelium via induction of the stemness-associated reprogramming factors OCT4 and SOX2

<p>Barrett's esophagus (BE) is essentially a metaplasia in which the normal stratified squamous epithelium is replaced by columnar epithelium. This study focuses on the involvement of OCT4 and SOX2, 2 key cell-reprogramming factors, in the deoxycholic acid (DCA)-induced expression of the intestinal hallmarks Cdx2 and MUC2 using both in vivo and in vitro models. Up-regulated expression of OCT4 and down-regulated expression of SOX2 were observed in BE compared with normal esophagus and esophagitis. Consistent with the data in vivo, DCA induced time-dependent expression of OCT4 at both the mRNA and protein levels and decreased nuclear expression of SOX2 in Het-1A cells. Down-regulation of OCT4 expression by siRNA abrogated DCA-induced expression of Cdx2 and MUC2, whereas siRNA against SOX2 significantly upregulated the expression of both Cdx2 and MUC2. Our data indicate that both OCT4 and SOX2 play important roles in the development of BE triggered by bile acid reflux.</p