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Background: Portal hypertension (PHT) is defined as a portal venous pressure gradient (PVPG) exceeding 5 mm Hg, which results in severe clinical manifestations. However, the validity of intraoperative PVPG monitoring and the association between PHT and bacterial translocation after liver transplantation remain unclear., Methods: In this retrospective study, 223 patients who underwent primary adult-to-adult living donor liver transplantation from 2008 to 2015 were divided into 2 groups based on the PVPG at the end of the operation: high PVPG (>5 mm Hg, n = 69) and low PVPG (≤5 mm Hg, n = 154). The clinical factors were compared between the groups, and the association between a high PVPG and posttransplant bacteremia/bacterial infections was investigated., Results: The high PVPG group had a significantly higher incidence of bacteremia (46% vs 24%, P < 0.001), higher 90-day mortality rate (20% vs 7%, P = 0.002), and poorer 1-year survival (71% vs 86%, P = 0.006). The high PVPG group had a particularly higher incidence of bacteremia caused by "gut bacteria" including Enterobacteriaceae, Bacteroides spp., and Enterococcus spp. (29% vs 12%, P = 0.003). Multivariate analysis showed that a PVPG greater than 5 mm Hg (odds ratio, 2.55; 95% confidence interval, 1.18-5.55; P = 0.017) was an independent predictor of bacteremia due to gut bacteria., Conclusions: Monitoring of the PVPG is clinically meaningful for predicting patients' prognosis. In particular, a high PVPG with a threshold of 5 mm Hg at the end of adult-to-adult living donor liver transplantation may increase gut-related bacteremia through the mechanism of bacterial translocation, resulting in early mortality. more...

Alcoholic liver disease is a major medical burden. Alcohol abuse is the cause for end-stage liver disease in approximately 50% of all patients with cirrhosis. Chronic alcohol consumption is associated with changes in the composition of the intestinal microbiota and gut barrier dysfunction. The portal vein is the major communication route between the intestine and the liver. Increased intestinal permeability allows microbial components, bacteria, and metabolites to translocate to the liver. The liver communicates with the intestine via mediators in the systemic circulation and the biliary system. In this review, the authors describe the changes that occur in the intestinal microbiota with chronic alcohol consumption. They further review the bilateral communication between the liver and the gut, and discuss how this interaction affects the progression of alcoholic liver disease., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.) more...

Background & Aims: Chronic infection with hepatitis B or C virus (HBV or HCV) is a leading cause of cirrhosis by unknown mechanisms of pathogenesis. Translocation of gut microbial products into the systemic circulation might increase because of increased intestinal permeability, bacterial overgrowth, or impaired clearance of microbial products by Kupffer cells. We investigated whether the extent and progression of liver disease in patients with chronic HBV or HCV infection are associated with microbial translocation and subsequent activation of monocytes., Methods: In a retrospective study, we analyzed data from 16 patients with minimal fibrosis, 68 with cirrhosis, and 67 uninfected volunteers. We analyzed plasma levels of soluble CD14 (sCD14), intestinal fatty acid binding protein, and interleukin-6 by enzyme-linked immunosorbent assay, and lipopolysaccharide (LPS) by the limulus amebocyte lysate assay, at presentation and after antiviral treatment., Results: Compared with uninfected individuals, HCV- and HBV-infected individuals had higher plasma levels of LPS, intestinal fatty acid binding protein (indicating enterocyte death), sCD14 (produced upon LPS activation of monocytes), and interleukin-6. Portal hypertension, indicated by low platelet counts, was associated with enterocyte death (P=.045 at presentation, P<.0001 after therapy). Levels of sCD14 correlated with markers of hepatic inflammation (P=.02 for aspartate aminotransferase, P=.002 for ferritin) and fibrosis (P<.0001 for γ-glutamyl transpeptidase, P=.01 for alkaline phosphatase, P<.0001 for α-fetoprotein). Compared to subjects with minimal fibrosis, subjects with severe fibrosis at presentation had higher plasma levels of sCD14 (P=.01) and more hepatic CD14+ cells (P=.0002); each increased risk for disease progression (P=.0009 and P=.005, respectively)., Conclusions: LPS-induced local and systemic inflammation is associated with cirrhosis and predicts progression to end-stage liver disease in patients with HBV or HCV infection., (Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.) more...