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Background and Aim: Alcohol‐associated hepatitis (AAH) is an acute, inflammatory liver disease with severe short‐term and long‐term morbidity and mortality. AAH can lead to severe complications including hepatic failure, gastrointestinal bleeding, sepsis, and the development or decompensation of cirrhosis. Rifaximin is an antibiotic that reduces bacterial overgrowth and gut translocation, and it may have a role in decreasing systemic inflammation and infection in patients with AAH. Therefore, we conducted a systematic review and meta‐analysis to evaluate the role of rifaximin in the management of AAH. Methods: A comprehensive search strategy was used to identify studies that met our inclusion criteria in Embase, MEDLINE (PubMed), Cochrane Library, Web of Science Core Collection, and Google Scholar. Outcomes of interest included rates of infection, 90‐day mortality, and overall mortality between the rifaximin versus non‐rifaximin group. Open Meta Analyst software was used to compute the results. Results: Three studies with a total of 162 patients were included in the final meta‐analysis. Of the three studies, two were randomized control trials (RCTs), and one was a case–control study. There was a significantly lower rate of infection in the rifaximin group versus the non‐rifaximin group (RR: 0.331, 95% CI: 0.159–0.689, I2 = 0%, P = 0.003). There was no significant difference in 90‐day mortality in the rifaximin versus non‐rifaximin group (RR: 0.743, 95% CI: 0.298–1.850, I2 = 24%, P = 0.523), nor was there a significant difference in overall mortality (RR: 0.624, 95% 95% CI: 0.299–1.3, I2 = 7.1%, P = 0.208). Conclusions: The use of rifaximin in AAH is associated with a lower rate of infection rate than the non‐rifaximin group. Additional research is needed to determine whether this effect is more pronounced in patients concurrently being treated with prednisolone. Differences in 90‐day or overall mortality did not reach statistical significance. Further studies, particularly large randomized controlled trials, are needed to establish the role of rifaximin in AAH, especially as an adjunct therapy with prednisolone. [ABSTRACT FROM AUTHOR]

Background and Aim: Inflammation plays a pivotal role in liver injury. Gabexate mesilate (GM, a protease inhibitor) inhibits inflammation by blocking various serine proteases. This study examined the effects of GM on hepatic encephalopathy in rats with acute and chronic liver failure. Methods: Acute and chronic liver failure (cirrhosis) were induced by intraperitoneal TAA administration (350 mg/kg/day for 3 days) and common bile duct ligation, respectively, in male Sprague-Dawley rats. Rats were randomized to receive either GM (50 mg/10 mL/kg) or saline intraperitoneally for 5 days. Severity of encephalopathy was assessed by the Opto-Varimex animal activity meter and hemodynamic parameters, mean arterial pressure and portal pressure, were measured (only in chronic liver failure rats). Plasma levels of liver biochemistry, ammonia, nitrate/nitrite, interleukins (IL) and tumor necrosis factor (TNF)-α were determined. Results: In rats with acute liver failure, GM treatment significantly decreased the plasma levels of alanine aminotransferase ( P = 0.02), but no significant difference of motor activity, plasma levels of ammonia, IL-1β, IL-6, IL-10 and TNF-α or survival was found. In chronic liver failure rats, GM significantly lowered the plasma TNF-α levels ( P = 0.04). However, there was no significant difference of motor activity, other biochemical tests or survival found. GM-treated chronic liver failure rats had higher portal pressure ( P = 0.04) but similar mean arterial pressure in comparison with saline-treated rats. Conclusions: Chronic GM treatment does not have a major effect on hepatic encephalopathy in rats with TAA-induced acute liver failure and rats with chronic liver failure induced by common bile duct ligation. [ABSTRACT FROM AUTHOR]

Background and Aim: Idiopathic portal hypertension (IPH) is thought to be benign if bleeding gastroesophageal varices can be controlled or prevented. A recent autopsy of a woman with IPH who died of hemorrhagic intestinal infarction related to mesenteric thrombosis prompted the authors to examine the terminal antemortem features and causes of death of IPH. Methods: Autopsy cases registered as IPH from 1986 to 1997 were surveyed in the records of the Annuals of Pathological Autopsy Cases in Japan, with permission from the Japanese Society of Pathology. The records of 65 of these cases were collected and examined pathologically. Results: It was found that the most frequent cause of death in these cases was (i) bacterial infection (20 cases). The next three causes of death were directly or indirectly related to hepatic disease or its altered portal hemodynamics as follows: (ii) progressive hepatic failure (16 cases); (iii) massive hemorrhage from ruptured gastroesophageal varices (11 cases); and (iv) hemorrhagic intestinal infarction due to mesenteric venous thrombosis (5 cases). Although portal venous thrombosis was closely associated with (iv), (ii) and (iii) seemed not to be associated with portal venous thrombosis. In addition, intracranial hemorrhage and other heterogeneous factors were identified as the cause of death in five cases and eight cases, respectively. Conclusion: These results suggest that progressive hepatic failure and intestinal hemorrhagic infarction should be considered in addition to rupture of gastroesophageal varices when monitoring patients with IPH. Clinicians should be also aware of severe bacterial infection and intracranial hemorrhage as a fatal complication of IPH. [ABSTRACT FROM AUTHOR]

Background: This study looked at the frequency of co-infection with multiple hepatotropic viruses and the effect of such infection on the course and outcome of acute sporadic viral hepatitis (AVH) and fulminant hepatic failure (FHF) in children. Methods: Consecutive children up to 15 years of age presenting with AVH or FHF between January 1998 and July 2002 were evaluated prospectively. The following viral markers were assessed in all children: immunoglobulin M (IgM) anti-hepatitis A virus (HAV), IgM anti-hepatitis E virus (HEV), hepatitis B surface antigen (HBsAg), IgM anti-hepatitis B core (HBc), and anti-hepatitis C virus (HCV). Results: A total of 149 children were included in the study, 122 with AVH and 27 with FHF. Co-infection with multiple viruses was detected in 30 (24.6%) AVH patients (A + E in 24, A + B in three, and E + B, A + C and A + E + B in one each) and seven (26%) FHF patients (A + E in five, and A + B and E + B in one each). The majority of single infections were due to HAV (AVH 70/92, FHF 14/20) followed by HEV (AVH 9/92, and FHF 5/20). HEV infection was associated with infection with another agent in 88% of patients with AVH (odds ratio 53, 95% confidence interval 15–186, P < 0.0001). Frequency of anicteric state, prolonged cholestasis, relapsing hepatitis, ascites, hemolysis and mortality rates were similar in the single and multiple infection groups for both AVH and FHF patients. Conclusions: Co-infection with multiple viruses is observed in one-quarter of patients with sporadic AVH in childhood. Such infection does not produce a more severe disease. HEV positivity is a strong marker for multiple infections. [ABSTRACT FROM AUTHOR]

Severe acute exacerbations of chronic hepatitis B virus (HBV) infection can spontaneously occur and rapidly progress to fatal hepatic failure. The purpose of the present paper was to identify factors that could influence the rapid progression of liver disease to hepatic failure, and assess the effects of lamivudine on serious disease.Twenty-five patients with spontaneous severe acute exacerbation (accompanied by jaundice and coagulopathy) were consecutively treated with lamivudine. Their clinical outcomes were compared with those of 25 lamivudine-untreated patients, as historical controls.Six lamivudine-treated patients (24%)and seven controls (28%) rapidly developed hepatic failure. Lamivudine monotherapy did not significantly prevent progression to hepatic failure. Multivariate analysis identified baseline serum bilirubin≥6 mg/dL (odds ratio[OR]: 5.61; 95% confidence interval[CI]: 1.66–21.61;P = 0.018), pre-existing cirrhosis (OR: 4.52; 95%CI: 1.26–30.42;P = 0.034), and baseline prothrombin time<40% (OR: 3.75; 95%CI: 1.03–43.86;P = 0.045) as independent determinants of the event. Of the aforementioned patients with hepatic failure, three lamivudine-treated patients (50%) and two controls (29%) survived (P > 0.15). However, lamivudine induced a sustained normalization of liver function and inhibited the development of cirrhosis in survivors.Lamivudine monotherapy conferred no significant protection against rapid progression of the disease to hepatic failure, but it resulted in long-term benefits. Lamivudine combined with other drugs could be more beneficial for patients with the aforementioned risk factors.© 2004 Blackwell Publishing Asia Pty Ltd [ABSTRACT FROM AUTHOR]

AbstractBackground and Aim: The serum hyaluronic acid (HA) concentrations reflect the degree of hepatic fibrosis and sinusoidal endothelial cell damage. The HA concentrations were examined to evaluate liver damage during the perioperative period of hepatectomy. Methods: The HA level of serum samples from 79 patients who underwent a hepatectomy was measured, and the results were compared to conventional liver function tests, the degree of fibrosis, liver regeneration and complications. Results: Hyaluronic acid concentrations correlated with the severe fibrosis or histological activity index, and also correlated with liver function tests including transaminase level, platelet counts, prothrombin time activity, indocyanine green retention rate at 15 min (ICG R15), liver activity at 15 min by technetium-99m galactosyl human serum albumin scintigraphy (LHL 15), and portal pressure. The HA level postoperatively correlated with liver function, especially with total bilirubin. Hyaluronic acid levels at day 28 postoperatively correlated with ICG R15 and LHL 15. The hyaluronic acid level before surgery and at day 28 postoperatively correlated with the regeneration of remnant liver in major hepatectomy. The HA levels were significantly higher in patients with hepatic failure or prolonged ascites. Conclusion: Our results indicate that the measurement of the HA level is useful for monitoring liver damage or predicting complications associated with liver surgery. [ABSTRACT FROM AUTHOR]