Superinfective Hepatitis E Virus Infection Aggravates Hepatocytes Injury in Chronic Hepatitis B.

Hepatitis E virus (HEV) infection is a major cause of morbidity in endemic areas. Its consequences among chronic hepatitis B (CHB) patients have been under-reported. The aim of this study was to assess the impact of superinfective HEV infection (acute and past) on virological and clinical features of patients with CHB infection. Clinical, biochemical, virological and immunological data of 153 CHB patients including 98 with hepatitis B virus (HBV) monoinfection and 55 with HBV-HEV superinfection with both HEV and HBV infection was retrospectively investigated and analyzed in this study conducted in Wuhan, China. An overall anti-HEV IgG seroprevalence was found to be 35.9% in CHB patients. HBV-HEV superinfection patients showed significantly higher rate of complications (ascites, hepato-renal syndrome & encephalopathy) (all with P=0.04), cirrhosis (P<0.001) and acute-on-chronic liver failure (P<0.001) than HBV monoinfection patients. They also displayed elevated ALTs (P<0.001) and total serum bilirubin (P<0.001) with diminished albumin (P<0.001) and HBV viral load (P<0.001). Cytokines assay revealed increased expression of IL-6 (P=0.02), IL-10 (P=0.009) and TNF-α (P=0.003) in HBV-HEV superinfection patients compared to HBV monoinfection patients. Our study demonstrated that HEV superinfection in CHB patients was associated with progressive clinical manifestation, which is likely due to the enhanced expression of cytokines related with hepatocytes necrosis. HEV was also associated with repressed HBV replication, but the underlying mechanism requires further investigation.

Course of disease and survival after onset of decompensation in hepatitis B virus-related cirrhosis.

BACKGROUND: Data regarding the outcome of hepatitis B virus (HBV)-related cirrhosis after the onset of decompensation is scanty. METHOD: From January 1998 to December 2008, a retrospective-prospective inception cohort study involving HBV-related decompensated cirrhotics was performed. Predictors of death and clinical events after the onset of decompensation were evaluated. Patients with co-infection with hepatitis C virus and/or human immunodeficiency virus, alcohol consumption to any degree and diabetes diagnosed before the detection of liver disease were excluded. RESULT AND ANALYSIS: Two hundred and fifty-three patients (231 males, 139 e-negative), including 102 untreated patients, were analysed. The mean (+/-SD) age was 43.0 (+/-12.0) years. The mean (+/-SD) follow-up period was 47 (+/-47) months. Decompensation was the first presentation of liver disease in 210 (83%) patients. Ascites (70%) and variceal bleed (28%) were predominant modes of decompensation. Forty-three (17%) patients died (22 vs 14% in untreated and treated cohort, respectively; P=0.002). Type 2 hepato-renal syndrome was the commonest cause of death (32%). Survival was independent of e-antigen status. In the total cohorts, predictors of death were occurrence of sepsis with systemic inflammatory response (SIRS), ascites as the initial mode of decompensation, absence of antiviral therapy and events of high-grade hepatic encephalopathy [hazards ratios (HR) of 4.4, 3.6, 2.2 and 1.7 respectively]. In the untreated cohort, initial decompensation with ascites and development of sepsis with SIRS were independent predictors of death (HR 8.5 and 2.3 respectively), while 5-year survival was higher in patients having initial decompensation with variceal bleed vs ascites (29 vs 16%, respectively, P=0.002). CONCLUSION: Decompensation with ascites and sepsis with SIRS predict reduced survival. Antiviral therapy beyond 6 months improves outcome.

Acute renal failure associated with the Rift Valley fever: a single center study.

Renal impairment is a frequent occurrence among patients with the Rift Valley fever (RVF), and is probably the result of hypovolemia and multiple organ dysfunctions in the majority of cases. This study was conducted to estimate the incidence of renal impairment in patients with RVF as well as to determine the associated mortality. Data of all patients admitted with renal impairment to the Gezira Hospital for Renal Diseases, Sudan, during the epidemic of RVF between September 2007 and January 2008 were analyzed. The total number of patients with RVF was 392 of whom, 194 were admitted to the Medani Teaching Hospital. Renal impairment was detected in 60% of the admitted patients; 90% of them needed dialysis treatment. The mortality rate was 31% in patients with acute renal failure, 25% in those with the hepatorenal syndrome and 31% in patients with primary hepatic involvement and mild renal impairment. The overall mortality was 40%. Our study suggests that RVF remains a major cause of acute renal failure with considerable mortality, although progression to chronic renal failure was not seen. Early renal substitution therapy fosters the best hope for survival.

Renal duplex Doppler ultrasound in patients with HCV related liver cirrhosis.

AIM: To study the renal resistive index (RI) and pulsatility index (PI) measured by renal Doppler in various stages of liver cirrhosis and their values to detect cirrhotic patients at risk for developing the hepatorenal syndrome. METHODS: This study included 60 cirrhotic patients divided into 4 groups (15 patients each): compensated liver cirrhosis (group A), diuretic responsive ascites (group B), refractory ascites (group C), hepatorenal syndrome (group D) and ten healthy persons as the control group (E). All patients were subjected to detailed history taking and clinical examination. Laboratory investigations included simple urine analysis, complete blood picture, liver function tests, blood urea and serum creatinine, serum sodium and serum potassium, 24-hour urine collection for sodium concentration, creatinine concentration and protein concentration. Ultrasonographic examination and renal duplex Doppler ultrasonography were undertaken to assess the RI and PI. RESULTS: The RI of both interlobar and arcuate arteries was significantly higher in all patient groups than in the control group (p<0.01). The RI was significantly higher in patients with refractory ascites than in patients with diuretic responsive ascites, and also in patients with diuretic responsive ascites than in patients with compensated cirrhosis (p<0.01); in patients with hepatorenal syndrome than in patients with diuretic responsive ascites and patients with compensated cirrhosis (p<0.0001). The PI was significantly higher in all patients groups than in the control group (p<0.01) and in patients with refractory ascites than in patients with diuretic responsive ascites and was also higher in patients with responsive ascites than in patients with compensated cirrhosis (p<0.0001). Also, the PI was significantly higher in patients with hepatorenal syndrome than in patients with responsive ascites and patients with compensated cirrhosis (p<0.0001). Creatinine clearance in patients with the hepatorenal syndrome was significantly lower than that of other different groups (p<0.0001) but there was no significant change in creatinine clearance between patients with compensated cirrhosis and control group. While creatinine clearance in patients with diuretic responsive ascites was significantly higher than that in patients with compensated cirrhosis (p<0.05) there was no significant change between patients with diuretic responsive ascites and patients with refractory ascites. CONCLUSION: Both renal resistive index and pulsatility index increase with the degree of hepatic decompensation. Renal duplex ultrasound which is a non-invasive, simple and easy method to study intrarenal hemodynamics in patients with liver cirrhosis may predict patients at risk of hepatorenal impairment.

Natural history of hepatitis B virus-related cirrhotic patients hospitalized to control ascites.

BACKGROUND AND AIM: Few studies have assessed the natural history of hepatitis B virus (HBV)-related cirrhotic ascites. We investigated the natural history of patients with HBV-related cirrhotic ascites hospitalized to control ascites and determined their prognosis, including survival rates and prognostic factors affecting survival. METHODS: Between January 1996 and December 2005, 203 consecutive patients with HBV-related cirrhotic ascites were followed for a median of 80.7 months (range, 15-149) after their first significant ascitic decompensation that required hospitalization. RESULTS: The mean age of all patients was 52.6 years. Male gender predominated (male/female, 138/65). A subgroup analysis of 165 patients who had ascitic decompensation as their first episode of hepatic decompensation revealed that gastrointestinal variceal bleeding developed after a median interval of 8 months following ascitic decompensation in 31 (18.8%) patients, hepatic encephalopathy occurred at 9 months in 53 (32.1%), spontaneous bacterial peritonitis appeared at 12.7 months in 24 (14.5%), hepatorenal syndrome occurred at 8.1 months in five (3%), and hepatocellular carcinoma was observed at 21.2 months in 10 (6.1%). The overall median survival was 12.4 months. The 1- and 3-year survival rates were 50.7 and 18.7%. The prognostic factors that independently correlated with survival at the time of ascitic decompensation were Child-Pugh classification B/C (P = 0.030), serum white blood cell (WBC; P = 0.035), serum creatinine (Cr; P = 0.039), serum sodium (Na; P = 0.010), and antiviral therapy (P = 0.040). CONCLUSIONS: The prognosis of HBV-related cirrhotic patients with ascitic decompensation is poor. Child-Pugh class, serum WBC/Cr/Na, and antiviral therapy primarily influenced survival.

Acute renal failure complicating non-fulminant hepatitis A.

Hepatitis, A is usually a mild and self-limiting infection of the liver. Whereas the clinical course is usually benign in children, complications such as prolonged cholestasis and fulminant liver failure have been reported in adults. Acute functional renal failure is an uncommon event in the absence of fulminating liver disease. So far, only cases of acute hepatitis A with biopsy-proven interstitial renal disease or tubular necrosis have been reported [Geltner et al. 1992. Kramer et al. 1986]. We present the case of a 35-year-old, previously healthy male with non-fulminant cholestatic viral hepatitis A, who developed progressive oliguric renal failure requiring dialysis therapy. Kidney biopsy ruled out glomerular disease and tubular necrosis. In the absence of bleeding and other causes of fluid depletion this case may be another variant of hepatorenal syndrome whose etiopathogenesis is only poorly understood.