Epatite B, il rischio occulto.

infezione da HBV, definita epatite B, rappresenta uno dei principali problemi sanitari a livello mondiale. Il virus responsabile di questa infezione si trasmette infatti in modo efficace attraverso il sangue e altri fluidi corporei, ragione per cui, fino a pochi decenni fa, le vie principali di diffusione del virus erano le pratiche ospedaliere e la trasmissione in ambito familiare. Nel decennio 1970-1980, l’Italia era un paese a media endemia, con ampie variazioni geografiche nella prevalenza dei portatori cronici della malattia (la prevalenza media era pari al 2-8% con i livelli più elevati nelle aree meridionali e insulari)

Virological analysis, genotypes and mutational patterns of the HBV pre-core/core gene in HBV/HCV-related hepatocellular carcinoma

We investigated the replicative profile of hepatitis B (HBV) and hepatitis C (HCV) viruses and the mutational pattern of the HBV precore/core (pre-C/C) domain in hepatocellular carcinoma (HCC). Thirty-eight consecutive patients with HCC were included in the study - 18 of them with HBV/HCV co-infection and 20 with HBV single infection. Twenty-three additional patients with co-infection, without HCC were recruited as the control group. Replication activity was evaluated by detecting and quantitating both HBV and HCV genomes. The HBV pre-C/C region, encompassing the pregenome encapsidation signal involved in viral replication, was analysed by direct sequencing. HBV viraemia levels were significantly lower (P = 0.04) in patients with co-infection in comparison with single-infected HCC, whereas two different HBV viraemia profiles were detected in co-infection with or without circulating HCV. HBV genotype D was prevalent in the three groups and HCV genotype 1b was found to be the infecting strain in all patients. Lower variability in the pre-C/C region was found in co-infection in comparison with HBV single infection (P = 0.0004). A synonymous T1936C mutation was found in all co-infected HCC cases not related to the presence or absence of circulating HCV, and a hypermutated pre-C strain, characterized by the same mutational pattern, was identified in three HCC cases. The mutational pattern of the pre-C/C region was closely related to HBV replication efficiency, and specific HBV mutations selectively associated with HCV co-infection could be linked with accelerated HBV/HCV-related disease progression. © 2006 The Authors

Genetic heterogeneity of hepatitis C virus in HBV/HCV co-infection

none8noneM.S. De Mitri; G. Morsica; R. Cassini; S. Bagaglio; P. Andreone; G. Bianchi; M. Margotti; M. BernardiM.S. De Mitri; G. Morsica; R. Cassini; S. Bagaglio; P. Andreone; G. Bianchi; M. Margotti; M. Bernard

A novel stop codon mutation within the hepatitis B surface gene is detected in the liver but not in the peripheral blood mononuclear cells of HIV-infected individuals with occult HBV infection.

To characterize occult HBV infection (OHB) in different compartments of HIV+ individuals. This retrospective study involved 38 consecutive HIV+ patients; 24 HBsAg negative (HBV)) and 14 HBsAg positive (HBV+). OHB was assessed in serum samples, liver tissue (LT) and peripheral blood mononuclear cells (PBMC) by genomic amplification of the partial S, X and precore/core regions. HBV genomic analysis was inferred by direct sequencing of PCR products. The intracellular HBV-DNA was measured by a quantitative real-time PCR. HBV+ patients were used as a control for HBV replication and genomic profile. In HBV) patients, HBV-DNA was undetectable in all serum samples, while it was found positive in 7/24 (29%) LT in which genotype D prevailed (57%). HBV-DNA was found in 6/7 (86%) PBMC of occultpositive and none of occult-negative LT. Significantly lower HBV-DNA load was present in both compartments in OHB+ with respect to the HBV+ group (LT: P = 0.002; PBMC: P = 0.026). In the occult-positive cases, HBV replication was significantly higher in LT than in PBMC (P = 0.028). A hyper- mutated S gene in PBMC and a nucleotide mutation at position C695 in LT that produces a translational stop codon at amino acid 181 of the HBs gene characterized OHB. In this group of HIV+ persons, OHB is frequent and exhibits lower replication levels than chronic HBV in the different compartments examined. HBV-DNA detection in PBMC may offer a useful tool to identify OHB in serum-negative cases. The novel HBs gene stop codon found in LT could be responsible for reduced production leading to undetectability of HBsAg

Influence of clinically significant portal hypertension on survival after hepatic resection for hepatocellular carcinoma in cirrhotic patients

BACKGROUND: The role of clinically significant portal hypertension on the prognosis of cirrhotic patients undergoing hepatic resection for hepatocellular carcinoma (HCC) is debated. AIMS: In this study, our aim was to assess the role of clinically significant portal hypertension after hepatic resection for HCC in patients with cirrhosis. METHODS: We assessed the prognostic role of the presence of clinically significant portal hypertension (oesophageal/gastric varices/portal hypertensive gastropathy or a platelet count <100 7 10(9) /L associated with splenomegaly) in 152 patients with compensated cirrhosis who underwent hepatic resection for HCC at the Italian Liver Cancer centres. Survival rates were assessed in the whole series, in the subgroup of Child-Pugh score 5 patients with uninodular HCC 64 5 cm, and in Child-Pugh score 5 patients with uninodular HCC 64 2 cm and normal bilirubin. RESULTS: Median survival was similar in patients with and without clinically significant portal hypertension (79 vs 77 months, P = 0.686). Child-Pugh score 5 was the only variable significantly associated with survival by Cox multiple regression (P = 0.007). In Child-Pugh score 5 patients with single HCC 64 5 cm or in those with single HCC 64 2 cm and normal bilirubin, there was no survival difference between patients with and without clinically significant portal hypertension (median survival: 94 vs 78 months, P = 0.121 and >100 vs 86 months, P = 0.742). CONCLUSIONS: Presence of clinically significant portal hypertension has no influence on survival of patients with well-compensated cirrhosis undergoing hepatic resection for HCC