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PubMed2005

Therapy of hepatitis C in patients with HIV infection.

Hepatitis C is found in approximately a third of patients infected with HIV. Therapy of hepatitis C in HIV patients is very important from several view points. First, hepatitis C in the setting of immunosuppression may progress faster, although recent data show that mortality from liver disease was decreased in highly active antiretroviral therapy. HIV/hepatitis C coinfection is associated with more frequent elevation in liver tests (drug-induced liver injury) during highly active antiretroviral therapy, and in some studies, hepatitis C has been associated with lower CD4+ recoveries. The therapeutic standard of care is a combination of peginterferon and ribavirin at a fixed dose, 800 mg/day, although higher ribavirin doses may further improve virologic outcomes. In patients that do not respond virologically, maintenance therapy with peginterferon monotherapy is a potential avenue to stem the advance of liver fibrosis, although controlled data in coinfected patients are needed to issue formal recommendations.

Antiviral Agents↗
PubMed1993

Mutations in core nucleotide sequence of hepatitis B virus correlate with fulminant and severe hepatitis.

Infection with hepatitis B virus leads to a wide spectrum of liver injury, including self-limited acute hepatitis, fulminant hepatitis, and chronic hepatitis with progression to cirrhosis or acute exacerbation to liver failure, as well as an asymptomatic chronic carrier state. Several studies have suggested that the hepatitis B core antigen could be an immunological target of cytotoxic T lymphocytes. To investigate the reason why the extreme immunological attack occurred in fulminant hepatitis and severe exacerbation patients, the entire precore and core region of hepatitis B virus DNA was sequenced in 24 subjects (5 fulminant, 10 severe fatal exacerbation, and 9 self-limited acute hepatitis patients). No significant change in the nucleotide sequence and deduced amino acid residue was noted in the nine self-limited acute hepatitis patients. In contrast, clustering changes in a small segment of 16 amino acids (codon 84-99 from the start of the core gene) in all seven adr subtype infected fulminant and severe exacerbation patients was found. A different segment with clustering substitutions (codon 48-60) was also found in seven of eight adw subtype infected fulminant and severe exacerbation patients. Of the 15 patients, 2 lacked precore stop mutation which was previously reported to be associated with fulminant hepatitis. These data suggest that these core regions with mutations may play an important role in the pathogenesis of hepatitis B viral disease, and such mutations are related to severe liver damage.

Adult↗
PubMed2003

Outcome of liver transplantation for patients infected by hepatitis C, including those infected by genotype 4.

Predictors of hepatitis C virus (HCV)-related liver disease posttransplantation are still unclear. The impact of HCV genotype on outcome of transplantation has been studied, but conclusions are not in agreement. The role of HCV genotype 4 on the result of liver transplantation requires further study. The aim of this study is to examine the outcome of liver transplantation for patients with HCV genotype-4 infection. The study group included 128 patients who underwent transplantation for HCV infection: 28 patients, genotype 1; 11 patients, genotype 2; 19 patients, genotype 3; and 32 patients, genotype 4. For 64 of 128 patients, genotype was known and an assessable histological specimen was available. Median interval from transplantation to biopsy was 1.92 years (range, 0.24 to 11.48 years). Twenty-six percent of HCV genotype-4 patients developed either severe fibrosis or cirrhosis versus 6.7% in the genotype non-4 group (P =.04). A statistically significant greater fibrosis progression rate was observed in genotype-4 than genotype non-4 patients. In univariate and multivariate analysis, rapid liver fibrosis was associated with the presence of HCV genotype-4 infection. In addition, donor and recipient age and graft warm ischemic time also were associated with rate of fibrosis progression. Five-year cumulative rates for the development of cirrhosis or severe liver fibrosis were 84% in genotype-4 and 24% in genotype non-4 patients (P =.02). Five-year survival rates for patients with genotypes 1, 2/3, and 4 were 72%, 80%, and 79%, respectively (P =.8). In conclusion, 5-year survival for patients who underwent transplantation for HCV genotype-4 infection was similar to that of genotype non-4 patients; however, more severe fibrosis and rapid fibrosis progression was observed after transplantation in patients with genotype-4 infection.

Adult↗
PubMed1977

Hepatitis B e antigen and infectivity of hepatitis B virus.

For confirmation of the difference in the infectivity of hepatitis B surface antigen (HBS Ag)-positive serum according to differences in the e antigen system, four chimpanzees were inoculated with serum positive for hepatitis B e antigen (HBe Ag), and three chimpanzees were inoculated with serum positive for antibody to HBe Ag (anti-HBe). Since the infectivity titrations are not yet completed, the end infectivity titer of each serum is not known. All four chimpanzees given injections of 10(-1), 10(-4), or 10(-8) dilutions of HBe Ag-positive serum developed hepatitis B virus infection, whereas the one chimpanzee injected with undiluted anti-HBe-positive serum became infected, and other chimpanzees injected with diluted anti-HBe-positive sera did not. As judged from the length of the incubation period before appearance of HBS Ag in blood, there seemed to be a remarkable difference in infectivity between the HBe Ag-positive serum and the anti-HBe-positive serum; the former serum was 10(8) times more infectious than the latter.

Animals↗
PubMed1998

High prevalence of hepatitis G virus infection compared with hepatitis C virus infection in patients undergoing chronic hemodialysis.

A recently discovered non-A-E hepatitis virus has been designated as hepatitis G virus (HGV) and identified as a new member of the Flaviviridae family. Infection by this virus is thought to be associated with blood-borne hepatitis and usually in the presence of hepatitis C or hepatitis B virus (HBV) infection. In this study, the presence of HGV-RNA in serum or plasma and the prevalence of antibodies against an HGV envelope protein (E2) were investigated in patients undergoing chronic hemodialysis using a sensitive reverse-transcriptase polymerase chain reaction and an enzyme-linked immunosorbent assay, respectively. HGV-RNA was detected in 19 of 112 patients investigated (17%) and anti-E2 antibodies were detected in 15 of 106 patients studied (14.2%). With the exception of two patients, the appearance of anti-E2 is associated with the clearance of serum HGV-RNA. The total prevalence of current (HGV-RNA positivity) and/or past (anti-E2 positivity) HGV infection in this patient population is thus 28.6% (32 of 112 patients were positive for serum HGV-RNA and/or anti-E2 antibodies). In apparently healthy blood donors, serum HGV-RNA was detected in four of 358 individuals (1.12%) and anti-E2 was not detected in 50 individuals investigated. From the 19 patients with serum HGV-RNA positivity, nine were coinfected with other hepatitis viruses (seven with HBV; one with HBV, hepatitis C virus [HCV], and hepatitis D virus; and one with HBV and cytomegalovirus). Thirteen of 15 patients with anti-E2 positivity (10 were positive for only anti-E2 and three were also positive for anti-HBc) had no detectable HGV-RNA. In two patients, both HGV-RNA and anti-E2 antibodies were concomitantly present (both patients were coinfected with HCV or HBV). Of the HGV-infected patients, only three who were coinfected with HBV showed elevated serum alanine aminotransferase levels. The serum HCV-RNA and/or anti-HCV were detected in five (4.5%) of 112 patients. From these findings, we conclude that there is a high prevalence of HGV infection (28.6%) compared with HCV (4.5%) in patients undergoing hemodialysis in our hospital. However, approximately 50% of patients had spontaneously lost the viremia and developed anti-HGV-E2 antibodies. We confirm that HGV infection alone is not associated with elevated serum transaminases, and the appearance of anti-HGV-E2 is usually accompanied with clearance of serum HGV-RNA. In contrast to the results of our previous study, the majority of patients infected with HGV are not coinfected with HCV, indicating that HGV is capable of independent transmission. It is likely that there is a preferential HGV acquisition in the hemodialysis unit. The clinical significance of long-term infection with HGV remains to be established.

Adult↗
PubMedDate not supplied

[A prevalence study of serum markers in hepatitis virus infection in the epidemiological anamnesis of the population].

Pandemic of the infections with hepatitis viruses is a priority in public health. In Romania, the very high acute and chronic morbidity by viral hepatitis demands the rapid implementation of a feasible preventive program. In the population of 5 districts from Transylvania we conducted a sero-epidemiological survey in order to find the real and specific characteristics of the prevalence of the infections with hepatitis viruses. The study was a cross-sectional study on the anamnestic presence of the infections in the population. The evolution of the cumulative prevalence of infections with HAV (74.3%) and HBV (31.7%) are proving a high endemoepidemicity. For the infections with HCV (4.9%) and HDV (1.7%) we observed an active process of endemicity. The high rate of persistent infections following HBV acute infections (19.1%) suggests a growing-up tendency of chronic hepatic diseases. In actual epidemiologic conditions, the rate of exposure to a potential hepatic viral infections in the population we studied could be 1.68 infections/person, during a period equal to life expectancy at birth.

Adolescent↗
PubMed1983

Incidence of infection with hepatitis B virus in 56 patients with haemophilia A 1971-1979.

During each of the four-year periods 1971-1975 and 1975-1979, the annual incidence of hepatitis B infection has been assessed in 56 patients with haemophilia A by measuring plasma HBsAg, anti-HBs and anti-HBc levels. Infection rates of 7% and 9.5% per annum respectively were observed for each four-year period despite the screening of individual blood donations for HBsAg by techniques up to the sensitivity of reversed passive haemagglutination. The highest incidence of seroconversion was amongst severe haemophiliacs many of whom had received treatment predominantly with cryoprecipitate. Of the 16 patients in whom serological evidence of hepatitis B infection was obtained only one had an accompanying clinical episode of hepatitis. We conclude that haemophiliacs are still at high risk of infection by hepatitis B virus despite the screening of individual blood donors for HBsAg.

Adolescent↗
PubMed2000

Biochemical and virological response to interferon therapy in patients with chronic hepatitis C, co-infected with hepatitis G virus.

It is still unclear whether hepatitis G virus (HGV) and hepatitis C virus (HCV) co-infection influences the natural course of chronic HCV infection and the response to interferon (IFN) therapy. In this study, we investigated the HGV RNA changes and responses to IFN therapy of HGV RNA-positive hepatitis C patients. The presence of HGV RNA in 264 patients who received IFN therapy at our institute was examined using the nested reverse transcription-polymerase chain reaction with primers deduced from the 5' non-coding region (5'-NCR) of the HGV. We also analysed the nucleotide sequences of the 5'-NCR and HGV before and after IFN therapy. Twelve (4.5%) of the 264 patients with chronic hepatitis C were HGV RNA positive. Of these 12 patients, full information was available in nine. Of those nine, seven became HGV RNA negative during IFN therapy but in six of the seven a relapse occurred. HCV RNA was not detected 1 year after IFN therapy in six patients. The serum alanine aminotransferase (ALT) levels of all the HCV RNA-negative patients post-treatment was within the normal range, irrespective of their HGV RNA status. Nucleotide sequences did not change after IFN therapy in any patient. Hence, we confirm that HGV is sensitive to IFN therapy but the liver damage caused by HGV infection is very mild or does not modify the liver function tests.

5' Untranslated Regions↗
PubMed1995

The role of bile acid secretion in the hepatic response to operation and infection.

Hepatic function is altered in many surgery-related diseases. Bile acid secretion is the major determinant of bile formation and an important indicator of overall hepatic function. To investigate the cause of intrahepatic cholestasis, which is frequently associated with sepsis, we studied the effects of cecal ligation and puncture (CLP) and surgical stress on bile acid secretion and composition. CLP or a sham operation was performed on 20 male Sprague-Dawley rats. Bile was collected from each rat by cannulation of the common bile duct for 10-minute intervals, at 5 and 20 hours after the initial procedure. Bile acid analysis was then performed by high performance liquid chromatography (HPLC). In CLP rats, there was a significant (P < 0.05) cholestatic effect. Bile flow was reduced to 70 +/- 13 per cent at 5 hours, and to 55 +/- 16 per cent at 20 hours (per cent of the sham mean value). In the sham-operated rats, there was a significant choleresis at 20 hours. Bile flow was increased to 146 +/- 13 per cent; bile acid secretion to 245 +/- 24 per cent; and total bile acid concentration to 175 +/- 19 per cent of the sham 5-hour value (P < 0.05). This increased secretion was significantly greater in the metabolites of chenodeoxycholate. However, these surgical stress-associated changes in bile acid secretion and composition did not occur in CLP rats. These findings are consistent with surgical stress-induced induction of 7 alpha-hydroxylase, which was not found in the septic animals. These observations may provide useful insights into the early stages of the pathogenesis of sepsis-related hepatic dysfunction and failure.

Animals↗
PubMed1993

[Mutation in core and pre-core amino acid sequences of hepatitis B virus correlate with fulminant and severe hepatitis].

Infection with hepatitis B virus leads to a wide spectrum of liver injury, including self-limited acute hepatitis, fulminant hepatitis and chronic hepatitis with progression to cirrhosis or acute exacerbation to liver failure, as well as, an asymptomatic chronic carrier state. To investigate why an extreme immunological attack occurs in fulminant hepatitis and severe exacerbation, the entire precore and core region were sequenced in 13 subjects. No significant change was noted in the 6 self-limited acute hepatitis patients. In contrast, clustering changes in a small segment of core codons #84 to #99 were found in all 7 fulminant and severe exacerbation patients. These data suggest that this mutation clustering region may play an important role in the pathogenesis, and such mutations appear to be related to severe liver damage.

Adult↗
PubMed1994

Sequential change of the hypervariable region of the hepatitis C virus genome in acute infection.

Hepatitis C virus (HCV) infection is characterized by persistence of liver inflammation that often leads to end-stage liver disease, although the mechanisms are not fully understood. A hypervariable region (HVR) has been reported in the E2/NS1 region of the HCV genome, in which striking diversity is found among different HCV isolates. To investigate the association of the HVR alterations with the clinical courses of HCV infection, a longitudinal analysis of the HVR in patients with acute HCV infection was carried out. Plasma samples were obtained at several times in three patients with acute hepatitis C. Plasma RNA was extracted and reverse transcribed, and DNA fragments that included the HVR were amplified by PCR. The sequences of the HVR were directly determined from the PCR products by the dideoxy chain termination method, from which amino acid sequences were deduced. In all cases, plasma HCV-RNA disappeared with the improvement of the initial alanine aminotransferase (ALT) elevation, but HCV-RNA reappeared about 1 year later with or without deterioration of the hepatitis. In a case of sporadic acute hepatitis, the HCV in the recurrent phase had seven amino acid substitutions in the HVR compared with that in the acute phase, although no amino acid changes were noted during the initial acute phase. In a case of posttransfusion hepatitis, a marked difference was observed between the acute and the recurrent phases, with an amino acid homology of 30% (8/27). The mutation rate of the HVR had a tendency to accelerate as the HCV infection progressed to the chronic stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1997

Multiple hepatitis virus infections in chronic HBsAg carriers in Naples.

In order to determine the prevalence of multiple infections with hepatitis viruses in chronic HBsAg carriers in Naples, to assess the interaction between HBV, HDV and HCV infections and to evaluate the influence of multiple virus hepatitis infections on the clinical presentation, we studied 198 HBsAg chronic carriers observed consecutively from 1971 to 1988 at our Liver Unit. Of the 198 HBsAg chronic carriers, 171 had undergone percutaneous liver biopsy. The presence of HBcAg or HDAg in the liver biopsy was considered a marker of HBV or HDV replication, respectively; the presence of anti-HCV was considered a marker of HCV infection. Anti-HCV was observed in 13.6% of the 22 subjects with normal liver, in 27.7% of the 47 patients with minimal chronic hepatitis, in 40% of the 50 with mild chronic hepatitis, in 70.6% of the 17 with moderate hepatitis, in 66.7% of the 3 with severe chronic hepatitis and in 65.6% of the 32 with active cirrhosis. Anti-HCV positive cases were antiHD positive more frequently than the anti-HCV negative (59.2% vs. 43%, p = 0.05). HDV infection exerted a clear inhibition on the HBV genome. Among the 171 HBsAg chronic carriers, the finding of an active chronic hepatitis (moderate chronic hepatitis + severe chronic hepatitis + active cirrhosis) is less frequent in subjects with HBV replication alone than in those with HDV replication or HCV infection. Patients with both HBV replication and HCV infection and those with both HDV replication and HCV infection showed a very high prevelance of active chronic hepatitis.

Adolescent↗
PubMed1997

Loss of serum HBsAg after interferon-A therapy in liver transplant patients with recurrent hepatitis-B infection.

Reinfection with hepatitis B virus after orthotopic liver transplantation is nearly universal in patients who have not received posttransplant immunoprophylaxis. Recurrence almost invariably leads to chronic liver disease. Interferon has been used both prophylactically and therapeutically but has not been effective. We treated 2 liver transplant patients with recurrent hepatitis B virus (HBV) infection (serum hepatitis B surface antigen [HBsAg] and HBV DNA positive on polymerase chain reaction, and positive liver biopsy result) with interferon, 3 to 6 MU three times weekly for 6 to 22 months. A full response to therapy was manifested in both patients by normalized serum alanine aminotransferase levels and the loss of serum HBsAg and HBV DNA. The effectiveness of interferon in our patients may have been related to coinfection with hepatitis D virus in the first case and the high interferon dose (6 MU, three times weekly) and long treatment period (22 months) in the second. No episodes of rejection were noted during therapy. We conclude that interferon can induce a complete response in liver transplant patients with recurrent HBV infection. Future studies should investigate the use of interferon therapy at higher doses and/or for longer periods.

Adult↗
PubMed1988

Delta infection and hepatitis B virus replication in Danish patients with fulminant hepatitis B.

The presence of hepatitis B virus and delta agent markers was investigated in 41 patients referred during the years 1970-1985 with fulminant hepatitis classified as type B or non-A non-B and compared to findings in patients with uncomplicated hepatitis B and chronic hepatitis B infection. 13 patients had no markers of hepatitis B and delta infection and were classified as non-A non-B hepatitis. The remaining 28 patients were all HBsAg and IgM anti-HBc positive and 14 (50%) had evidence of delta infection. In contrast, only 13/71 patients (18%) with acute benign hepatitis B had evidence of delta coinfection (p less than 0.005). This corresponds to an odds ratio of 4.5 for development of fulminant hepatitis among patients with hepatitis B and delta coinfection. In 100 chronic HBsAg carriers 29% were positive for delta markers. 12 of the delta infected patients with fulminant hepatitis were positive for total antibody to the delta antigen, and 2 were delta antigen positive. Three were HBeAg positive/anti-HBe negative. None had hepatitis B virus DNA. Among the 14 patients without delta infection, hepatitis B virus DNA was found in 2/4 HBeAg positive/anti-HBe negative patients and in 1/8 patients negative for both markers. The present data indicate that a high proportion of Danish patients with fulminant hepatitis B have hepatitis B and delta agent coinfection. Further, the findings suggest that hepatitis B and delta coinfection may be associated with an increased risk of development of fulminant hepatitis as compared to that of hepatitis B alone.

Adolescent↗
PubMed2003

[Hepatitis C virus infection and primary hepatic large B-cell lymphoma: a non-fortuitous association. Case report and review of literature].

We report a case of hepatitis C virus infection in association with primary hepatic large B-cell non-Hodgkin's lymphoma. Primary hepatic non-Hodgkin's lymphoma is a rare disease. Association of hepatitis C virus infection with primary hepatic B-cell non-hodgkin's lymphoma is probably not fortuitous. Indeed, in case of primary hepatic non-hodgkin's lymphoma' patients are often hepatitis C virus positive. Moreover, several studies have reported a high prevalence of chronic hepatitis C virus infection among patients with B-cell non-Hodgkin's lymphoma whatever the localization of the lymphoma. A recent study found a high rate of remission of a splenic form of lymphoma after treatment of hepatitis C virus infection. Our case report confirms the hypothesis of a key role of hepatitis C virus in the pathogenesis of various forms of B-cell lymphoproliferative disorders and in particular in primary hepatic lymphoma.

Aged↗
PubMed2006

Entecavir: a new nucleoside analog for the treatment of chronic hepatitis B infection.

BACKGROUND: Chronic hepatitis B infection carries considerable risk for the development of cirrhosis and hepatocellular carcinoma. Treatment options are increasing but are limited to interferon alfa-2b, pegylated interferon alfa-2a, lamivudine, adefovir dipivoxil, and entecavir. Entecavir, a nucleoside analog, is the newest oral antiviral approved in the United States for treatment of chronic hepatitis B. OBJECTIVE: To review the available data for entecavir regarding its pharmacology, pharmacokinetics, safety, efficacy, and clinical use. METHODS: A MEDLINE, EMBASE, and Cochrane search of the English-language literature from January 1997-May 2006 was performed. Preapproval studies provided by the manufacturer and abstracts from recent scientific meetings on infectious disease and hepatology were also reviewed. RESULTS: Three phase III clinical trials representing more than 1600 subjects established the superior efficacy and equivalent safety of entecavir compared with lamivudine for treating patients who are hepatitis B early antigen (HBeAg) positive, HBeAg negative, or refractory to lamivudine. Entecavir resistance has not occurred in nucleoside-naïve patients but may develop in those who already possess lamivudine resistance mutations. CONCLUSION: Trial results, along with previously published response rates for adefovir dipivoxil and interferon monotherapy, make entecavir the preferred first-line treatment option for patients with chronic hepatitis B who are nucleoside naïve, HBeAg positive or negative, and have compensated liver disease. Both entecavir and adefovir dipivoxil maintain activity against hepatitis B virus in patients with chronic hepatitis B who are refractory to lamivudine, and both agents are reasonable first-line treatment options. Longer trials involving nucleoside-naïve, lamivudine-refractory patients are needed to determine entecavir's optimal treatment duration, long-term safety, and durability of response, including rate of resistance.

Animals↗