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Chronic Hepatitis B Virus Infection (chronic + hepatitis_b_virus_infection)
Selected AbstractsChronic hepatitis B virus infection in Asian countriesJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2000I Merican Of the estimated 50 million new cases of hepatitis B virus (HBV) infection diagnosed annually, 5,10% of adults and up to 90% of infants will become chronically infected, 75% of these in Asia where hepatitis B is the leading cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC). In Indonesia, 4.6% of the population was positive for HBsAg in 1994 and of these, 21% were positive for HBeAg and 73% for anti-HBe; 44% and 45% of Indonesian patients with cirrhosis and HCC, respectively, were HBsAg positive. In the Philippines, there appear to be two types of age-specific HBsAg prevalence, suggesting different modes of transmission. In Thailand, 8,10% of males and 6,8% of females are HBsAg positive, with HBsAg also found in 30% of patients with cirrhosis and 50,75% of those with HCC. In Taiwan, 75,80% of patients with chronic liver disease are HBsAg positive, and HBsAg is found in 34% and 72% of patients with cirrhosis and HCC, respectively. In China, 73% of patients with chronic hepatitis and 78% and 71% of those with cirrhosis and HCC, respectively, are HBsAg positive. In Singapore, the prevalence of HBsAg has dropped since the introduction of HBV vaccination and the HBsAg seroprevalence of unvaccinated individuals over 5 years of age is 4.5%. In Malaysia, 5.24% of healthy volunteers, with a mean age of 34 years, were positive for HBsAg in 1997. In the highly endemic countries in Asia, the majority of infections are contracted postnatally or perinatally. Three phases of chronic HBV infection are recognized: phase 1 patients are HBeAg positive with high levels of virus in the serum and minimal hepatic inflammation; phase 2 patients have intermittent or continuous hepatitis of varying degrees of severity; phase 3 is the inactive phase during which viral concentrations are low and there is minimal inflammatory activity in the liver. In general, patients who clear HBeAg have a better prognosis than patients who remain HBeAg-positive for prolonged periods of time. The outcome after anti-HBe seroconversion depends on the degree of pre-existing liver damage and any subsequent HBV reactivation. Without pre-existing cirrhosis, there may be only slight fibrosis or mild chronic hepatitis, but with pre-existing cirrhosis, further complications may ensue. HBsAg-negative chronic hepatitis B is a phase of chronic HBV infection during which a mutation arises resulting in the inability of the virus to produce HBeAg. Such patients tend to have more severe liver disease and run a more rapidly progressive course. The annual probability of developing cirrhosis varies from 0.1 to 1.0% depending on the duration of HBV replication, the severity of disease and the presence of concomitant infections or drugs. The annual incidence of hepatic decompensation in HBV-related cirrhosis varies from 2 to 10% and in these patients the 5-year survival rate drops dramatically to 14,35%. The annual risk of developing HCC in patients with cirrhosis varies between 1 and 6%; the overall reported annual detection rate of HCC in surveillance studies, which included individuals with chronic hepatitis B and cirrhosis, is 0.8,4.1%. Chronic hepatitis B is not a static disease and the natural history of the disease is affected by both viral and host factors. The prognosis is poor with decompensated cirrhosis and effective treatment options are limited. Prevention of HBV infection thorough vaccination is still, therefore, the best strategy for decreasing the incidence of hepatitis B-associated cirrhosis and HCC. [source] Does Cerumen Have a Risk for Transmission of Hepatitis B?,THE LARYNGOSCOPE, Issue 3 2004M. Tayyar Kalcioglu MD Abstract Objectives/Hypothesis Chronic hepatitis B virus infection is a significant worldwide health problem. It affects 350 to 400 million people. The patients with chronic hepatitis B virus infection have a significant risk for the development of cirrhosis or hepatocellular carcinoma. Full awareness of the mechanisms of transmission can allows susceptible individuals to refrain from this infection. Cerumen has never been studied as a route for hepatitis B transmission. The aim of the study was evaluate the importance of cerumen in transmission of hepatitis B virus infection. Study Design This study was performed on forty patients with confirmed hepatitis B virus infection. Methods Forty cerumen specimens collected from the patients with hepatitis B virus DNA in their sera were prospectively analyzed for the presence of hepatitis B virus DNA by real-time polymerase chain reaction. Results Eleven of 40 cerumen specimens (27.5%) were positive for hepatitis B virus DNA, with counts ranging from 4.2 × 102 to 4.7 × 106 copies per sample. There was positive correlation between hepatitis B virus DNA concentrations of serum and cerumen. Half of hepatitis B e antigen (HBeAg),positive patients had detectable hepatitis B virus DNA levels (5.7 × 102 to 4.7 × 106 copies) in cerumen specimens, whereas 12.5% of cerumen specimens from anti-HBe,positive patients had hepatitis B virus DNA levels (4.2 × 102 to 7.0 × 103 copies). Conclusion Cerumen can be a potential source of transmission. Therefore, this route should be investigated in further studies for horizontal, nosocomial, and occupational transmission of hepatitis B. [source] Immunomodulatory therapy for chronic hepatitis B virus infectionFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2005D. Sprengers Abstract Hepatitis B virus (HBV) is one of the most prevalent viral pathogens of man with around 350 million chronically infected patients. It has been postulated that in persistently infected individuals the HBV-specific immune response is too weak to eliminate HBV from all infected hepatocytes, but sufficiently strong to continuously destroy HBV-infected hepatocytes and to induce chronic inflammatory liver disease. The primary aim in the treatment of chronic hepatitis B is to induce sustained disease remission and prevent serious complications like liver failure and/or hepatocellular carcinoma. The recent emergence of drug-resistant HBV mutants and post-treatment relapse as a consequence of nucleoside analogue monotherapy emphasizes that the principal goal should be to stimulate a successful immune response. In this paper we will focus on the immune response to HBV and we will review reported data on immunotherapeutic strategies like immunomodulatory drugs (cytokines and Thymic derivates) and vaccine therapies using currently available recombinant anti-HBV vaccines, lipopeptide-based T cell vaccine and newly developed genetic vaccines. [source] Serum hepatitis B virus-DNA cutoff levels in hepatitis B e antigen,negative chronic hepatitis B virus infection,HEPATOLOGY, Issue 2 2007George V. Papatheodoridis No abstract is available for this article. [source] Association of estrogen receptor , polymorphisms with susceptibility to chronic hepatitis B virus infectionHEPATOLOGY, Issue 2 2004Guohong Deng Several studies have demonstrated that estrogen receptor , (ESR1) participates in the pathogenesis of persistent hepatitis B virus (HBV) infection. To examine whether polymorphisms at the ESR1 gene locus are associated with persistent HBV infection, we resequenced ESR1 genomic region for single nucleotide polymorphisms (SNPs) in 27 unrelated Chinese. Two haplotype-tagged SNPs (htSNP), T29C and A252966G, were selected for genotyping in 1,277 persistent HBV-infected cases, 748 spontaneously recovered controls, and 293 nuclear families using polymerase chain reaction (PCR)-restriction fragment length polymorphism (PCR-RFLP) analysis. We observed that the subjects bearing ESR1 29T/T genotype had an increased susceptibility to persistent HBV infection compared to those bearing at least one 29C allele (odds ratio 1.41; 95% CI, 1.17-1.71, P < .001). Consistent with the results of population-based association study, a significantly greater than expected transmission of the 29T allele (56.4%) from heterozygous parents to offspring with persistent HBV infection was observed (,2 = 4.60, P = .033) using the transmission-disequilibrium test (TDT) in 293 nuclear families. Linkage disequilibrium (LD) mapping analysis indicated that the T29C polymorphism contained within a LD block located from promoter region to intron 3 of ESR1, suggesting that the strong association detected with T29C in ESR1 originated from ESR1 itself. In conclusion, our results suggest that the genetic variation at the ESR1 locus influences susceptibility to persistent HBV infection in a Chinese population. (HEPATOLOGY 2004;40:318,326.) [source] Safety and efficacy of oral entecavir given for 28 days in patients with chronic hepatitis B virus infectionHEPATOLOGY, Issue 3 2001Ph.D., Robert A. de Man M.D. Entecavir is an oral antiviral drug with selective activity against hepatitis B virus (HBV). We conducted a randomized, placebo-controlled, dose-escalating study in patients with chronic hepatitis B infection in which we evaluated the efficacy and safety of entecavir given for 28 days. Follow-up was 24 weeks. All doses of entecavir (0.05 mg, 0.1 mg, 0.5 mg, and 1.0 mg) showed a pronounced suppression of replication of the HBV with a 2.21, 2.29, 2.81, and 2.55 mean log10 reduction of viral load, respectively. Approximately 25% of patients on entecavir showed a decline of HBV DNA below the limit of detection of the Chiron HBV-DNA assay (<0.7 MEq/mL). In the postdosing follow-up period patients who were treated with 0.5 and 1.0 mg of entecavir showed a considerably slower return in their HBV DNA levels to baseline compared with those patients treated with lower dosages (P < .05). All doses of entecavir were well tolerated with no significant difference between treated patients and those receiving placebo. No significant changes in alanine transaminase (ALT) levels within the dose groups and the placebo group between baseline and the end of treatment were observed. Three patients (9%) (1 each in the 0.05-, 0.1-, and 0.5-mg groups) experienced asymptomatic hepatitis flares 16 weeks (2 patients) and 24 weeks (1 patient) after withdrawal of entecavir. In conclusion, in this 28-day study of entecavir a pronounced decrease of HBV DNA was observed and there were no significant side effects in entecavir patients in comparison with placebo-treated patients. (HEPATOLOGY 2001;34:578-582.) [source] Usefulness of transient elastography for assessment of liver fibrosis in chronic hepatitis B: Regression of liver stiffness during entecavir therapyHEPATOLOGY RESEARCH, Issue 9 2010Masaru Enomoto Aim:, The usefulness of transient elastography remains to be validated in chronic hepatitis B, particularly as a tool for monitoring the degree of liver fibrosis during treatment. Methods:, The subjects were 50 patients with chronic hepatitis B virus infection. Liver biopsy was performed in 38 patients, and in 12 patients with platelet counts of 50 × 109/L or less, cirrhosis was clinically diagnosed on the basis of specific signs of portal hypertension. Liver stiffness was measured by transient elastography at baseline and after 12 months of treatment in 20 nucleos(t)ide-naïve patients who started entecavir within 3 months after study entry. Results:, Twenty (40%) patients were classified as F1, 10 (20%) as F2, 5 (10%) as F3, and 15 (30%) as F4 (cirrhosis). Median liver stiffness (interquartile range) was 7.0 kPa (5.6,9.4), 9.8 kPa (5.6,14.7), 9.8 kPa (7.6,12.9), and 17.3 kPa (8.2,27.6) in fibrosis stages F1 to F4, respectively. Liver stiffness significantly correlated with fibrosis stage (r = 0.46; P = 0.0014). Of the patients who started entecavir, median liver stiffness significantly decreased from 11.2 kPa (7.0,15.2) to 7.8 kPa (5.1,11.9; P = 0.0090) during 12 months of treatment. Median levels of amino-terminal peptide of type III procollagen and type IV collagen 7S domain in serum significantly decreased from 0.9 (0.6,1.3) to 0.6 (0.5,0.7) U/mL (P = 0.0010) and from 5.0 (4.4,6.7) to 3.9 (3.2,4.4) ng/mL (P = 0.015), respectively. Conclusion:, Liver stiffness measurement can be useful for monitoring regression of liver fibrosis during entecavir treatment in patients with chronic hepatitis B virus infection. [source] Effects of structural variations of APOBEC3A and APOBEC3B genes in chronic hepatitis B virus infectionHEPATOLOGY RESEARCH, Issue 12 2009Hiromi Abe Aim:, Human APOBEC3 deaminases induce G to A hypermutation in nascent DNA strand of hepatitis B virus (HBV) genomes and seem to operate as part of the innate antiviral immune system. We analyzed the importance of APOBEC3A (A3A) and APOBEC3B (A3B) proteins, which are potent inhibitors of adeno-associated-virus and long terminal repeat (LTR)-retrotransposons, in chronic HBV infection. Methods:, We focused on the common deletion polymorphism that spans from the 3, part of A3A gene to the 3, portion of A3B gene. An association study was carried out in 724 HBV carriers and 469 healthy control subjects. We also analyzed hypermutated genomes detected in deletion and insertion (non-deletion) homozygous patients to determine the effect of APOBEC3 gene deletion. Further, we performed functional analysis of A3A gene by transient transfection experiments. Results:, The association study showed no significant association between deletion polymorphism and chronic HBV carrier state. Context analysis also showed a negligible effect for the deletion. Rather, mild liver fibrosis was associated with APOBEC gene deletion homozygosity, suggesting that A3B deletion is not responsible for chronic HBV infection. Functional analysis of A3A showed that overexpression of A3A induced hypermutation in HBV genome, although the levels of hypermutants were less than those introduced by A3G. However, overexpression of A3A did not decrease replicative intermediates of HBV. Conclusion:, These results suggest that A3A and A3B play little role in HBV elimination through anti-viral defense mechanisms. The significance of hypermutation induced by A3A should be investigated further. [source] Physiological hepatic nuclear vacuolation,how long does it persist?HISTOPATHOLOGY, Issue 4 2010Adam P Levene Levene A P & Goldin R D (2010) Histopathology56, 426,429 Physiological hepatic nuclear vacuolation,how long does it persist? Aims:, Nuclear vacuolation\glycogenation is a characteristic histological feature of non-alcoholic fatty liver disease (NAFLD) that can help distinguish it from alcohol-induced liver disease. There are, however, other associations of nuclear vacuolation of which the commonest is as a normal feature of childhood. The aim of this study was to identify how long this physiological nuclear vacuolation persists. Methods and results:, Liver biopsy specimens from 872 patients with chronic hepatitis B virus infection (a condition known not to be associated with nuclear vacuolation) were studied to assess the frequency of nuclear vacuolation at different ages. All the patients studied had a body mass index of <25 kg/m2 and an alcohol intake of <15 units/week, as well as no other risk factors for liver disease. It was found that the frequency of nuclear vacuolation, in the absence of NAFLD, fell from 13% at age 20,24 years to 4% in the early 30s and to 0% at age 60,64 years. Conclusions:, Physiological hepatic nuclear vacuolation is common in the 20s and persists into the 30s. This knowledge can help in the assessment of liver biopsy specimens in which nuclear vacuolation is a feature. [source] Infliximab therapy in a patient with Crohn's disease and chronic hepatitis B virus infectionINFLAMMATORY BOWEL DISEASES, Issue 5 2004María del Valle García-Sánchez MD No abstract is available for this article. [source] A great deal of learning from the natural course of chronic hepatitis B virus infectionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2007Rong-Nan Chien [source] How do naturally occurring YMDD-motif mutants influence the clinical course of lamivudine-naïve patients with chronic hepatitis B virus infection?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2006Akihito Tsubota [source] Genetic susceptibility to chronic hepatitis B virus infectionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2006Ian R Mackay [source] Identification of a pre-S2 mutant in hepatocytes expressing a novel marginal pattern of surface antigen in advanced diseases of chronic hepatitis B virus infectionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2000Yu-Fen Fan Abstract Background and Aims: The expression of hepatitis B viral (HBV) antigens in liver tissue reflects the replicative status of chronic HBV infection. We have previously recognized a novel marginal pattern of hepatitis B surface antigen (HBsAg) in hepatocytes, which usually clusters in groups and emerges at the late non-replicative phase. This study was designed to investigate whether the marginal-type HBsAg represented the gene product of a specific HBV-surface mutant. Methods: Microdissection of cirrhotic nodules homogeneously expressing marginal HBsAg was performed on two of 12 resected livers from HBsAg-seropositive patients with hepatocellular carcinoma. The gene presumably encoding marginal HBsAg was polymerase chain reaction (PCR)-cloned, sequenced and analysed. In vitro transfection and expression of the cloned surface mutant plasmids were performed on the Huh7 cell line to illustrate intrahepatic HBsAg expression. Results: Immunohistochemical staining revealed that the marginal HBsAg was positive for pre-S1 and thus contained large surface proteins. The PCR cloning and sequencing of the genes presumably encoding marginal-type HBsAg in both cases revealed the same deletion at the 5, terminus (nt 2,55) of pre-S2. A point mutation on the small-surface (S) antigen was also found in one case. The pre-S2 deletion sequence and the mutation sites of the S gene coincide with human lymphocyte antigen-restricted T- and/or B-cell epitopes. In vitro transfection of the mutant plasmid revealed a blot-like retention or accumulation of HBsAg in the cytoplasm or at the periphery of hepatocytes, accompanied by a decreased secretion of HBsAg in the culture supernatant, mimicking intrahepatic expression. Conclusion: A natural pre-S2 deletion mutant was identified in hepatocytes expressing a novel marginal pattern of HBsAg, which probably contains mutant, large, surface proteins. The biological significance of the pre-S2 deletion mutant should be interesting in view of the clustering proliferation of hepatocytes expressing marginal HBsAg. [source] Treatment of chronic hepatitis B virus infection in special groups of patients: decompensated cirrhosis, immunosuppressed and paediatric patientsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2000Ismail Merican [source] Current limitations to nucleoside analogue therapy for chronic hepatitis B virus infection in the liver transplant and non-transplant settingsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2000John S Freiman No abstract is available for this article. [source] B7-H1 expression is upregulated in peripheral blood CD14+ monocytes of patients with chronic hepatitis B virus infection, which correlates with higher serum IL-10 levelsJOURNAL OF VIRAL HEPATITIS, Issue 11 2006L. Geng Summary., Chronicity in hepatitis B virus (HBV) infection is maintained by increased type 2 T-helper cell response, possibly because of increased interleukin-10 (IL-10) productions. B7-H1 can negatively regulate T-cell responses via its receptor, programmed death 1. Ligation of B7-H1 to T-cells can result in the preferential secretion of IL-10. In this study, we investigated whether there was an upregulated expression of B7-H1 in peripheral blood mononuclear cells in patients chronically infected by HBV and further explored the correlation between B7-H1 expression and serum interleukin 2, interferon- ,, IL-10, HBeAg, alanine aminotransferase (ALT) levels and viral load. Fifty-five patients with chronic HBV infection and 20 healthy controls (HCs) were enrolled in the present study. The results showed that in patients with chronic hepatitis B CD14+ monocytes but not CD3+ and CD19+ cells had a significantly increased expression of B7-H1 compared with HCs, which positively correlates with serum IL-10 levels and the presence of HBeAg and negatively correlates with serum ALT levels. In conclusion, chronic HBV patients harbour an increased B7-H1 expression in CD14+ monocytes compared with controls, which may be responsible for the increased serum IL-10 levels. This might be an important way by which HBV evades an adequate immune response, leading to viral persistence and disease chronicity. [source] 48 weeks pegylated interferon alpha-2a is superior to 24 weeks of pegylated interferon alpha-2b in achieving hepatitis B e antigen seroconversion in chronic hepatitis B infectionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2006C.-K. HUI Summary Background/aim, Although 48-week therapy with pegylated-interferons has been shown to be effective for the treatment of chronic hepatitis B virus infection, the efficacy of a shorter duration of therapy with pegylated interferons is unknown. Method, We reviewed 53 hepatitis B e antigen positive Chinese patients treated with 48 weeks of pegylated interferon alpha-2a or 24 weeks of pegylated interferon alpha-2b. Sustained virological response was defined as hepatitis B e antigen seroconversion and hepatitis B virus DNA <105 copies/mL at week 72. Results, Twenty-nine patients were treated with 48 weeks of pegylated-interferon-alpha-2a and 24 patients with 24 weeks of pegylated-interferon-alpha-2b. At the end-of-therapy, hepatitis B e antigen seroconversion and hepatitis B virus DNA <105 copies/mL were similar between the two groups of patients [9/29 (31.0%) vs. 2/24 (8.3%), respectively, P = 0.09]. At week 72, 10 of the 29 patients (34.5%) treated with 48 weeks of pegylated-interferon-alpha-2a compared with two of the 24 patients (8.3%) treated with 24 weeks of pegylated-interferon-alpha-2b had sustained virological response (P = 0.04). By logistic analysis, 48 weeks of pegylated-interferon-alpha-2a was independently associated with sustained virological response (P = 0.04 adjusted hazards-ratio 9.37). Conclusion, Further studies are required to determine the optimal duration of therapy with pegylated interferons in chronic hepatitis B. [source] Does Cerumen Have a Risk for Transmission of Hepatitis B?,THE LARYNGOSCOPE, Issue 3 2004M. Tayyar Kalcioglu MD Abstract Objectives/Hypothesis Chronic hepatitis B virus infection is a significant worldwide health problem. It affects 350 to 400 million people. The patients with chronic hepatitis B virus infection have a significant risk for the development of cirrhosis or hepatocellular carcinoma. Full awareness of the mechanisms of transmission can allows susceptible individuals to refrain from this infection. Cerumen has never been studied as a route for hepatitis B transmission. The aim of the study was evaluate the importance of cerumen in transmission of hepatitis B virus infection. Study Design This study was performed on forty patients with confirmed hepatitis B virus infection. Methods Forty cerumen specimens collected from the patients with hepatitis B virus DNA in their sera were prospectively analyzed for the presence of hepatitis B virus DNA by real-time polymerase chain reaction. Results Eleven of 40 cerumen specimens (27.5%) were positive for hepatitis B virus DNA, with counts ranging from 4.2 × 102 to 4.7 × 106 copies per sample. There was positive correlation between hepatitis B virus DNA concentrations of serum and cerumen. Half of hepatitis B e antigen (HBeAg),positive patients had detectable hepatitis B virus DNA levels (5.7 × 102 to 4.7 × 106 copies) in cerumen specimens, whereas 12.5% of cerumen specimens from anti-HBe,positive patients had hepatitis B virus DNA levels (4.2 × 102 to 7.0 × 103 copies). Conclusion Cerumen can be a potential source of transmission. Therefore, this route should be investigated in further studies for horizontal, nosocomial, and occupational transmission of hepatitis B. [source] Association between tumour necrosis factor gene polymorphisms and the clinical types of patients with chronic hepatitis B virus infectionCLINICAL MICROBIOLOGY AND INFECTION, Issue 1 2005X.-W. Xu Abstract A PCR restriction fragment length polymorphism assay was used to analyse single-nucleotide polymorphisms in the tumour necrosis factor (TNF)-, and TNF-, genes of 56 patients with chronic severe hepatitis B virus (HBV) infection, 71 patients who either had chronic mild HBV infection or who were asymptomatic carriers, and 90 healthy controls. The serum TNF-, concentrations in patients with chronic severe HBV infection were compared to those of 30 healthy controls by radioimmunoassay. The frequencies of the TNF1/2 genotype and the TNF2 allele were greater in patients with chronic severe HBV infection than in healthy controls (25% vs. 11.1%, p 0.015; 12.5% vs. 5.6%, p 0.036, respectively) and patients with chronic mild HBV infection and asymptomatic carriers (25% vs. 8.8%, p 0.011; 12.5% vs. 4.2%, p 0.015, respectively). Heterozygotes carrying the TNF2 allele had higher levels of serum TNF-, than homozygotes for the wild-type allele among all patients with chronic severe HBV infection (p < 0.01). The genotype distribution and allele frequency of TNF-, were similar for patients with chronic severe HBV infection and healthy controls, but the frequency of the TNF-,*2/2 genotype in patients with chronic mild HBV infection and asymptomatic controls was lower than for healthy controls (9.9% vs. 22.4%, p 0.043) or patients with chronic severe HBV infection (9.9% vs. 26.8%, p 0.043), although this was not significant after correction for multiple testing. It was concluded that TNF-, gene polymorphisms may play an important role as a host factor in the progression of HBV infection. [source] | ||||||||||||||||||||||