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At least 127 records · Page 7Linked to original sources
PubMed2001

Quantitation of hepatic hepatitis C virus RNA in patients with chronic hepatitis C. Relationship with severity of disease, viral genotype and response to treatment.

BACKGROUND/AIMS: To determine the correlation between hepatic hepatitis C virus (HCV) RNA and histological lesions, viral genotype or response to alpha interferon therapy. METHODS: Forty-three patients with chronic hepatitis C (14 sustained responders (SR) and 29 non-sustained responders (NSR)) were studied. A liver tissue sample was obtained before and 1 year after treatment. Quantitation of hepatic HCV-RNA was performed by competitive PCR. RESULTS: Before treatment, HCV-RNA was detectable in all liver samples. There was no association between hepatic HCV-RNA and the severity of liver lesions. There was a significant association between old age and hepatic HCV-RNA (P = 0.03). There was an association, at the limit of significance, between genotype 1 and high hepatic HCV-RNA amounts (15 x 106 and 4.1 x 10(6) copies/g, P = 0.05). Pre-treatment hepatic HCV-RNA amounts were lower in SRs than in others (0.65 x 10(6) and 13.2 x 10(6) copies/g, P = 0.0002). After treatment, no liver HCV-RNA was detectable in the SRs while in the NSRs, the HCV-RNA amounts were unchanged. CONCLUSIONS: The amount of hepatic HCV-RNA is correlated to genotype and response to interferon therapy but not to histologic lesions. Hepatic HCV-RNA clearance is observed in SRs, suggesting viral eradication.

Adult↗
PubMed2000

Clinical implications of hepatitis G virus (HGV) infection in patients of acute viral hepatitis & fulminant hepatic failure.

BACKGROUND & OBJECTIVES: Viral hepatitis is a major public health problem especially in developing countries such as India. Hepatitis viruses A, B, C, D and E are all well characterized and molecularly defined agents with unequivocal association with human liver disease but there is evidence of hepatitis in humans caused by certain transmissible agents which cannot be classified with the above hepatotoric viruses. The role of recently discovered hepatitis G virus (HGV/GBV-C) as an independent heaptitis agent is controversial. Recently, we have shown a relatively high frequency of HGV infection in fulminant hepatic failure but the virus was often detected in co-infection with hepatitis B or E virus. The present study has therefore been carried out to evaluate the clinical significance of HGV infection in acute viral hepatitis (AVH) and fulminant hepatic failure (FHF) through follow up of HGV positive patients till their clinical and biochemical recovery. METHODS: The study included 50 patients comprising 35 of AVH and 15 of FHF. These patients were evaluated on the basis of history, physical examination, liver function profile and serological markers for hepatitis A, B, C and E. Those patients serologically negative for HBV and HCV infection were further screened for HBV DNA and HCV RNA by PCR. All the samples were screened for presence of HGV-RNA by RT-PCR using inner and outer primers sequences selected from NS3 helicase region of the HGV genome. FHF patients who died were subjected to postmortem liver biopsy and these biopsy specimens were also screened for HGV-RNA. Repeat detection of HGV-RNA was done after clinical and biochemical recovery of the patients. RESULTS: Of 35 AVH patients, HGV infection was detected in 5 patients (14.3%) while 4 of 15 patients (26.6%) in the FHF group were positive for HGV-RNA. Five HGV positive AVH patients were followed till clinical and biochemical recovery and all of them tested positive for HGV-RNA at follow up (6 weeks to 6 months). Out of 4 HGV positive FHF patients, only one survived and his repeat sample after clinical and biochemical recovery tested positive for HGV-RNA. INTERPRETATION & CONCLUSIONS: The results suggest that HGV infection does occur in patients of AVH and FHF and HGV viraemia persists for a long time even after clinical and biochemical recovery. These observations point towards a possible non-pathogenic role of hepatitis G virus infection.

Base Sequence↗
PubMed1979

Demonstration of hepatitis B e antigen in hepatitis B core particles obtained from the nucleus of hepatocytes infected with hepatitis B virus.

Liver tissue infected with hepatitis B virus was homogenized and nuclei were separated by centrifugation. Hepatitis B core particles were obtained from the nucleus by the digestion with pronase followed by ultracentrifugation in a sucrose density gradient. Hepatitis B core particles were then treated with sodium dodecyl sulphate and 2 mercaptoethanol and tested for hepatitis B e antigen (HBeAg) by the haemagglutination method. The antigenicity of HBeAg was clearly demonstrated in hepatitis B core particles so treated, although untreated core particles did not reveal any detectable HBeAg activity. The localization of HBeAg in hepatitis B core particles was further supported by the results of a fluorescent antibody technique. When a frozen section of the liver infected with hepatitis B virus was stained with the specific rabbit antibody against HBeAg labelled with fluorescent isothiocyanate, only nuclei of hepatocytes were stained, in a similar distribution to hepatitis B core antigen visualized by fluorescent antibody against hepatitis B core antigen in a nearby section.

Cell Nucleus↗
PubMed2000

Immunoreactivity to various human cytochrome P450 proteins of sera from patients with autoimmune hepatitis, chronic hepatitis B, and chronic hepatitis C.

Numerous human Cytochrome P450 enzymes (CYPs) associated with 'phase I' drug metabolism have been identified. Among them, CYP2D6 is thought to be the major target autoantigen to anti-liver kidney microsome (LKM)-1 autoantibody, a characteristic feature of autoimmune hepatitis (AIH) type II. In this study, we were able to clone CYP2D6 cDNA from a human liver cDNA library and express the CYP2D6 recombinant protein, and also to prepare four other representative human CYP proteins (CYP1A2, 2C9, 2E1, and 3A4). These preparations were used to assay the immunoreactivity of patients with AIH type I (n=35) and type II (n=9). As comparison groups, sera from patients with chronic hepatitis B (n=15), chronic hepatitis C (n=55; 24 anti-LKM-1-positive, 31 anti-LKM-1-negative), and from normal controls (n=30) were included. The five CYP proteins did not react with sera from normal controls nor from patients with chronic hepatitis B. CYP2D6 reacted with sera from 100% (9/9) of AIH type II patients, 79% (19/24) of patients with anti-LKM-1-positive chronic hepatitis C, and 6.5% (2/31) of patients with anti-LKM-1-negative chronic hepatitis C. In contrast, CYP1A2 reacted with serum from one patient with AIH type I, CYP2E1 reacted with sera from two patients with AIH type I, one patient with anti-LKM-1-positive chronic hepatitis C, and two patients with anti-LKM-1-negative chronic hepatitis C, and CYP3A4 reacted with sera from one patient with AIH type II and one patient with anti-LKM-1-positive chronic hepatitis C. CYP2C9 did not react with any of the sera included in this study. From these results, it is suggested that CYPs other than CYP2D6 can function as immunotargets in certain disease conditions.

Adult↗
PubMed1993

Post-transfusional anti-HCV-negative non-A non-B hepatitis (II) serological and polymerase chain reaction analysis for hepatitis C and hepatitis B viruses.

Hepatitis C virus (HCV) is a major etilogical agent of post-transfusional and sporadic acute and chronic hepatitis in various geographical areas. However, anti-HCV seroconversion was uncommon in a recent study of patients with post-transfusional hepatitis in Paris, France (N. Asar et al., companion paper). The aim of the present study was to detect viral markers, in particular HCV RNA and hepatitis B virus (HBV) DNA, in these patients. A combination of second-generation assays for anti-HCV antibodies and the polymerase chain reaction were used to identify HCV RNA and HBV DNA sequences in serum samples collected before and after transfusion from patients who developed non-A, non-B hepatitis. Eighteen cases of acute, post-transfusional, non-A, non-B hepatitis were identified in the prospective clinical survey. Only three of these 18 subjects developed anti-HCV antibodies in second-generation tests. HCV RNA was identified in the serum of these three subjects but in none of the others. Two patients who were anti-HCV-negative had polymerase chain reaction evidence of HBV DNA. Known viral markers were not identified in 13 of the 18 patients with acute post-transfusional non-A, non-B hepatitis. These results raise the issue of HCV strains or 'non-A, non-B, non-C' viruses not identified by current HCV and HBV markers and implicated in post-transfusional hepatitis in France.

Base Sequence↗
PubMed2003

Search for hepatitis delta virus (HDV) infection in hepatitis C patients in north-eastern Poland. Comparison with anti-HDV prevalence in chronic hepatitis B.

Hepatitis C virus and hepatitis D virus have been shown to suppress HBsAg synthesis. Thus it is possible that HDV infection occurs despite the lack of detectable HBsAg. The aim of our study was to (a) determine the prevalence of HDV infection in patients with chronic hepatitis C (b) compare it with the prevalence of HDV infection in HBsAg positive patients with hepatitis B. The study group consisted of 51 chronic hepatitis C patients, 30 HIV infected drug addicts (27 of them were also positive for anti-HCV) and 102 hepatitis B patients. The participants were tested for anti-HDV, anti-HCV and HBsAg. All anti-HCV positive patients were negative for anti-HDV. Four individuals with anti-HDV belonged to hepatitis B group and constituted 3.9% of all HBsAg positive subjects. We conclude that (a) there is currently no evidence of HDV infection among HCV infected patients in our region (b) hepatitis delta infection is rare in north-eastern Poland.

Adult↗
PubMed2005

Fatal reactivation of hepatitis B post-chemotherapy for lymphoma in a hepatitis B surface antigen-negative, hepatitis B core antibody-positive patient: potential implications for future prophylaxis recommendations.

In the absence of prophylaxis, the reactivation of hepatitis B in oncology patients who are hepatitis B carriers is a well-known and often fatal complication of chemotherapy. The current recommendations in Canada and the USA are that patients who are positive for hepatitis B surface antigen (HBsAg) receive antiviral prophylaxis prior to chemotherapy. We report a 67-year-old man with B-cell lymphoma who developed hepatitis B reactivation following chemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone and rituximab. Pre-chemotherapy, the patient was negative for HBsAg, positive for hepatitis B core antibody (anti-HBc) and weakly positive for hepatitis B surface antibody. Despite treatment with lamivudine, the patient died of fulminant hepatic failure. Our experience indicates that patients who are negative for HBsAg but positive for anti-HBc are still at risk for reactivation of latent hepatitis B during and after chemotherapy and may be considered for prophylaxis.

Aged↗
PubMed2006

Aberrant hepatic expression of PPARgamma2 stimulates hepatic lipogenesis in a mouse model of obesity, insulin resistance, dyslipidemia, and hepatic steatosis.

Insulin-resistant apoB/BATless mice have hypertriglyceridemia because of increased assembly and secretion of very low density apolipoprotein B (apoB) and triglycerides compared with mice expressing only apoB (Siri, P., Candela, N., Ko, C., Zhang, Y., Eusufzai, S., Ginsberg, H. N., and Huang, L. S. (2001) J. Biol. Chem. 276, 46064-46072). Despite increased very low density lipoprotein secretion, apoB/BATless mice have fatty livers. We found that hepatic mRNA levels of key lipogenic enzymes, acetyl-CoA carboxylase, fatty-acid synthase, and stearoyl-CoA desaturase-1 were increased in apoB/BATless mice compared with levels in apoB mice, suggesting increased lipogenesis in apoB/BATless mice. This was confirmed by determining incorporation of tritiated water into fatty acids. Neither the hepatic mRNA of the lipogenic transcription factor, SREBP-1c (sterol-response element-binding protein 1c), nor the nuclear levels of the mature form of SREBP-1 protein were elevated in apoB/BATless mice. By contrast, hepatic levels of peroxisomal proliferator-activated receptor 2 (PPARgamma2) mRNA and protein were specifically increased in apoB/BATless mice, as were hepatic mRNA levels of two targets of PPARgamma, CD36 and aP2. Treatment of apoB/BATless mice for 4 weeks with intraperitoneal injections of a PPARgamma antisense oligonucleotide resulted in dramatic reductions of both PPARgamma1 and PPARgamma2 mRNA, PPARgamma2 protein, and mRNA levels of fatty-acid synthase and acetyl-CoA carboxylase. These changes were associated with decreased hepatic de novo lipogenesis and hepatic triglyceride concentrations. We conclude that hepatic steatosis in apoB/BATless mice is associated with elevated rates of hepatic lipogenesis that are linked directly to increased hepatic expression of PPARgamma2. The mechanism whereby hepatic Ppargamma2 gene expression is increased and how PPARgamma2 stimulates lipogenesis is under investigation.

Adipose Tissue, Brown↗
PubMed2005

Hepatic attenuation differences associated with obstruction of the portal or hepatic veins in patients with hepatic abscess.

OBJECTIVE: The purpose of our study was to determine the nature of the association between the attenuation difference of the hepatic parenchyma surrounding an abscess and obstruction of the regional portal vein or of the hepatic vein. MATERIALS AND METHODS: Helical CT scans of 60 patients with hepatic abscess were analyzed for the presence of complete or partial obstruction of the portal or hepatic veins and for attenuation differences in the surrounding parenchyma. Clinical (age, sex, underlying disease, and microorganism) and CT (obstruction of the portal or hepatic vein and number, location, and size of abscesses) findings were analyzed statistically for possible associations with each of regional parenchymal hyper- and hypoattenuation by using the chi-square test and multivariate logistic regression analysis. RESULTS: Regional parenchymal hyperattenuation was identified in 40 patients (67%). More patients with portal vein obstruction showed regional parenchymal hyperattenuation than patients without portal vein obstruction (22/27 patients vs 18/33, p = 0.028), and more patients with hepatic vein obstruction showed regional parenchymal hypoattenuation than those without hepatic vein obstruction (11/21 vs 3/39, p = 0.0003). Multivariate logistic regression analysis showed that portal venous obstruction was the only statistically significant predictor of regional parenchymal hyperattenuation (p = 0.032; odds ratio, 3.7) and that parenchymal hypoattenuation was associated with hepatic venous obstruction (p = 0.001; odds ratio, 44.9). CONCLUSION: Parenchymal hypo- and hyperattenuation are frequently observed in the hepatic region surrounding an abscess on dynamic CT. Moreover, these parenchymal attenuation differences are associated with regional portal or hepatic vein obstruction.

Adult↗
PubMed1986

Persistent elevation of the aminoterminal peptide of procollagen type III in serum of patients with acute viral hepatitis distinguishes chronic active hepatitis from resolving or chronic persistent hepatitis.

We measured the serum concentration of the aminoterminal propeptide of collagen type III (PIIIP) in 22 patients with acute viral hepatitis (19 hepatitis B, 3 hepatitis non-A, non-B). Nine patients showed persistent biochemical remission, 13 patients developed chronic active hepatitis (CAH); 6 of those underwent therapy with methylprednisolone and azathioprine. Thirteen patients with chronic persistent viral hepatitis (CPH) and 38 healthy individuals were also investigated. In the control group, PIIIP values were 9.5 +/- 2.25 ng/ml (chi +/- SD; range 4-14 ng/ml). All patients with acute hepatitis showed elevated PIIIP values (range 20-125 ng/ml). In the 9 patients with biochemical resolution, PIIIP normalized after a maximum of 6.5 months (range 7.5-14 ng/ml). In CAH, PIIIP was persistently elevated on the day of the diagnostic biopsy (range 15.6-35.7 ng/ml). In comparison, the patients with chronic persistent hepatitis showed a range of 5.0-15.4 ng/ml. Differences between controls and CAH and CPH/CAH were statistically highly significant (P less than 0.001). Treatment of patients with CAH by immunosuppression resulted in normal PIIIP values in 3 and persistently elevated values in 3. One additional patient had normal PIIIP after treatment with an increased dose of methylprednisolone of 16 mg p.d. Serum concentrations of PIIIP offer a non-invasive index for the development of chronic active hepatitis from acute viral hepatitis. This blood test may also be useful for monitoring immunosuppressive treatment in CAH.

Acute Disease↗
PubMed2001

Projecting severe sequelae of injection-related hepatitis C virus epidemic in the UK. Part 2: Preliminary UK estimates of prevalent injection-related hepatitis C carriers, and derivation of progression rates to liver cirrhosis by gender and age at hepatitis C virus infection.

BACKGROUND: In Part 2, we illustrate how available data can be used to obtain preliminary estimates for Scotland of prevalent injection-related hepatitis C carriers and of maternally hepatitis C virus (HCV)-infected infants. Novel approaches to reducing uncertainty about the number of Scotland's HCV infected children of injector parents are discussed in brief. Three approaches, one direct and two indirect, to estimating the number of current and ever-injectors are presented for England and Wales. METHODS: Diagnosed HCV infections in injectors and HCV test uptake by current injectors are combined with survey estimates for the ratio of ever-injectors to current injectors to estimate prevalent injection-related hepatitis C carriers. Household surveys give direct but potentially biased estimates of the number of current and ever-injectors. Indirect estimates make use of hepatitis C diagnoses in injectors, HCV prevalence and test-uptake by injectors, or exploit international comparisons. We comment on key reporting problems that inhibit synthesis of HCV progression studies; and suggest how to derive preliminary gender-and-age specific progression rates to liver cirrhosis for use in projections. RESULTS: Preliminary estimates for Scotland of prevalent injection-related hepatitis C carriers are: central estimate 39,000, inner uncertainty 16,000-59,000; of maternally hepatitis C virus (HCV)-infected infants central estimate 260, uncertainty 110-1100; and for England and Wales estimates of the number of prevalent ever-injectors are central estimate 360,000, uncertainty 240,000-835,000. Both hepatitis C prevalence in injectors and estimated numbers of current injectors are similar in Australia, and England and Wales (but not so for Scotland), Australian work on projections of severe HCV sequelae from hepatitis C infections may therefore be a suitable starting point for projections for England and Wales. Australia anticipates a doubling in the number of persons living with hepatitis C cirrhosis from 8500 in 1997 to over 17,000 in 2010. DISCUSSION: Australian projections of severe HCV sequelae used progression rates that, for simplicity, were independent of gender and of age at HCV infection. Faster HCV progression for males, and their higher injector prevalence, means that the impact of HCV infection on, for example, liver cancer may be evident to a greater extent and earlier in males.

Adolescent↗
PubMed2001

[Effects of hepatitis G virus coinfection on hepatic pathological changes of patients with chronic hepatitis B: a long-term comparative study].

OBJECTIVE: To observe the long-term effect of hepatitis G virus (HGV) coinfection on hepatic pathological changes of patients with chronic hepatitis B (CHB) and explore the pathogenicity of HGV. METHODS: Menghini method liver biopsy was performed on 45 patients with CHB twice with an interval of 5 years on a voluntary basis. The liver tissue of 21 cases was HGV nonstructural region 5 (HGV NS5) antigen positive by peroxidase anti-peroxidase (PAP) immunohistochemical staining assay (HGV coinfection group) in these two tests, and 24 cases were negative (HGV noncoinfection group). There was no significant difference in age, sex, course of disease, amount of serum HBV-DNA by competitive quantitative polymerase chain reaction assay and severity of hepatic pathological leisions between these two groups (P < 0.05) and they were treated with the same scheme and without sustained curative effeect. The hepatic pathological changes of the two groups after 5 years were compared and analysed retrospectively. RESULTS: There was no significant difference in basic hepatic pathological change, severity of inflammatory activity grade and fibrosis stage in these two groups. The numbers of cases of inflammatory activity grade G1, G2, G3, and G4 were 3, 7, 7, and 4 in HGV coinfection group, and 5, 8, 7, and 4 in HGV noncoinfection group in the beginning of observation; and were 3, 5, 7, and 6 in HGV coinfection group, and 4, 6, 8, and 6 in HGV noncoinfection group after 5 years. The numbers of cases in fibrosis stages S1, S2, S3, and S4 were 4, 7, 7, and 3 in HGV coinfection group, and 6, 8, 6, and 4 HGV noncoinfection group in the beginning of observation; and were 3, 6, 5, 7 in HGV coinfection group, and 4, 7, 5, and 8 in HGV noncoinfection group after 5 years (P > 0.05). CONCLUSION: HGV coinfection does not lead to the activation of hepatic pathological changes and does not speed up the progression of fibrosis in patients with CHB. HGV coinfection does not play an obvious role in long-term hepatic pathological changes of patients with CHB. HGV has at most a mild hepatic pathogenicity.

Adult↗
PubMed1998

Prompt hepatitis C virus suppression following hepatitis B virus superinfection in chronic untreated hepatitis C.

The natural course of chronic hepatitis C virus infection after hepatitis B virus superinfection is not clear since it is difficult to determine the chronology of the double infections. We report on a case of de novo hepatitis B virus infection in the course of chronic untreated hepatitis C, in which the time of hepatitis B virus infection is actually known. The patient eliminated HCV-RNA, both from serum and from liver tissue, soon after the clinical onset of the acute hepatitis B. Liver histology featured hepatitis with severe portal inflammation and high-grade periportal and intralobular necro-inflammatory lesions. This observation demonstrates that hepatitis C virus replication can be promptly and spontaneously suppressed by acute hepatitis B virus superinfection.

Acute Disease↗
PubMedDate not supplied

Hepatitis B virus, hepatitis non-A, non-B virus and hepatitis delta virus in lyophilized antihemophilic factor: relative sensitivity to heat.

Lyophilized plasma derivatives are more stable to heat than when they are in the liquid state. Commercial Factor VIII (antihemophilic factor) was seeded with a measured quantity of hepatitis B virus. The contaminated material was then lyophilized and subjected to heat of 60 degrees C for 30 hr. Chimpanzees were inoculated with the heat-treated antihemophilic factor or sham-treated antihemophilic factor that had been held at 4 degrees C. Surprisingly, hepatitis B virus survived the heating procedure with no apparent loss in titer: the incubation period to appearance of HBsAg was that expected for the challenge dose of virus. Even more surprising, one chimpanzee (the recipient of the unheated antihemophilic factor) also developed non-A, non-B hepatitis and two chimpanzees (recipients of the heated antihemophilic factor) also developed delta hepatitis. Neither of these agents was a contaminant of the hepatitis B virus challenge pool, since the purity of this hepatitis B virus pool was established previously in chimpanzees. Thus, both a non-A, non-B agent and the delta agent apparently contaminated the commercial antihemophilic factor. This is the first direct evidence for contamination of antihemophilic factor with the delta agent and confirms previous seroepidemiologic evidence for its presence in pooled plasma derivatives. Subsequent inactivation studies were performed with antihemophilic factor experimentally contaminated with the Hutchinson strain of non-A, non-B hepatitis virus. In these studies, heating at 60 degrees C for 30 hr in the dry state rendered antihemophilic factor free of detectable non-A, non-B hepatitis virus.

Animals↗
PubMed2005

Genotype C hepatitis B virus infection is associated with a higher risk of reactivation of hepatitis B and progression to cirrhosis than genotype B: a longitudinal study of hepatitis B e antigen-positive patients with normal aminotransferase levels at baseline.

BACKGROUND/AIMS: Longitudinal studies on the relationship between hepatitis B virus (HBV) genotypes and reactivation of hepatitis B and progression to cirrhosis were very rare. METHODS: Liver biochemistry, virological markers and ultrasound were monitored in 202 hepatitis B e antigen (HBeAg)-positive patients with normal alanine aminotransferase (ALT) at baseline for 3-20 (average 10.8) years, and the outcome was correlated with HBV genotypes. RESULTS: There were 150 genotype B and 52 genotype C patients. Hepatitis activity during the HBeAg-positive phase showed no significant difference. However, genotype B was associated with a significantly earlier and higher rate of HBeAg seroconversion. HBeAg seroconversion correlated with age at entry for genotype B and with ALT levels for genotype C. Reactivation of hepatitis B was significantly more common in genotype C patients. Five genotype B and 10 genotype C patients progressed to cirrhosis. Multivariate analysis revealed that genotype C (P = 0.03) and reactivation of hepatitis B (P = 0.0004) were independent factor predictive of cirrhosis. CONCLUSIONS: Rate and factors of HBeAg seroconversion, and rate of reactivation of hepatitis B differed between genotype B and genotype C patients. Genotype C and reactivation of hepatitis B were associated with increased risk of cirrhosis.

Adult↗
PubMed2003

Previous hepatitis B virus infection is associated with worse disease stage and occult hepatitis B virus infection has low prevalence and pathogenicity in hepatitis C virus-positive patients.

BACKGROUND: Anti-hepatitis C virus (anti-HCV) patients with chronic liver disease (CLD) frequently show markers of previous hepatitis B virus (HBV) infection. Moreover, they may carry occult HBV infection. These features might influence clinical and biochemical features as well as stage of disease. AIM: To assess the prevalence and clinical associations of previous (positivity for anti-HBs and/or anti-HBc antibodies) and occult HBV infection (positivity for HBV-DNA by nested-PCR) in the serum of anti-HCV-positive, HCV-RNA-positive, HBsAg-negative patients with various degrees of CLD seen at a tertiary referral centre. PATIENTS: A total of 119 patients fulfilled the inclusion criteria (84 chronic hepatitis and 35 liver cirrhosis). RESULTS: Forty-eight patients (40.3%) showed markers of previous HBV infection. This feature was more frequent (P = 0.02) among cirrhotics (57%) as compared to chronic hepatitis patients (33%). Chronic hepatitis patients positive for markers of previous HBV infection had worse histology as compared to negative ones (grading: 6.4 +/- 2.7 versus 4.6 +/- 3.0, P = 0.004; staging: 1.6 +/- 1.2 versus 1.0 +/- 1.0, P = 0.01). Eight patients were positive for HBV-DNA in serum (6.7%). No difference in the presence of occult HBV infection was seen between various degrees of liver disease (7.1% of chronic hepatitis, 5.7% of cirrhosis) and among patients who were positive (10.4%) or negative (4.2%) for markers of previous HBV infection. No significant biochemical, virological, or histological difference was observed between age, age at infection, duration of infection, marker patterns of previous HBV infection-matched HBV-DNA-positive and negative chronic hepatitis patients. CONCLUSIONS: Our findings suggest that previous HBV infection among anti-HCV patients is associated with worse disease stage. In these patients, the prevalence of occult HBV infection is low and there is no difference in distribution among patients with or without markers of previous HBV infection. Furthermore, it does not seem to be associated with disease stage. Lastly, at least among patients with chronic hepatitis, it does not seem to affect the severity of disease.

Adult↗
PubMed2005

Response to hepatitis B vaccine in HIV-1-positive subjects who test positive for isolated antibody to hepatitis B core antigen: implications for hepatitis B vaccine strategies.

BACKGROUND: Whether human immunodeficiency virus type 1 (HIV-1)-positive subjects who test positive for isolated antibody to hepatitis B core antigen (anti-HBc) should be vaccinated with hepatitis B vaccine is not certain. Development of an anamnestic response after vaccination would suggest previous hepatitis B virus (HBV) infection, in which case vaccination is not necessary. METHODS: Sixty-nine HIV-1-positive subjects who tested negative for hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs) received vaccination with standard hepatitis B vaccine. Twenty-nine subjects (42%) tested positive for anti-HBc, and 40 (58%) tested negative for anti-HBc. An anamnestic response was defined as an anti-HBs titer of >or=10 IU/L within 4 weeks of the first vaccination. RESULTS: The overall anamnestic response rate was 16% and was not significantly different between subjects who tested positive for anti-HBc (24%) and those who tested negative for anti-HBc (10%) before vaccination (P=.18). Approximately 50% of subjects who tested positive for anti-HBc also tested positive for antibody to hepatitis Be antigen (anti-HBe). The anamnestic response rate was higher in subjects who tested positive for both anti-HBc and anti-HBe (43%) than in subjects who tested positive for anti-HBc but negative for anti-HBe (7%) (P=.035). After a complete series of vaccinations, HIV-1/hepatitis C virus (HCV)-coinfected subjects were less likely to achieve high anti-HBs titers than were subjects infected with HIV-1 alone. CONCLUSIONS: After hepatitis B vaccination, the anamnestic response rate in HIV-1-positive subjects who tested positive for isolated anti-HBc but negative for anti-HBe was low and was comparable to that in subjects who tested negative for anti-HBc. This finding suggests that testing for anti-HBc alone may not be a reliable assessment of protection from HBV infection. HIV-1/HCV coinfection may be associated with impaired responses to hepatitis B vaccine, and evaluation of strategies to improve immunogenicity of the vaccine in such individuals is warranted.

Adult↗