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PubMed1985

Prevention of hepatitis B infection by hepatitis B immune globulin in infants born to mothers with acute hepatitis during pregnancy.

Eleven infants born to mothers with acute hepatitis B during the third trimester of pregnancy who were hepatitis B surface antigen-positive at delivery were treated with hepatitis B immune globulin within 24-48 h of birth. Five infants received one dose of hepatitis B immune globulin and 6 infants received a second dose at 1 mo of age. During the average 12.5-mo follow-up period, only 1 of 11 (9%) treated infants became hepatitis B surface antigen-positive and this individual developed acute hepatitis B at 9.5 mo of age and recovered. Twenty-four infants born to mothers with acute hepatitis B during the third trimester of pregnancy who were untreated served as historical controls. Of these, 17 (71%) showed evidence for hepatitis B infection and 15 (62.5%) became chronic hepatitis B virus carriers. This study shows that administration of hepatitis B immune globulin to infants born to mothers with acute hepatitis B is effective in preventing perinatal transmission of the hepatitis B virus. With the availability of the hepatitis B virus vaccine, the current recommendation is to give hepatitis B immune globulin to such infants within 24 h of birth, followed by three doses of the hepatitis B virus vaccine beginning soon after birth, and again 1 and 6 mo later.

Adult↗
PubMed1994

Displacement of hepatitis B virus by hepatitis C virus as the cause of continuing chronic hepatitis.

BACKGROUND/AIMS: It has been shown that hepatitis C virus (HCV) superinfection may suppress hepatitis B virus (HBV) leading to hepatitis B surface antigen (HBsAg) clearance and that hepatitis may persist after HBsAg clearance in a few patients. The role of HCV in continuing hepatitis after termination of chronic HBsAg antigenemia remains to be explored in a series of patients. METHODS: HCV markers were studied using second generation enzyme immunoassay and polymerase chain reaction with reverse transcription and were compared between 41 patients with persistent alanine aminotransferase (ALT) elevation (hepatitis group) and 82 age/sex-matched patients with normal ALT (control group) after HBsAg clearance. RESULTS: Twenty-six (63%) of the 41 hepatitis group patients were seropositive for antibodies to HCV (anti-HCV) compared with only 4 (5%) of 82 controls (P < 0.0001). Six patients of the hepatitis group and 1 control had an episode of acute hepatitis C with seroconversion of anti-HCV 1-68 months before HBsAg clearance. Of those seropositive for anti-HCV, serum HBV DNA was not detectable, and serum HCV RNA was detected in 23 (88.5%) of the 26 hepatitis patients but none of the 4 controls (P < 0.001). Liver biopsy in 6 anti-HCV positive patients with continuing hepatitis showed features compatible with chronic hepatitis C. HCV RNA, but not HBV DNA, was detected in liver tissues of these 6 patients. CONCLUSIONS: The results suggest that HCV may usurp the role of HBV in chronic hepatitis and act as the major cause of continuing hepatitis or ALT elevation after HBV/HBsAg clearance.

Adult↗
PubMed1999

Fulminant hepatic failure in acute hepatitis C: increased risk in chronic carriers of hepatitis B virus.

BACKGROUND/AIMS: The role of hepatitis C virus (HCV) in fulminant hepatitis remains controversial. This study was conducted to investigate the risk of fulminant hepatitis C in relation to HCV genotypes and concurrent infection of other viruses. PATIENTS: 109 HCV RNA positive patients from 334 consecutive cases hospitalised to a medical centre in northern Taiwan for overt acute viral hepatitis were prospectively evaluated. METHODS: HCV RNA was detected by a combined reverse transcription-polymerase chain reaction assay. HCV genotypes were analysed using a genotype specific probe based assay in the 5' untranslated region. RESULTS: 39 patients tested positive for hepatitis B surface antigen but negative for IgM antibody to hepatitis B core antigen, indicating concurrent chronic hepatitis B virus (HBV) infection. Twelve patients were hepatitis G virus (HGV) RNA positive. Genotyping of HCV disclosed 1b in 93, 1b mixed with 2a/2c or 1b mixed with 2b in 11, and not classified in five. Serum titres of HCV RNA were <10(5) copies/ml in 77, 10(5)-10(7) copies/ml in 25, and >10(7) copies/ml in seven. Eleven patients (10.1%) had fulminant hepatitis as a complication. Development of fulminant hepatitis did not correlate with age and gender of the patients, concurrent HGV infection, HCV genotypes, or serum titre of HCV RNA. However, the incidence (95% confidence interval) of fulminant hepatitis in patients with underlying chronic HBV infection was 23. 1% (9.9 to 36.3%), which is significantly higher than in those without (2.9% (-1.0 to 6.8%)). In 39 patients with concurrent chronic HBV infection, the clinical and virological characteristics showed no significant difference between those with fulminant hepatitis and those without. CONCLUSIONS: Acute hepatitis C in patients with concurrent chronic HBV infection is associated with a substantial risk of fulminant hepatitis.

Acute Disease↗
PubMed1995

Long-term follow-up of hepatitis B virus and hepatitis C virus replicative levels in chronic hepatitis patients coinfected with both viruses.

Dual infection with hepatitis B and C viruses is often encountered in endemic areas of both viruses. However, understanding of the clinical and virological implications is limited. The aim of this study was to investigate the role of each virus in liver injury and the interaction between the two viruses in dual infection with hepatitis B and C viruses. Three patients who had chronic infection with both hepatitis B and C viruses were examined, and a longitudinal study of both serum hepatitis B virus DNA and hepatitis C virus RNA levels over 4 years was undertaken. The results were correlated with serum alanine aminotransferase levels. Serum alanine aminotransferase values showed a relationship with hepatitis B virus replicative levels, but not with hepatitis C virus replicative levels in all 3 patients. Serial changes of replicative levels of both viruses were studied, and it was found that hepatitis C virus replicative levels were enhanced after the decline of hepatitis B virus replication in 1 of the 3 patients. In the remaining 2 patients, a transient rise of hepatitis C virus replicative levels in association with a decrease of hepatitis B virus replication was also observed during part of the follow-up period. These findings indicate that hepatitis B virus may play a dominant etiological role in liver injury, and that a suppressive action between hepatitis B and C viruses may occur in dual infection with both viruses.

Adult↗
PubMed2001

Risks associated with hepatitis A and hepatitis B in patients with hepatitis C.

Individuals with hepatitis C virus (HCV) are at risk for acquiring hepatitis A virus (HAV) or hepatitis B virus (HBV) because of shared risk factors. A number of organizations recommend vaccination against HAV and HBV for patients with HCV. The rationale for vaccinating these patients is to prevent hepatic superinfections. Acute HAV superinfection causes more severe disease, acute hepatic failure, and higher fatality rates in patients with underlying chronic liver disease, specifically chronic HBV infection and chronic HCV infection. Available data, although limited, suggest that HBV coinfection with HAV and HCV causes more severe hepatic injury than infection with HAV or HCV alone. At standard doses, hepatitis A and hepatitis B vaccines are safe and immunogenic in patients with mild-to-moderate hepatitis C or chronic liver disease. Regardless of disease severity, vaccination should be routinely administered to patients upon diagnosis of HCV infection. Early vaccination is important because response to vaccination is reduced as liver disease progresses. Prevaccination and postvaccination serology testing is recommended in specific populations. A new combination hepatitis A and hepatitis B vaccine has been shown to be as safe and effective as monovalent hepatitis A and B vaccines and is currently under review by the United States Food and Drug Administration. A combination vaccine would offer ease of administration and convenience and could increase compliance in patients with hepatitis C or other chronic liver disease: two groups that should be more aggressively targeted by healthcare professionals.

Adult↗
PubMed2000

Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis.

Among the many mutations found in the hepatitis B virus (HBV) genome, some have been associated with fulminant hepatitis, as exemplified by precore-defective mutations. The aim of this study was to determine whether such mutations also are found in Vietnamese cases of fulminant hepatitis B. The full-genome nucleotide sequence of HBV in three patients with fulminant hepatitis (F-2, F-3, and F-6) and one with acute hepatitis (A-3), who were admitted to Cho Ray Hospital, Ho Chi Minh City, Vietnam was ascertained. Additionally, two patients with fulminant hepatitis (F-1 and F-7) and three with acute hepatitis (A-1, A-2, and A-5) were examined only for the precore/core region of HBV. Remarkably, the nonsense mutation at precore codon 28 (Trp82Stop) was found in four of the five patients with fulminant hepatitis, while all the acute hepatitis patients harbored wild type (one had a mixture of wild and mutant types). The missense mutations within the core region, Ile97Leu and Pro130Ile/Thr/Ser, were also remarkable in fulminant hepatitis. Only F-2 was free from these precore/core mutations, but F-2 was unique in that it possessed a chimeric genotype: it could be classified into genotype C as a whole, but its X region was of genotype B, like the other four fulminant hepatitis isolates (F-1, F-3, F-6, and F-7). The codon 41 of the X protein was Pro in all three fulminant hepatitis cases examined for this region, while it was Ser in the wild-type isolates of genotype B. Of note as negative data, the mutations C1653T and T1753M of the enhancer II (Enh II) and A1762T and G1764A of the precore/core promoter regions, once reported to be relevant to severe or fulminant hepatitis, were not found in the present cases. The results with the Vietnamese cases of fulminant hepatitis corroborated results of previous studies with respect to the mutations Trp28Stop of precore and Ile97Leu and Pro130Ile/Thr/Ser of core, but not for the mutations within Enh II and precore/core promoter region. Whether the Ser41Pro mutation in the X region of genotype B HBV is Vietnam-specific or disease-specific deserves further investigation.

Adult↗
PubMed1990

[Clinical problems in non-A, non-B viral hepatitis. I. Diagnosis of non-A, non-B viral hepatitis and its role in the occurrence of acute viral hepatitis in the Czechoslovak population].

Using RIA and ELISA methods the authors examined HBsAg, anti-HBc IgM and anti-HAV IgM antibodies in 830 adult patients and 101 children with acute viral hepatitis from the catchment area of the South Moravian region. In these groups also the most frequent hepatotropic infectious agent as the possible cause of hepatitis was examined. It was revealed that in adults viral hepatitis A accounted for 22%, viral hepatitis B for 48.5%, viral hepatitis non-A, non-B for 28.8% of the group. The percentage distribution of viral hepatitis in children is different: hepatitis A predominates (65%), hepatitis B is less frequent (22%) and viral hepatitis non-A, non-B is least frequent (13%). It was demonstrated that viral hepatitis non-A, non-B is under our conditions a very frequent disease, it accounts for one quarter of all cases of viral hepatitis and if we take into account that non-A, non-B hepatitis has frequently permanent serious sequelae, then proper attention must be paid to this disease. The authors demonstrate that differentiation of types of viral hepatitis by routine methods is possible which leads to a substantially more accurate differentiation of hepatitis.

Acute Disease↗
PubMed1998

Detection of hepatitis C and E virus genomes in sera of patients with acute viral hepatitis and fulminant hepatitis by their simultaneous amplification in PCR.

A study was undertaken to investigate the role of hepatitis C virus (HCV) and hepatitis E virus (HEV), either alone or together, in the causation of sporadic acute viral hepatitis (AVH) and fulminant hepatitis (FH) by simultaneous detection of their genomes in serum samples using the reverse transcription and nested polymerase chain reaction (RT-PCR). A total of 50 patients were enrolled in the study of which 34 had AVH and 16 had sporadic FH. The serum samples were first tested for hepatitis B surface antigen (HBsAg) and immunoglobulin (Ig)M antibodies against hepatitis A virus (HAV), hepatitis B core antigen (HBcAg) and HEV and also antibodies against HCV using commercially available enzyme-linked immunosorbent assay (ELISA) kits. All samples were then subjected to RT-PCR using primers for both HCV and HEV simultaneously in the same reaction mixture. Hepatitis C or hepatitis E was diagnosed when either the antibodies or PCR or both were positive for the respective viruses. Evidence of hepatitis C was present in six of the 34 (17.6%) cases of AVH and two out of 16 (12.5%) cases of FH. Four patients in the AVH group and one of the fulminant hepatic failure (FHF) group were found to be positive by PCR and the rest by serology. But as a sole aetiological agent, HCV infection was found in only one (2.9%) case of AVH and in none of the FHF cases. Evidence of HEV infection was found in 22/34 (64.7%) and 8/16 (50%) cases of AVH and FHF, respectively. Excluding co-infection with other viruses, HEV was found to be the sole aetiological agent in 15/34 (44.1%) of AVH and 7/16 (43.7%) cases of FHF. In five (10%) (four AVH and one FHF) of the 50 cases, evidence of infection with both HCV and HEV was present. But only in two of these five cases, genomes of both HCV and HEV were co-amplified. In seven (four AVH and three FHF) out of 50 (14%) cases, no known viral agent could be detected. Our results suggest that HEV is the most common aetiological agent for both acute viral hepatitis and fulminant hepatic failure and that HCV is a rare cause of acute liver diseases although along with other viruses, evidence of either present or past HCV infection may be present in a substantial number of cases. Furthermore, advanced-stage pregnancy appears to be a potential risk factor for HEV infection and high rate of mortality in women. The study suggests that the method of simultaneous amplification of both HCV and HEV genomes could reduce the time, labour and cost involved in diagnostic work up of acute liver disease patients.

Acute Disease↗
PubMedDate not supplied

Viral hepatitis in the 1990s, Part III: Hepatitis C, hepatitis E, and other viruses.

Acute hepatitis can be caused by a number of viruses, especially A, B, C, E, delta, Epstein-Barr virus, and cytomegalovirus. Hepatitis A and B have been discussed previously in this series. The virus responsible for most cases of what commonly has been referred to as non-A non-B hepatitis has been tracked, and antibodies to certain proteins of this virus have been identified. This virus is now referred to as hepatitis C. The possible clinical outcomes after acute hepatitis C virus infection are similar to those for hepatitis B virus infection, except that hepatitis C is far more likely to become chronic. Clinical testing for hepatitis C virus infection is in its infancy and has certain limitations. Successful treatment of at least some cases of hepatitis C is possible. Hepatitis E has recently been described, primarily in third-world countries. It causes an acute hepatitis that may be particularly lethal for pregnant women. Herpesviruses may also cause hepatitis, particularly in the newborn or the immunocompromised. Exotic viruses causing acute hepatitis are enumerated.

Cytomegalovirus↗
PubMed1981

Determination of immunoglobulin M antibodies against hepatitis B core antigen and hepatitis A virus by reorienting sucrose gradient high-speed centrifugation for diagnosis of acute viral-hepatitis.

Immunoglobulin M (IgM) antibodies against hepatitis B core antigen (anti-HBc) and hepatitis A virus (anti-HAV) were determined in 41 cases of acute viral hepatitis. In sera positive for anti-HBc or anti-HAV, IgM was separated from IgG by reorienting sucrose gradient high-speed centrifugation, and the IgG- and IgM-containing serum fractions were tested for the presence of specific antibody by radioimmunoassay. At the onset of illness, 4 of the 41 cases were classified as hepatitis A, 31 were hepatitis B, and 6 were non-A, non-B hepatitis, based on the results of these tests and of assays for hepatitis B surface antigen and antibody and hepatitis B e antigen and antibody. Fourteen of these 41 patients (34%) required IgM anti-HBc or IgM anti-HAV testing or both for appropriate classification. IgM anti-HBc persisted for at least 7 weeks after onset but no longer than 17 weeks in all patients tested with transient hepatitis B surface antigen-positive acute hepatitis. IgM anti-HAV persisted up to but not longer than 62 days in the patients with hepatitis A. Therefore, IgM anti-HBc and IgM anti-HAV determinants are valuable tools for the differential diagnosis of acute A, B, and non-A, non-B hepatitis.

Antibodies, Viral↗
PubMed2006

[Relation of serological markers of hepatitis B virus and alanine transaminase to hepatic tissue pathology in patients with chronic hepatitis B].

OBJECTIVE: To investigate the association of serological markers of hepatitis B virus (HBV) and alanine transaminase (ALT) with hepatic tissue pathology in patients with chronic hepatitis B. METHODS: The serological marker of HBV, liver function and liver biopsy of 133 patients with chronic hepatitis B were measured and evaluated. The patients were divided into 4 groups according to HBeAg and HBV DNA positivity. Hepatic necrosis/inflammation grade and hepatic fibrosis were compared between the groups. RESULTS: Hepatic histological examination of all these patients showed inflammation, necrosis and different degrees of fibrosis. In patients with normal serum ALT, liver biopsy showed different degrees of inflammation, hepatic fibrosis, and even hepatocirrhosis. In patients with abnormal serum ALT negative for HBeAg, hepatic tissue inflammation and fibrosis were more serious. Hepatic tissue pathology was not paralleled with the level of HBV replication. CONCLUSION: Evaluation of the liver disease can not depend solely on serum ALT and viral loading in these patients. Hepatic tissue pathology in patients with chronic hepatitis B should be served as the most reliable evidence for evaluating hepatitis conditions and making the decision on antiviral therapy.

Adolescent↗
PubMed1991

Detection of hepatitis B virus DNA in paraffin-embedded liver tissues in chronic hepatitis B or non-A, non-B, hepatitis using the polymerase chain reaction.

We developed a polymerase chain reaction assay for the direct detection of hepatitis B virus in paraffin-embedded liver tissue and applied this assay to determine whether hepatitis B virus DNA exists in livers with chronic hepatitis non-A, non-B. Fifty five liver biopsy samples were studied: 11 from patients with HBeAg-positive chronic hepatitis (paraffin-embedded) and 44 from patients with chronic hepatitis non-A, non-B (21 paraffin-embedded; 25 fresh frozen). Thirty three (75%) of the non-A, non-B cases were positive for hepatitis C virus antibodies. Approximately 1 to 10 ng of DNA was extracted from the paraffin-embedded tissue and amplified using oligonucleotide (23-mer) primers specific for the S gene (positions 261 to 692). The beta-globin gene was used as an internal control for sensitivity because this is a single copy gene and allows for relative quantification. In each of the chronic hepatitis B livers, the expected 432-base-pair amplification product for hepatitis B virus DNA and beta-globin gene product were both detected. On the other hand, in the 21 paraffin-embedded chronic hepatitis non-A, non-B livers, no hepatitis B virus DNA was detected, although beta-globin gene was observed in all. Furthermore, in all 25 frozen non-A, non-B livers, beta-globin gene was observed, but no hepatitis B virus band was seen. The limit of detection of hepatitis B virus DNA by this method was estimated to be one genomic copy of hepatitis B virus DNA per cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Expression of the chemokine IP-10 correlates with the accumulation of hepatic IFN-gamma and IL-18 mRNA in chronic hepatitis C but not in hepatitis B.

The pathogenesis of hepatitis C virus-induced chronic liver disease is still poorly understood. Previous studies revealed enhanced hepatic expression of the Th1 prototype cytokine IFN-gamma in individuals with chronic hepatitis C. In accordance with several animal models of experimentally induced hepatitis, a Th1 lymphocyte driven inflammatory process, which involves newly infiltrated as well as resident monocytes/macrophages, has been proposed. An involvement of the interferon-gamma-inducible chemokine IP-10, which is chemoattractive for stimulated Th1 cells and monocytes, is also suggested. Using an HBV transgenic mouse model, a reduction of hepatic infiltration and liver disease was achieved recently by administration of antibodies directed against the interferon-gamma-inducible chemokine Mig and against IP-10. In the present study, expression of IP-10 was investigated both in serum and in the liver of patients with chronic hepatitis C and hepatitis B. Patients with liver diseases of non-viral etiologies served as controls. IP-10 expression was highest in hepatitis C. In chronic hepatitis C, but not in chronic hepatitis B nor in liver disorders unrelated to viral infections, IP-10 expression was strongly correlated with the amount of transcripts for IFN-gamma and to the amount of transcripts for the constitutively expressed macrophage derived cytokine IL-18. Hepatic inflammatory activity, however, was found to be associated more closely with IFN-gamma than with IP-10 or IL-18 mRNA expression. The data support the hypothesis that IP-10 is responsible for the recruitment of Th cells and monocytes in chronic hepatitis C, and suggest that its role in chronic hepatitis B is less determining. Moreover, they deliver additional support for the view that IFN-gamma still has to be considered as a mediator that determines the outcome of inflammation, e.g., via its ability to activate IL-18 expressing cells and to initiate a delayed type hypersensitivity reaction.

Adolescent↗
PubMed1977

Nuclear fluorescence of liver cells for IgG in viral hepatitis B: significance and relation to hepatitis B-core and anti-hepatitis B-core formation.

The occurrence of anti-HBcAg antibodies in the blood as determined by indirect immunofluorescence and its relation to the occurrence of HBsAg in the cytoplasm and of HBcAg and IgG in the nuclei of hepatocytes were studied in the following groups of patients (total of 123 biopsies): I. 64 HBAg-negative patients with various liver diseases; II. 51 HBAg-positive patients without therapeutical immunosuppression (6 acute hepatitis, 10 nonspecific reactive and 10 chronic persistent hepatitis, 19 chronic aggressive hepatitis, 6 "Hippie"-hepatitis); III. 8 kidney transplant recipients. It could be shown that nuclear IgG is found only if both parameters can be demonstrated at the same time: HBcAg in liver cell nuclei and anti-HBcAg antibodies in the serum in titers higher than 1:64. Accordingly, all types of hepatitis with excess formation of nuclear HBcAg (early phase of acute hepatitis, chronic aggressive hepatitis and chronic non-aggressive forms with generalized core formation, i.e. carrier state or chronic persistent hepatitis of the HBc type) may show nuclear fluorescence for IgG. All forms of hepatitis B without detectable core formation (acute hepatitis in the elimination phase, chronic non-aggressive hepatitis with isolated HBsAg expression, i.e. carrier state or chronic persistent hepatitis of the HBs type, posthepatitic phase) do not present nuclear IgG despite eventual anti-HBcAg formation. Finally, lack of anti-HBcAg or very low titers associated with lack of IgG in hepatocytic nuclei do not exclude generalized core formation in liver cell nuclei in chronic persistent hepatitis of effectively immunosuppressed patients. Although the demonstration of nuclear IgG has several diagnostic and prognostic consequences in common with the demonstration of HBcAg, a specific search for the core antigen in the tissue is needed for the correct appraisal of the HBcAg- and HBsAg tissue expression pattern and the associated disease.

Antigen-Antibody Complex↗
PubMed2000

Hepatectomy for hepatitis B-, hepatitis C-, and dual hepatitis B- and C-related hepatocellular carcinoma in Taiwan.

To evaluate the surgical results of patients with hepatitis B-, hepatitis C- and dual hepatitis B- and C-related hepatocellular carcinoma (HCC), we reviewed the clinical records 252 patients (196 men and 56 women) with complete profiles of hepatitis B and hepatitis C infection who had hepatectomies to treat HCC from March, 1992, to August, 1998. The patients were divided into four groups, 30 patients (11.9%) without either hepatitis B surface antigen or anti-hepatitis C antibody (N-HCC group), 133 patients (52.8%) with hepatitis B infection only (B-HCC group), 66 patients (26.2%) with hepatitis C infection only (C-HCC group), and 23 patients (9.1%) with dual hepatitis B and C infection (BC-HCC group). Compared with the patients in the other groups, the patients in the C-HCC group were older and had more severe cirrhotic change of the liver. The surgical complication rates and hospital mortalities in the C-HCC and BC-HCC groups were 30.3% and 12.1% and 30.4% and 17.4%, respectively, which were higher than those in the N-HCC (13.3%, 3.3%) and B-HCC (15.8%, 3.8%) groups. The mean disease-free survivals for the N-HCC, B-HCC, C-HCC, and BC-HCC groups were 31.4, 25.4, 38.9 and 13.8 months, respectively, with the difference between the four groups being significant (P < 0.05). However, the mean overall survival times, 38.3 months for the N-HCC group, 37.2 months for the B-HCC group, 52.1 months for the C-HCC group, and 32.7 months for the BC-HCC group, were not significantly different (P = 0.146). In conclusion, surgical treatments for HCC related to hepatitis C or dual hepatitis B and C infection were associated with a higher surgical complication rate and hospital mortality. Hepatocellular carcinoma related to dual hepatitis B and C infection recurred earlier after hepatectomy, but the overall survival of the four groups was not significantly different.

Adult↗
PubMed2004

Elevated resistive index in the hepatic artery as a predictor of fulminant hepatic failure in patients with acute viral hepatitis: a prospective study using Doppler ultrasound.

To assess the sensitivity and specificity of the resistive index of the hepatic artery, which is related to the vascular resistance of the artery, for the prediction of fulminant hepatic failure, we performed Doppler ultrasonography examinations on the hepatic arteries of 72 patients with acute viral hepatitis (25 of whom developed fulminant hepatic failure and 47 of whom recovered without developing fulminant hepatic failure) as well as the hepatic arteries of age- and sex-matched controls. The mean resistive index of the hepatic arteries in patients who developed fulminant hepatic failure was significantly larger than that of patients who recovered without developing fulminant hepatic failure (P < 0.01). When a resistive index cutoff level of 0.74 was used, an 84% sensitivity and a 94% specificity were obtained for the prediction of fulminant hepatic failure. An elevated resistive index of the hepatic artery may be useful for predicting the patient's clinical outcome and determining the need for a liver transplantation in patients with acute viral hepatitis.

Acute Disease↗
PubMed1998

Outbreak of enterically-transmitted hepatitis due to hepatitis A and hepatitis E viruses.

BACKGROUND/AIMS: One hundred and eleven patients with acute hepatitis and 61 controls were investigated for hepatitis serological markers in order to determine the viral etiology of cases involved in a waterborne epidemic of hepatitis observed in 1993 in Djibouti, Republic of Djibouti (East Africa). These cases occurred both in indigenous Djiboutians, and in French soldiers and their families in Djibouti. A retrospective study of the viral etiology of acute hepatitis cases observed in French soldiers and relatives living in Djibouti during the 3-year period preceding the epidemic was also undertaken. METHODS: HAV, HBV and HCV infections were investigated using commercial ELISA tests. HEV infections were investigated by testing IgG and IgM-specific antibodies by means of three different ELISA tests using recombinant proteins or synthetic peptides. RESULTS: Hepatitis A was observed in 37 (33%) and hepatitis E in 43 (39%) of the 111 cases of acute hepatitis recorded during this epidemic. Hepatitis B represented only 6% of the indigenous cases and hepatitis C was not observed among the cases investigated. Anti-HEV IgG antibodies were also detected in 19% of the indigenous control group. CONCLUSION: These results suggest that both HAV and HEV were responsible for this waterborne epidemic of acute hepatitis. However, HAV and HEV infections were not equally distributed between French expatriates and Djibouti residents. Whereas HAV infections were mainly observed in French patients, HEV was almost exclusively found in indigenous patients. This study reports for the first time a waterborne outbreak of acute hepatitis simultaneously due to HAV and HEV.

Adolescent↗
PubMed1998

Clearance of persistent hepatitis B virus infection in Chinese bone marrow transplant recipients whose donors were anti-hepatitis B core- and anti-hepatitis B surface antibody-positive.

Thirteen hepatitis B surface antigen-positive Chinese patients who received hepatitis B surface antibody-positive marrow (hepatitis B core antibody-positive or -negative: 6 and 7, respectively) via allogeneic bone marrow transplantation (BMT) were studied. After BMT, 4 recipients had serologic clearance of hepatitis B surface antigen from hepatitis B core antibody-positive marrow, but none of the recipients of hepatitis B core antibody-negative marrow had serologic clearance (P=.02). There was no significant difference in the donors' hepatitis B surface antibody titer before BMT for patients with or without serologic clearance of hepatitis B surface antigen (2255.2+/-4244.0 vs. 854.2+/-2306.7 mIU/mL; P=not significant). Adoptive immunity clearance of hepatitis B surface antigen was favored by hepatitis B core antibody positive-donor marrow and was not related to donor pre-BMT hepatitis B surface antibody titer.

Adolescent↗