Acute hepatic failure in infective hepatitis with a report of six cases.
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A NON-ENVELOPED VIRUS: The hepatitis E virus is non-enveloped and measures approximately 32-34 nm in diameter. Its genome is a single stranded 7.5 kb RNA with three open-reading frames designated ORFI, 2 and 3. There is only one genotype, but several strains have been identified, with relatively high homology. LARGE OUTBREAKS: The virus is transmitted by the teco-oral route, usually from contaminated drinking water. Large outbreaks, sometimes involving over 100,00 cases, have been reported in many developing countries in Asia, Africa, the Middle East and Central America. FULMINANT HEPATITIS: The overall frequency of fulminant hepatitis is 0.5 to 3 p. 100, and, for unknown reasons, in pregnant women it reaches 15 to 25 p. 100. Vertical transmission from mother to infant appears to be frequent, with occurrence of clinical, occasionally fatal hepatitis. ELISA TEST: Detection of IgG and IgM antibodies is possible with current ELISA tests. PERSPECTIVES: Recombinant vaccines are currently being tested in animals and should allow an efficient prevention in the near future.
In 39 unselected patients with acute infective hepatitis diagnosed on clinical, epidemiological, and pathological findings, smooth muscle (S.M.) antibody was found in 87% and hepatitis-associated antigen in 33%. The incidence of S.M. antibody was highest during the first month after the onset of symptoms, and the antibody was preponderantly IgM at this stage.S.M. antibody and hepatitis-associated antigen occurred independently, and unlike hepatitis-associated antigen, which was strongly associated with possible parenteral exposure to infection, the incidence of S.M. antibody was not related to the presumed mode of exposure. It is concluded that production of S.M. antibody is more directly related to liver cell damage than to the presence of hepatitis-associated antigen in the serum.
Tumour necrosis factor alpha (TNFalpha) is a pivotal cytokine in host defences with broad ranging effects on the innate and adaptive immune systems. Clinically, TNFalpha inhibitors have demonstrated remarkable efficacy in a wide range of autoimmune and inflammatory disorders but clearly at the cost of heightened susceptibility to a variety of infections in those treated with these agents. Most reports to date have described increased susceptibility to intracellular pathogens in patients with underlying chronic viral infections, but little in the way of adverse event reporting in these patients has occurred. While the reported experience to date is rather limited, TNFalpha inhibitors have displayed a reasonable safety profile in the setting of some chronic viral infections and in certain circumstances have demonstrated adjunctive activity in the treatment of these infections. Given the high prevalence of chronic viral infections in patients who are candidates for anti-TNF therapy and the potential for these agents in the treatment of chronic viral illness, additional studies are urgently needed to assess the risks and benefits of such therapy in these populations.
Forty-six patients with chronic hepatitis delta virus infection were followed between 6 and 116 mo (mean = 32.8 mo; median = 24 mo). Nineteen patients (41%) demonstrated clinical courses with episodes of biochemical reactivation (ALT levels greater than or equal to 10 times baseline values [group A]). Twenty-seven patients (59%) had stable clinical courses without biochemical reactivation (group B). Patients in group A were younger than those in group B (30.5 vs. 35.3 yr; p = 0.03), were less likely to be intravenous drug abusers (16% vs. 52%; p = 0.01) and were more likely to be homosexual (58% vs. 22%; p = 0.01). Serum hepatitis B virus DNA, hepatitis delta virus RNA, IgM antibody to HBc, HBeAg, antibody to HBe and IgG and IgM antibody to hepatitis delta virus were measured in all patients. In group A, these markers were studied before and during reactivation and during remission. In group B, these parameters were studied in a random fashion at 7- to 10-mo intervals. The presence of antibodies to human immunodeficiency virus and hepatitis C virus was assessed in all patients. A total of 38 biochemical reactivation episodes was noted among the 19 patients in group A. Eleven had sequential changes in hepatitis delta virus markers, suggesting that the exacerbations were due to hepatitis delta virus. In three, the sequential changes of viral markers were consistent with the exacerbations due to hepatitis B virus. In five other patients, no sequential changes in viral markers could be demonstrated to correlate with the biochemical exacerbations.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Viral hepatitis is a cause of hepatic dysfunction in children with ALL in remission during maintenance therapy is debated. The aims of the current study were (1) to explore the incidence of hepatic dysfunction in a group of children (Egyptian and Saudi) with ALL under maintenance therapy, (2) to study the prevalence of hepatitis B (HBV) and/or C (HCV) infection and their contributions to chronic liver disease that might be induced by maintenance therapy. PROCEDURE: The current study included 105 children with ALL (54 Egyptian and 51 Saudi). All eligible patients had been on maintenance therapy for at least 12 months and all had serial assessments of liver function. These included determination of total bilirubin, AST, ALT, and alkaline phosphatase. Markers for HBV and HCV including HBsAg, anti-HBC, and anti-HCV and for some patients HCV RNA by PCR were studied. Percutaneous liver biopsy was performed for a group of children. RESULTS: The prevalence of hepatitis infection (HBV and/or HCV) among Egyptian children was found to be high (43/54-80%). Only five Saudi children had evidence of exposure to HBV (5/51-9.8%), P<0.0001. During the period of study, 22 Egyptian patients vs. four Saudi patients (41 vs. 7.8%, P<0.0001) experienced at least one episode of elevation of liver enzymes, three times the upper limit of normal or more. Twenty-six of the 48 patients (54%) with HBV and/or HCV infection had episodes of elevated liver enzymes, while there was no occurrence among the patients negative for HBV and HCV. In patients with HBV infection, the presence of HBsAg was strongly associated (100%) with elevated liver enzymes. Histopathologic examination of liver biopsies obtained from 35 patients revealed that all five patients negative for HBV and HCV had normal liver biopsies in spite of being under maintenance therapy. CONCLUSION: In children undergoing treatment for ALL, elevations in liver enzymes may be primarily due to hepatitis viruses. However, maintenance therapy using known hepatotoxic drugs, may have additive deleterious effects. Liver enzymes are normalized in affected patients when maintenance therapy is temporarily suspended.
Viral hepatitis is an important health problem worldwide. Globally, three major viruses are the leading cause of hepatitis: hepatitis A, B, and C. In this study, we have investigated the pattern of hepatitis among the National Guard personnel and their extended families seen in the central region of Saudi Arabia. The most dominant type of hepatitis infection was hepatitis B virus (HBV), followed by hepatitis C virus (HCV), and to a lesser extent hepatitis A virus (HAV). Our results showed three different age groups at risk of acquiring the infection: HAV, which is mainly a disease of the young; HBV, a disease of adolescents and adults; and HCV, a disease of the elderly. There was no significant difference in the male:female ratio in HAV and HCV; however, as seen in the developed countries, more males were affected with HBV than females. These data will pave the way for further studies by identifying the risk groups for the three major hepatitis infections and by using the data as a preventive tool to educate those risk groups.
Imaging plays a significant role in the detection, characterization and treatment of hepatic infections. Infectious diseases of the liver include pyogenic and amoebic abscesses and parasitic, fungal, viral and granulomatous infections. With increases in worldwide travel, immunosuppression and changing population demographics, identification of cases of hepatic infection is becoming more common in daily practice. Knowledge of the imaging features seen with hepatic infections can assist in early diagnosis and timely initiation of appropriate therapy. This review presents the imaging appearances of hepatic infections, emphasizing specific features that may contribute to the diagnosis. Examples of the imaging findings seen with pyogenic and amoebic abscesses, infection with Echinococcus granulosus (Hydatid), schistosomiasis, candidiasis and tuberculosis (TB) are presented.
We describe an unusual case involving an infected hepatic cyst. An 88-year-old woman presented with acute onset of right upper quadrant abdominal pain, mild left lower abdominal pain, diarrhea, and fever. On admission, computed tomography revealed multiple hepatic cysts including an 8-cm cyst located in the left medial segment of the liver, which demonstrated a thickened wall enhanced with contrast media. Ultrasonography showed an 8-cm hypoechoic lesion which differed in appearance from the other, anechoic hepatic cysts. The serum concentration of C-reactive protein was 29.8 mg/dL; white blood cell count, 12,800/microL; CA19-9, 96 U/mL; and CEA, 2.2 ng/mL. Diagnosis of infected hepatic cyst was made by percutaneous transhepatic drainage of the cyst. Milky fluid was obtained and the patient's right upper quadrant abdominal pain resolved after drainage. The cyst fluid CA19-9 concentration was 18,000 U/mL. Cytology of the cyst fluid was negative. Serum CA19-9 (41 U/mL) and CEA (1.8 ng/mL) concentrations were improved 1 week after drainage. Escherichia coli was cultured from the drainage fluid. The patient was discharged 27 days after admission. Percutaneous transhepatic drainage is effective in the treatment of infected hepatic cysts.
Despite the low susceptibility of BALB/c mice to hepatic infection by Plasmodium berghei, this animal model is routinely used to investigate the basic biology of the malaria parasite and to test vaccines and the immune response against exoerythrocytic (EE) stages derived from sporozoites. A murine model in which a large number of EE parasites are established would be useful for furthering such investigations. Therefore, we assayed six mouse strains for susceptibility to erythrocytic and hepatic infections. The administration of 50 sporozoites by intravenous inoculation was sufficient to establish erythrocytic infections in five of five C57BL/6 mice compared with 10,000 sporozoites required to infect 100% of BALB/c mice. To assay for hepatic infections, mice received an intravenous inoculum of 10(6) sporozoites, and liver sections for light microscopy and histology were obtained at 29 and 44 h postinoculation. EE parasites were visualized by immunofluorescence, using an antibody to a P. falciparum heat shock protein. The mean number of EE parasites per 100 cm2 for C57BL/6 and A/J strains was significantly higher than that for BALB/c (2,190 +/- 260, 88 +/- 38, and 6 +/- 2, respectively). The proportion of inoculated sporozoites transforming into liver schizonts was 8.2% in C57BL/6 and < 1% in C3H/HeJ, DBA/1, and Swiss CD-1/ICR mice. Nonspecific inflammatory infiltrates around EE parasites were less prevalent in liver sections from C57BL/6 mice than in those from BALB/c mice, which contributed to the decrease in developing EE stages in BALB/c mice. These data indicate that the C57BL/6-P. berghei system is preferable for investigating the biology and immunology of liver stage parasites.
Determining the possible association of viral hepatitis infection and degree of pruritus is the primary concern of this study. Ninety-six adequately dialyzed CAPD patients (47 male and 49 female) and 526 normal controls (266 male and 260 female) were enrolled. Blood hemoglobin, ferritin, electrolytes, calcium, phosphate, albumin, urea, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase, and bilirubin were analyzed by routine methods. Serum HBsAg was examined, using a radioimmunoassay method and the anti-HCV, an enzyme immunoassay method. All cases were interviewed with a standardized questionnaire. The highest possible pruritus score (PS) was 22. The prevalences of HBsAg(+) and anti-HCV(+) were 14.6% and 17.7%, respectively. The mean PS in all 96 CAPD patients was 11.6 (range 7-22). The mean PS were 11.8 +/- 0.6 and 12.5 +/- 1.0 for patients infected with HBV and HCV, respectively. Both were significantly higher than that (10 +/- 0.9) of patients without hepatitis infection. AST and ALT were significantly higher in patients infected with viral hepatitis than those without. The other biochemical parameters were not significant. Thirty-seven (38.5%) of our 96 patients had mild pruritus (PS < or = 7) and 11 (15.9%) had severe pruritus (PS > or = 15). Of the 83.9% (26/31) patients with viral hepatitis, the grades of skin itching were moderate to severe; whereas those of the patients without viral hepatitis, 53.6% (37/69) belonged to the group of moderate to severe pruritus (p = 0.003, chi 2 test with Yates' correction). The authors recommended screening of viral hepatitis infection to be undertaken for uremic patients with unexplained skin itching.
Naturally occurring malaria, arbovirus infection and hepatitis in monkeys can be a hazard for the investigator and might interfere with the outcome of experiments. 63 young adult Macaca fascicularis from Malaysia were screened for these infections. About 1 year after their arrival in France, parasitaemia due to Plasmodium spp., was present in 6.4% of the animals and specific antibodies in 55.5%. 19 of 35 initially positive monkeys were tested again 2 years later. Parasitaemia was found in 1 of 4 monkeys and antibodies in 11 of 19 monkeys which were initially positive. 9 of the monkeys initially tested had low titres of antibodies to the Flavivirus genus. All animals were negative for the hepatitis B surface antigen and anti-HBc. The prevalence of IgG antibodies against hepatitis A was 46.0%. The implications in terms of control are discussed.
Structural chromosomal aberrations, in the form of breaks, were found in a significantly higher proportion of bone marrow cells in patients with infective hepatitis than in controls. These anomalies were observed during the first and third weeks after the onset of jaundice but had subsided by the sixth week. Chromosomal aberrations did not appear to be related to the severity of infective hepatitis or to the sex or age of the patients.The distribution of chromosomal abnormalities did not appear to be random; they were observed predominantly in the A(2) and B(4-5) series. Since no abnormalities were detected in the G-group chromosomes, no evidence in support of a relationship between infective hepatitis and Down's syndrome was obtained. Numerical chromosomal aberrations were not observed, nor was any evidence obtained that mitotic activity of bone marrow cells is suppressed in patients with infective hepatitis.
Cellular DNAs from human livers chronically infected with hepatitis B virus (HBV) were analyzed by Southern blot hybridization for the presence of integrated HBV DNA. In 15 of 16 chronically infected hepatic tissues, random HBV DNA integration was evident. By molecular cloning and structural analyses of 19 integrants from three chronically infected hepatic tissues, deletion of cellular flanking DNA in all cases and rearrangement of HBV DNA with inverted duplication or translocation of cellular flanking DNA at the virus-cell junction in some cases were noted. Thus, the rearrangement of HBV DNA or cellular flanking DNA is not a specific incident of hepatocellular carcinoma formation. Detailed analyses of various integrants bearing rearranged viral DNA failed to indicate any gross structural alteration in cellular DNA, except for a small deletion at the integration site, indicating that viral DNA rearrangement with inverted duplication possibly occurs before integration of HBV DNA. Based on nucleotide sequencing analyses of virus-virus junctions, a one- to three-nucleotide identity was found. A mechanism for this inverted duplication of HBV DNA is proposed in which illegitimate recombination between two complementary viral strands may take place by means of a nucleotide identity at the junction site in a weakly homologous region (patchy homology) on one side of adjoining viral sequences. For virus-cell junctions, the mechanism may be basically similar to that for virus-virus junctions.
BACKGROUND: There are conflicting reports on the prevalence of hepatitis B and C virus (HBV and HCV) mediated chronic liver disease (CLD) in India. AIM: To study the prevalence of HBV and HCV associated in CLD in north India. MATERIAL AND METHODS: Eighty five patients (66 males, 19 females; age range 16-70 years) with unequivocal CLD were analysed. CLD patients with nonviral aetiologies were excluded. All sera were tested for anti-HCV by EIA (third generation), HBsAg, IgM and IgG anti-HBc, HBeAg/Anti-HBe by EIA (Abbott Diagnostics, IL). Positive anti-HCV results were confirmed by RIBA-II assay. RESULTS: Sixteen (18.8%), 22 (25.9%) and 21 (24.7%) patients had HBV, HCV and HBV + HCV infection, respectively. Twenty six (30.6%) CLD patients had no viral markers. CONCLUSION: HCV is emerging as an important cause of CLD in India. Dual infection (HBV + HCV) is seen in 25% patients. Dual infection influences the prognosis and response rates to interferon therapy.
Experimental duck virus hepatitis infection of 11-day-old white Pekin ducklings having specific maternal antibodies revealed significant changes in some biochemical constituents and enzymes of the serum during the 3 weeks following exposure. These changes included a marked decrease in the total proteins and the albumin fraction, together with a significant elevation in levels of alkaline phosphatase, glutamic pyruvic transaminase, bilirubin, and creatinine. Most of these changes were attributed primarily to a deranged liver function associated with duck virus hepatitis infection.
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The safety of blood and blood products is based on three interdependent activities: selection of safe donors, laboratory testing, and, where applicable, treatment of the product to reduce residual infectivity. Posttransfusion hepatitis has provided both the initial stimulus and the model for these procedures. The procedures have resulted in a progressive increase in the safety of the blood supply, which is continuing, as evidenced by a 50% decrease in the frequency of reported posttransfusion hepatitis over the past two years.