non-B Fulminant Hepatitis Research Articles

Etiologic considerations of fulminant non-A, non-B viral hepatitis in Japan: analyses by nucleic acid amplification method.

The etiology of fulminant non-A, non-B hepatitis has remained unclear, even after the identification of hepatitis C and E viruses. To study the possible involvement of hepatitis B, C, D, and E virus infections, viral genomes were amplified by a sensitive polymerase chain reaction method in sera and liver tissues obtained from 20 patients serologically diagnosed with non-A, non-B fulminant hepatitis (n = 14), acute hepatitis severe type (n = 2), and ordinary acute hepatitis (n = 4). Hepatitis C or E virus RNA could not be detected in sera obtained at admission from these patients. Hepatitis B virus DNA was detected in sera from 3 patients with fulminant hepatitis and in liver from 9 patients with fulminant hepatitis or acute hepatitis severe type. These results suggest that HCV might not be involved in fulminant non-A, non-B hepatitis, and HBV might be related to some of the serologic "non-A, non-B" viral hepatitis cases in Japan.

Hepatitis C virus infection involved in fulminant hepatitis in Japan

Serum samples obtained from 32 patients with fulminant hepatitis (FH) of varying etiology were tested for anti-hepatitis C virus antibody (anti-HCV) and HCV RNA. Both anti-HCV and HCV RNA were detected in one of eight patients (13%) with FH due to hepatitis A virus (HAV) and three of nine hepatitis B virus (HBV)-induced FH patients (33%) in serum samples obtained prior to plasma exchange therapy and blood transfusion. Of the four patients positive for anti-HCV, three had an anti-HCV exceeding the cut-off index of 5.00. On the other hand, all 15 patients with non-A, non-B FH were negative for anti-HCV in the initial samples. However, HCV RNA was detected in four of the 15 patients (27%) negative for anti-HCV. These results strongly suggest that acute HCV infection may exist in some patients with non-A, non-B FH. Moreover, it is suggested that superinfection of HAV or HBV to HCV carrier may enhance the risk of FH in some patients.

Contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan

To assess the contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan, we compared 10 major clinical features among 7 patients with type B fulminant hepatitis (type B group), 13 patients with non-A, non-B fulminant hepatitis with evidence of hepatitis C virus infection (type C group) and 10 patients without evidence of hepatitis C virus infection (NANB group). Duration from first symptom to coma and that from onset of jaundice to coma was significantly longer in the type C group (median = 39 and 25 days, respectively) and in the non-A, non-B group (median = 29 and 12 days, respectively) than in the type B group (median = 9 and 2 days, respectively) (p < 0.01). The maximum median AST level was significantly lower in the type C (1,689 U/L) and non-A, non-B groups (1,353 U/L) than in the type B group (5,780 U/L) (p < 0.05). Serum transaminase levels showed a single peak in six of seven of the type B patients, whereas they formed two or more peaks in all of the type C patients and in most of the non-A, non-B group (p < 0.05). Six of seven in the type B group, 6 of 13 in the type C group and 4 of 10 in the non-A, non-B group survived (p < 0.05). We found no significant difference in any of the 10 clinical features between the type C and non-A, non-B groups. Compared with type B fulminant hepatitis, type C and most cases of non-A, non-B fulminant hepatitis in Japan are, thus, characterized by slower and less severe but more persistent hepatocyte destruction. (HEPATOLOGY 1994;19:829–835.)

Contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan

To assess the contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan, we compared 10 major clinical features among 7 patients with type B fulminant hepatitis (type B group), 13 patients with non-A, non-B fulminant hepatitis with evidence of hepatitis C virus infection (type C group) and 10 patients without evidence of hepatitis C virus infection (NANB group). Duration from first symptom to coma and that from onset of jaundice to coma was significantly longer in the type C group (median = 39 and 25 days, respectively) and in the non-A, non-B group (median = 29 and 12 days, respectively) than in the type B group (median = 9 and 2 days, respectively) (p < 0.01). The maximum median AST level was significantly lower in the type C (1,689 U/L) and non-A, non-B groups (1,353 U/L) than in the type B group (5,780 U/L) (p < 0.05). Serum transaminase levels showed a single peak in six of seven of the type B patients, whereas they formed two or more peaks in all of the type C patients and in most of the non-A, non-B group (p < 0.05). Six of seven in the type B group, 6 of 13 in the type C group and 4 of 10 in the non-A, non-B group survived (p < 0.05). We found no significant difference in any of the 10 clinical features between the type C and non-A, non-B groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Etiological role of hepatitis E virus in sporadic fulminant hepatitis.

Non-A, non-B hepatitis viruses have been implicated as the etiological agent(s) in up to 60% of patients with fulminant hepatitis. These agents are reported to induce a higher mortality than other causes of fulminant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV) at present constitute the major identifiable non-A, non-B hepatitis agents. Of these, HEV has been established as the sole cause of epidemic hepatitis in Afro-Asian countries, and fulminant hepatitis has been recorded during such epidemics. However, in sporadic cases, the etiological role of HEV in fulminant hepatitis has remained uncertain. The role of HCV in acute liver disease and fulminant hepatitis remains unclear. The present study was undertaken to investigate the association of HEV and HCV in patients with fulminant hepatitis by direct detection of the viral genome using reverse transcription-polymerase chain reaction (RT-PCR). Serum samples from 50 serologically identified non-A, non-B fulminant hepatitis cases negative for cryptic hepatitis B virus (HBV) infection examined via PCR were tested for HEV and HCV RNA using RT-PCR. For HEV primers from the nonstructural region (ORF-1) were used, and for HCV primers from the highly conserved 5' untranslated regions were used. The products were analysed using agarose gel electrophoresis and confirmed by hybridisation with radiolabelled internal oligonucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non-A, non-B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In 11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (40%) cases, HEV was detected alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Non-A, non-B fulminant hepatitis is also non-E and non-C.

to define the roles of the hepatitis C and E viruses (HCV and HEV) in non-A, non-B (NANB) fulminant hepatitis. we utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANB fulminant hepatic failure (FHF) patients. none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitis patients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA. we did not find evidence implicating HCV or HEV in presumed viral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with autoimmune hepatitis, drug-induced hepatotoxicity, or halothane hepatotoxicity.

Minimal role of hepatitis C virus infection in childhood liver diseases in an area hyperendemic for hepatitis B infection

To investigate the role of hepatitis C virus (HCV) in childhood liver disease in Taiwan, an area hyperendemic for hepatitis B, we studied antibody to HCV (anti-HCV) with a second generation enzyme immunoassay in 195 infants and children, including 96 hepatitis B surface antigen (HBsAg) positive children (66 with chronic hepatitis B, 23 children with hepatocellular carcinoma, and 7 with fulminant hepatitis B), 6 children with fulminant non-A, non-B hepatitis, 42 infants with neonatal hepatitis, 11 with biliary atresia, and 40 prospectively followed blood recipients. For comparison, another 748 apparently healthy children (from neonates to 12 years) were also screened for anti-HCV. The positive rate of anti-HCV was low in both apparently healthy children (0.13%) and patients with various liver disorders (0 to 4.4%) except fulminant hepatitis. The seropositive rate in 6 cases of non-A, non-B fulminant hepatitis was higher (16.7%) although the case number was too small. We conclude that HCV is generally not a major etiologic factor in the liver diseases of Taiwanese children.

Anti-HCV immunoglobulin M antibody in patients with hepatitis C.

Anti-hepatitis C virus (HCV) immunoglobulin M antibody titres were measured by an enzyme-linked immunosorbent assay method in 16 patients with non-A, non-B acute hepatitis (NANB AH), 13 with non-A, non-B fulminant hepatitis (NANB FH) and nine with type C chronic hepatitis. Anti-HCV IgM was positive in one of the 16 patients with NANB AH, six of the 13 with NANB FH, and five of the nine with type C chronic hepatitis. Anti-HCV IgG was positive in eight of the 16 patients with NANB AH and eight of the 13 with NANB FH. Either anti-HCV IgM or anti-HCV IgG were positive in 10 of the 13 patients with NANB FH. All of the five anti-HCV IgM positive patients with type C chronic hepatitis were undergoing an exacerbation of the diseases, while all of the anti-HCV IgM negative patients were in a remission stage which had lasted for more than 6 months. The findings of this study suggest that anti-HCV IgM is useful for the early diagnosis of type C FH and may be a useful marker of diseases activity in type C chronic hepatitis.

Toga‐Like virus as a cause of fulminant hepatitis attributed to sporadic non‐a, non‐b

Virus-like particles (60-70 nm) with spiked surfaces budding into cell vacuoles and rod-shaped inclusions were detected in nuclei of hepatocytes from a British patient transplanted for sporadic non-A, non-B fulminant hepatitis (NANB-FHF), probably contracted in Kenya. Identical particles were seen in two successive grafts (days 2 and 10) at regrafting for recurrent FHF. Ultrastructural features resembled those of the RNA-containing arbovirus, Rift Valley fever virus, but serological markers against a representative panel for arboviruses (Togaviruses) and transmission in mice proved negative. The particles shared features with the different arboviruses seen in the hepatectomy specimen of a second patient with NANB-FHF, and in both patients an insect vector was implicated in the clinical history. The particles were identical in size to those of a third patient with NANB-FHF, who had remained in the United Kingdom. These findings, together with the recent report of isolation of an RNA-containing virus resembling the Togaviridae, in parenteral NANB, suggest that several exotic virus-like agents resembling the arboviruses may be involved in the aetiology of NANB, including in the sporadic forms of FHF in the United Kingdom.

Non-A, non-B fulminant viral hepatitis in France in returnees from Asia and Africa.

Among 61 patients admitted for non-A, non-B fulminant viral hepatitis to Hôpital Beaujon, 10 had returned from Asia or Africa, and 51 had not been outside France, within the month preceding jaundice. This suggests that hepatitis might have been contracted in Asia or Africa in the former, and in France in the latter. The interval between the onset of jaundice and the onset of hepatic encephalopathy was 10 days in the former and 26 days in the latter (P less than 0.03). The serum of the patient returning from Asia contained, and the sera of the nine patients returning from Africa did not contain, antibodies to a virus isolated from the stools of patients suffering from an epidemic fecal-oral non-A, non-B viral hepatitis in Central Asia. It is concluded that infection with Asian-African non-A, non-B viruses can be the cause of fulminant hepatitis in persons returning from these countries, that the course of this type of non-A, non-B fulminant viral hepatitis is shorter than that of non-A, non-B fulminant hepatitis contracted in France, and that different viruses might be responsible for non-A, non-B hepatitis in Asia and Africa.