Hepatic decompensation associated with hepatitis B e antigen clearance in chronic type B hepatitis

Sheen, I‐Shyan; Liaw, Yun–Fan; Tai, Dar‐In; Chu, Chia–Ming

doi:10.1016/0016-5085(85)90566-9

Cited by 134 publications

(72 citation statements)

References 17 publications

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“…Our failure to detect anti-HDV in the sera of patients experiencing severe exacerbation suggested that HDV infection may not play an important role in severe acute exacerbation in chronic carriers of HBsAg in Japan. Our findings are compatible with reports from Greece (Tassopoulos et al 1986), Maryland in the United States (Davis et al 1984a) and Taiwan (Sheen et al 1985), while inconsistent with those from Italy (Smedile et al 1982) and California in the United States (Govindarajan et al 1984). The difference may be attributed to the lower prevalence of HDV infection in the former areas (and in Japan) than in the latter (Rizzetto et al 1980).…”

Section: Discussionsupporting

confidence: 55%

“…These clinical features resemble those of acute type B hepatitis (Bortolotti et al 1986). The histological findings of liver showed severe hepatic injuries such as massive hepatic necrosis and bridging hepatic necrosis, which suggest that hepatocytes were affected by drastic immune responses (Sheen et al 1985). It has been also reported that bridging hepatic necrosis is a predictive indicator of the progress of chronic active hepatitis to cirrhosis (Cooksley et al 1986).…”

Section: Discussionmentioning

confidence: 94%

“…Although patients suffer elevation of hepatic enzymes, the clinical symptoms are mild, or, like the physical findings of chronic liver diseases, often absent (Hoofnagle and Alter 1984). In rare cases, severe exacerbations with hepatic decompensation have also been reported in such patients (Sheen et al 1985;Tassopoulos et al 1986). During the past 10 years, of 297 HBsAg carriers we have examined, there have been 10 cases with severe acute exacerbation.…”

mentioning

confidence: 99%

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Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Kanno

Suzuki²,

Miyazaki³

et al. 1988

Tohoku J. Exp. Med.

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In order to examine the clinical features of severe acute exacerbation in chronic hepatitis B virus (HBV) infection, 297 hepatitis B surface antigen (HBsAg) carriers were followed for 35+22 months (mean+s.D.) in Tohoku University Hospital from 1976 to 1987. Of these, 10 experienced severe acute exacerbation with hepatic decompensation. All of these patients had intense subjective symptoms related to the hepatitis. They were all icteric and 8 had ascites. Three developed to fulminant hepatic failure, eventually died. Histology after the exacerbation showed severe hepatic damage such as massive hepatic necrosis and bridging hepatic necrosis in a half of them. Six cases were suspected to result from spontaneous reactivation and 2 from drug-induced reactivation of chronic HBV infection, and the other 2 from superinfection with non-A, non-B hepatitis agent (s). These results suggest that the reactivation of chronic HBV infection is an important factor of severe acute exacerbations in chronic HBV infection in Japan.severe acute exacerbation ; HBsAg carrier ; reactivation of chronic HBV infection Patients with chronic type B hepatitis positive for hepatitis B e antigen (HBeAg) are considered to experience frequent acute exacerbations (Perrilo et al. 1984;Liaw et al. 1987). However, the exacerbations occasionally occur in hepatitis B surface antigen (HBsAg) carriers negative for HBeAg (Liaw et al. 1987). Such exacerbations are considered to be induced by the spontaneous reactivation of chronic hepatitis B virus (HBV) infection and superinfections with hepatitis A virus (HAY) (Zachoval et al. 1983;Davis et al. 1984b), non-A, non-B (NANB) hepatitis agent (s) (Papaevangelou et al. 1984) and hepatitis delta

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

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Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Kanno

Suzuki²,

Miyazaki³

et al. 1988

Tohoku J. Exp. Med.

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“…This reflects the host's attempt to eradicate the virus and is associated with HBeAg seroconversion and disappearance of DNA polymerase [12][13][14]. Such a seroconversion was also noted in HBsAg carriers during HAV [10,15,16], Delta [17] and Non-A, Non-B viruses superinfection [18].…”

Section: Discussionmentioning

confidence: 99%

Dissociation of alanine aminotransferase values in acute hepatitis A patients with and without past experience to the hepatitis B virus

Papachristou¹,

Katsouyannopoulos

1991

Epidemiol. Infect.

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SUMMARYSerological markers and peak serum alanine aminotransferase (ALT) values of 140 in-patients with acute hepatitis, either type A (n = 90), or type B (n = 50) were prospectively assessed. In 23 out of the 90 patients with acute hepatitis A, evidence of previous experience with hepatitis B virus (HBV) was found, whereas 35 out of the 50 patients with acute hepatitis B had past contact with hepatitis A virus (HAV). The mean peak ALT values [S.D.] were significantly higher in hepatitis A patients with previous experience with HBV (1413 [704] i.u./l), when compared to those without such experience (842 [464] i.u./l, P < 0-001). Such a difference was not evident between acute hepatitis B patients, whether or not they had previous contact with HAV. We conclude that when acute hepatitis A is superimposed on past HBV infection an augmented transaminaemia, indicative of enhanced liver cell necrosis, takes place although a definite explanation is lacking. We suggest that individuals with markers of HBV infection should be early candidates for HAV immunization.

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“…1 The exacerbation can accelerate the progression of liver disease. 2 Hepatitis B virus (HBV) evolves rapidly in chronic hepatitis B patients, and the correlation of HBV variation with the onset of AE has been extensively studied. [3][4][5] Previously, we investigated sequential full-length viral sequences in patients with AE 6,7 and found that most exacerbations were preceded by an upsurge of serum HBV identical to the preexisting HBV strain.…”

mentioning

confidence: 99%

Origin of serum hepatitis B virus in acute exacerbation: Comparison with HBV in the liver and from other exacerbation

et al. 2004

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Acute exacerbation (AE) of chronic hepatitis B is usually preceded by reemergence or increase of hepatitis B virus (HBV) in the serum. To investigate the origin of the reemergence or increase, we compared the identity of the serum viral genome to that in the liver and in previous AE by full-length sequencing. The full-length viral genome and extent of quasispecies were obtained from serum and liver biopsy specimens at the same time from 9 subjects with hepatitis B exacerbation (group I). Composition of viral quasispecies was compared by the genetic diversity and the average number of nucleotide substitutions within and between different viral sources. Another 2 patients with repeated AEs (group II) were also enrolled, and their serial serum alanine aminotransferase, HBV DNA levels and full-length sequences were determined. In all group I patients, serum viral genome was identical to that in the liver. The genetic diversity and the average number of nucleotide difference were also comparable between serum and liver tissue. In 2 group II patients, the viral variant that emerged after previous AE was not identical to that caused by the subsequent AE. Dominant viral strains for serial AEs in a single patient did not show a sequential evolution, but presented as a horizontal selection of a minor population from the original viral pool. In conclusion, the findings suggest that viral strain in serum reflects the intrahepatic strain of the AE. Random reactivation of the original HBV pool, rather than a sequential evolution of one strain, also contributes to the onset of repeated AE. A cute exacerbation (AE) occurs frequently in hepatitis B surface antigen carriers. 1 The exacerbation can accelerate the progression of liver disease. 2 Hepatitis B virus (HBV) evolves rapidly in chronic hepatitis B patients, and the correlation of HBV variation with the onset of AE has been extensively studied. [3][4][5] Previously, we investigated sequential full-length viral sequences in patients with AE 6,7 and found that most exacerbations were preceded by an upsurge of serum HBV identical to the preexisting HBV strain. After exacerbation, however, about half of the patients were repopulated by a different viral variant in the circulation.The pathogenesis of AE actually takes place in the liver. Therefore, it is better to directly characterize the viral genome from the liver biopsy specimen. As noted previously, some potential pathogenic strains may replicate actively within the liver but not be released into the circulation. 8 Thus, HBV genomic changes that are correlated with the development of hepatitis B exacerbation might occur and be retained within the liver but not be detected in the specimens obtained from the circulation. To resolve these questions, the representation of the serum viral genome to the corresponding intrahepatic one was first determined by comparing the dominant viral nucleotide sequence and genetic complexity of the viral quasispecies between both tissue specimens obtained si-

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Hepatic decompensation associated with hepatitis B e antigen clearance in chronic type B hepatitis

Cited by 134 publications

References 17 publications

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Dissociation of alanine aminotransferase values in acute hepatitis A patients with and without past experience to the hepatitis B virus

Origin of serum hepatitis B virus in acute exacerbation: Comparison with HBV in the liver and from other exacerbation

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