Influence of Delta Infection on Severity of Hepatitis B

Smedile, Antonina; Verme, G; Cargnel, Antonietta; Dentico, P; Opolon, P; Vergani, Diego; Farci, Patrizia; Caredda, F.; Caporaso, N.; Trépo, C.; Gimson, Alex; Williams, Roger; Rizzetto, Mario

doi:10.1016/s0140-6736(82)90156-8

Cited by 411 publications

(185 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: 59%

“…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 virus (HDV) (Smedile et al 1982; Govindarajan et al 1984). 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).…”

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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: 59%

mentioning

confidence: 99%

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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“…So, vaccination against HBV will remain the only efficacious and safe prophylaxis against HDV, as it prevents the infection upon which the defective HDV thrives. [15][16][17][18][19][20][21] We emphasize the importance of HBsAg immunization programs that have been implemented here since January 1991, certain that this will be reflected in the HDV control.…”

Section: Discussionmentioning

confidence: 99%

Seroepidemiological Prevalence of Hepatitis Delta Virus in Eastern Saudi Arabia

Fathalla

Abdulazziz

Sabri

et al. 1994

Annals of Saudi Medicine

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Four hundred and eleven (411) confirmed hepatitis B surface antigen (HBsAg) positive individuals were tested for hepatitis delta antibodies (anti HDV) by the enzyme immunoassay method (EIA) from June 1988 through December 1993. An overall prevalence rate of 4.87% was recorded while rates for liver diseased patients, subjects on hemodialysis programs, intravenous drug addicts and blood donors showed 7.69%, 6.85%, 5.77% and 2.75% respectively. Breaking down rates according to the country of origin of our subjects showed the highest prevalence among Middle Easterners (8.22%) and Saudis (6.22%), while it was 2.63% among the India subcontinent subjects. No HDV case has been recorded from the Southeastern Asia samples despite the known higher HBsAg anemia in this region. This study could suggest that although HDV infection is limited to HBV carriers, the HDV prevalence does not seem to be a simple function of HBV, as some other factors (environmental, genetic, cultural, and/or viral strains) could modify the HDV/HBV relationship. However, limitation of the currently available tests for HDV could be the cause of the underestimation of HDV prevalence here as well as elsewhere. Ann Saudi Med 1994;14(6):503-506. This single strand RNA virus is considered as a mini-defective virus that requires a complementary helper function of hepatitis B virus (HBV) for its synthesis; hence, it can only develop in persons infected with HBV and it is well established that the HDV pathology is mainly due to its direct cytopathic effect on the hepatocytes as opposed to the immunological damage of HBV.2,3

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“…It has been reported that upto 70% cases of pregnant women with acute hepatitis E progress to acute liver failure with a short pre-encephalopathy period, rapid development of cerebral edema and high occurrence of disseminated intravascular coagulation [3]. Acute viral hepatitis is defined as those cases which have acute self limited disease and a serum aspartate aminotransferase elevation of at least five fold or clinical jaundice or both [4]. In our case the serum AST was less than two fold increased.…”

Section: Discussionmentioning

confidence: 68%

An Atypical Presentation of Hepatitis E in Pregnancy

Maji¹,

Dey²,

Saraswat³

et al. 2016

Med-Science

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Hepatitis E is water born disease and transmitted by feco-oral route and it is an emerging infectious agent causing acute viral hepatitis all over the world. During pregnancy, especially in the third trimester, hepatitis E infection is characterized by a more severe infection with many fold increase in hepatic enzyme levels that sometimes results in fulminant hepatitisleading to increasing maternal and fetal morbidity and mortality. We are presenting an atypical case of hepatitis E in pregnancy which showed mild increase in enzyme levels with very high bilirubin levels.

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Influence of Delta Infection on Severity of Hepatitis B

Cited by 411 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.

Seroepidemiological Prevalence of Hepatitis Delta Virus in Eastern Saudi Arabia

An Atypical Presentation of Hepatitis E in Pregnancy

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