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Fulminant hepatitis in asymptomatic hepatitis B surface antigen carriers in Greece
Insights
Reactivation of chronic hepatitis B is a significant cause of fulminant hepatitis in HBsAg carriers. This study highlights its role, especially in heterosexual males, in areas with high hepatitis B virus prevalence.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Fulminant hepatitis (FH) in HBsAg carriers lacking IgM anti-HBc suggests superimposed acute hepatitis or reactivation.
- Hepatitis B virus (HBV) infection is endemic in many regions, with reactivation posing a clinical challenge.
Purpose of the Study:
- To investigate the causes of fulminant hepatitis in HBsAg carriers negative for IgM anti-HBc.
- To determine the role of HBV reactivation and other viral agents in FH.
Main Methods:
- Analysis of 11 male FH patients positive for HBsAg but negative for IgM anti-HBc.
- Detection of hepatitis A virus (HAV), HBV, and hepatitis delta virus (HDV) using serologic markers and molecular hybridization.
- Review of patient history, including chemotherapy and risk factors.
Main Results:
- Reactivation of chronic hepatitis B accounted for FH in 7 out of 11 patients (4 spontaneous, 3 chemotherapy-induced).
- HDV superinfection was identified in one patient.
- Three patients had possible superinfection by non-A, non-B, HDV, or HDV-like agents.
Conclusions:
- Reactivation of chronic hepatitis B is a major cause of apparent acute FH in HBsAg carriers, particularly heterosexual males in HBV-endemic areas.
- Immunosuppressive therapy can trigger HBV reactivation leading to FH.
- Diagnostic challenges exist for FH in HBsAg carriers due to atypical presentations.
Abstract:
Eleven male fulminant hepatitis (FH) patients (mean age: 47.7 +/- 16 years) positive for hepatitis B surface antigen (HBsAg) but negative for IgM antibody to hepatitis B core antigen (IgM anti-HBc) were admitted consecutively to the Athens Hospital for Infectious Diseases between May 1981 and November 1983. Because of the absence of IgM anti-HBc, determined by an enzyme immunoassay, these patients were considered to be HBsAg carriers with a superimposed acute hepatitis. Three of the 11 patients received immunosuppressive chemotherapy during the six months before the onset of the acute hepatitis. None of the patients was homosexual or a drug addict. Infection with hepatitis A virus (HAV), hepatitis B virus (HBV), or hepatitis delta virus (HDV) was detected with serologic markers and/or molecular hybridization techniques. Fulminant hepatitis was attributed to spontaneous reactivation of chronic hepatitis B in four patients, chemotherapy-induced reactivation of chronic hepatitis B in three patients, HDV superinfection in one patient and possible superinfection by non-A, non-B agent(s), HDV, or HDV-like agents in three patients. Reactivation of chronic hepatitis B was an important cause of apparent acute hepatitis in heterosexual male HBsAg carriers from an area with a high prevalence of HBV infection.