We looked for hepatitis A virus (HAV) infection as an etiological agent among patients with fulminant hepatitis and chronic active hepatitis. Among 42 patients with hepatitis B surface antigen (HBsAg)-negative fulminant disease, we detected seroconversion by immune adherence hemagglutination for antibody to HAV (anti-HAV) in 3 of 10 survivors, as well as an increasing anti-HAV score by immune electron microscopy. In the 32 HBsAg-negative nonsurvivors, we found 3 patients with anti-HAV detectable by immune electron microscopy and radioimmunoassay, but not by immune adherence hemagglutination. We classified the latter cases as presumptively attributable to HAV. In 10 survivors among 30 HBsAg-positive patients with fulminant disease, we did not detect any instances of anti-HAV seroconversion. In the 20 HBsAg-positive nonsurvivors, 1 case had anti-HAV detectable by immune electron microscopy and radioimmunoassay but not by immune adherence hemagglutination. This case was also considered to be presumptively caused by HAV. In addition, we studied anti-HAV in patients with chronic active hepatitis. The incidence of anti-HAV in 13 HBsAg-positive cases was 31%, which did not differ from the 32% found in 22 HBsAg-negative cases. There was one seroconversion for anti-HAV in 1 patient with HBsAg-negative chronic active hepatitis, but this appeared to be an epiphenomenon. We looked for fecal shedding of HAV in 14 patients with HBsAg-negative chronic active hepatitis without success.
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