Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 879-882 |
| Number of pages | 4 |
| Journal | Gastroenterology |
| Volume | 74 |
| Issue number | 5 PART 1 |
| State | Published - 1978 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Gastroenterology
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Hepatitis a virus infection in fulminant hepatitis and chronic active hepatitis. / Rakela, Jorge; Redeker, Allan G.; Edwards, Virginia M.; Decker, Richard; Overby, Lacy R.; Mosley, James W.
In: Gastroenterology, Vol. 74, No. 5 PART 1, 1978, p. 879-882.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hepatitis a virus infection in fulminant hepatitis and chronic active hepatitis
AU - Rakela, Jorge
AU - Redeker, Allan G.
AU - Edwards, Virginia M.
AU - Decker, Richard
AU - Overby, Lacy R.
AU - Mosley, James W.
PY - 1978
Y1 - 1978
N2 - 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.
AB - 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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UR - http://www.scopus.com/inward/citedby.url?scp=0017819509&partnerID=8YFLogxK
M3 - Article
C2 - 205479
AN - SCOPUS:0017819509
VL - 74
SP - 879
EP - 882
JO - Gastroenterology
JF - Gastroenterology
SN - 0016-5085
IS - 5 PART 1
ER -