BACKGROUND/AIMS: The role of hepatitis C virus in fulminant hepatitis remains controversial and needs further investigation. The aim of this study was to examine the role of hepatitis C virus in fulminant hepatitis in an area with endemic hepatitis A and B. METHODS: Serological markers of hepatitis C virus were studied in 62 adults from Taiwan with fulminant viral hepatitis. RESULTS: Of 62 patients, 5 (8.1%) were infected with acute type B hepatitis, 11 (17.7%) were infected with acute non-A, non-B hepatitis, and the remaining 46 (74.2%) were hepatitis B surface antigen (HBsAg) positive but immunoglobulin M (IgM) antibody to hepatitis B core antigen negative. Of the latter, 11 (23.9%) were IgM antibody to hepatitis D virus positive, 16 (34.8%) had high-titered serum hepatitis B virus DNA (> 1000 pg/mL) and were suspected to have hepatitis B virus reactivation, and the other 19 (41.3%) had no identified causes. Serum hepatitis C virus RNA was found in 5 (45.5%) of 11 patients with fulminant non-A, non-B hepatitis, 3 (27.3%) of 11 HBsAg carriers with delta superinfection, and 6 (31.6%) of 19 HBsAg carriers with fulminant hepatitis of undetermined cause. CONCLUSIONS: Nearly half of fulminant non-A, non-B hepatitis and about 20% of HBsAg carriers with superimposed fulminant hepatitis in Taiwan could be attributed to hepatitis C virus infection.
BACKGROUND/AIMS: The role of hepatitis C virus in fulminant hepatitis remains controversial and needs further investigation. The aim of this study was to examine the role of hepatitis C virus in fulminant hepatitis in an area with endemic hepatitis A and B. METHODS: Serological markers of hepatitis C virus were studied in 62 adults from Taiwan with fulminant viral hepatitis. RESULTS: Of 62 patients, 5 (8.1%) were infected with acute type B hepatitis, 11 (17.7%) were infected with acute non-A, non-B hepatitis, and the remaining 46 (74.2%) were hepatitis B surface antigen (HBsAg) positive but immunoglobulin M (IgM) antibody to hepatitis B core antigen negative. Of the latter, 11 (23.9%) were IgM antibody to hepatitis D virus positive, 16 (34.8%) had high-titered serum hepatitis B virus DNA (> 1000 pg/mL) and were suspected to have hepatitis B virus reactivation, and the other 19 (41.3%) had no identified causes. Serum hepatitis C virus RNA was found in 5 (45.5%) of 11 patients with fulminant non-A, non-B hepatitis, 3 (27.3%) of 11 HBsAg carriers with delta superinfection, and 6 (31.6%) of 19 HBsAg carriers with fulminant hepatitis of undetermined cause. CONCLUSIONS: Nearly half of fulminant non-A, non-B hepatitis and about 20% of HBsAg carriers with superimposed fulminant hepatitis in Taiwan could be attributed to hepatitis C virus infection.