Epidemiological, clinical and biological characteristics of acute non-A, non-B hepatitis with and without hepatitis C virus infection

Abstract

Serially collected serum samples from 81 patients with acute non-A, non-B hepatitis were tested for the presence of antibodies to hepatitis C virus (anti-HCV) by a second-generation enzyme immunoassay (EIA) test. Anti-HCV was detected in 56 cases (69%) during the first month, in 61 cases (75%) at 3 months and in 63 cases (78%) at 6 months. In those 18 patients showing anti-HCV negative results in the three determinations, hepatitis C virus (HCV) RNA was tested using a nested polymerase chain reaction (PCR) in the first serum sample and was detected in only one case. Anti-HCV or HCV-RNA positive episodes were considered as acute hepatitis C, while those negative for both markers were classified as acute non-A, non-B, non-C hepatitis. On comparing acute hepatitis C with the non-A, non-B, non-C episodes, no significant differences were found in the presence of jaundice, mean maximum alanine-aminotransferase (ALT) levels and positivity of markers of past hepatitis B virus (HBV) infection. However, patients with hepatitis C were significantly younger than those with non-A, non-B, non-C hepatitis (p = 0.002). Male sex (78.1% vs. 35.3%; p = 0.001), history of parenteral exposure (90.6% vs. 11.8%; p = 0.0001), and progression to chronicity (73.4% vs. 5.9%; p = 0.0001) were significantly more frequent in the HCV-related group. Although other possibilities cannot be excluded, these results suggest that there might be a different infectious agent implicated in the etiology of acute non-A, non-B, non-C hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidemiological characteristics, risk factors, and clinical manifestations of acute non‐A–E hepatitis

“…No patients with acute non-A±E hepatitis in this series admitted intravenous drug use nor reported parenteral exposures or household contact. The present results are in agreement with most of the published data [Alter et al, 1992[Alter et al, , 1997Buti et al, 1994;Navascues et al, 1994;Ghabrah et al, 1995;Corwin et al, 1996;Rochling et al, 1997;Frider et al, 1998;Kanda et al, 1999;Parana et al, 1999] except one study from Russia that identi®ed parenteral routes of transmission in acute non-A±E hepatitis as common as in acute hepatitis C [Favorov et al, 1994]. Acute non-A±E hepatitis is likely to represent several etiological factors.…”

“…The incidence of chronic evolution of acute non-A±E hepatitis in seven published series varied from 0 to 29% [Buti et al, 1994;Navascues et al, 1994;Alter et al, 1997;Rochling et al, 1997;Kanda et al, 1999;Parana et al, 1999;Romano et al, 2000]. Overall, the average rate (95% con®dence interval) of chronic evolution was 8.5% (5.5±11.5%), as shown in Table III. In conclusion, from the present ®ndings and the published data, the general epidemiological characteristics of acute non-A±E hepatitis can be summarized as follows: acute non-A±E hepatitis is worldwide in distribution, accounting for 20±60% of sporadic acute NANB hepatitis.…”

Acute hepatitis C virus (HCV) infection in chronic carriers of hepatitis B virus (HBV): the impact of underlying active HBV replication on persistence of HCV infection and antibody responses to HCV

“…However, this value is similar to those in previous reports in which 65-89% of patients with presumed acute HCV infection had anti-HCV detectable in initial serum specimens using second or third generation enzyme immunoassays. [15][16][17][18][19] Serum levels of bilirubin and prothrombin time were significantly higher in chronic HBsAg carriers with acute HCV infection than in non-HBsAg carriers (see table 1). Asymptomatic HBsAg carriers are known to harbour various liver lesions that may aggravate the severity of acute hepatitis.…”