title: Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: etiology and natural history.
abstract: In a 4-year follow-up study, patients with acute sporadic non-A, non-B (NANB) hepatitis were evaluated to determine the etiology and natural history of the disease. Acute hepatitis C virus (HCV) was detected in 13 of 43 (30%) of patients, anti-hepatitis E virus (HEV) IgG in 5 (12%), and 25 (58%) were considered non-A-E. The HCV RNA was detected in all HCV patients but none of the non-A-E cases. The initial clinical and biochemical presentation of the HCV and non-A-E cases was quite similar, although 2 of the non-A-E patients had severe disease. The 5 patients who were found to be anti-HEV IgG-reactive recovered within 6 months of follow-up. Of the 13 HCV cases, alanine transaminase (ALT) levels returned to normal in 7 (53. 8%), while 6 (46.2%) continued to show abnormal ALT after 6 months of follow-up. However, 9 (69.2%) of them remained HCV-RNA-positive, denoting virological/biochemical dissociation. Long-term follow-up showed a reappearance of HCV RNA in 2 of the 4 patients who were in virological remission performing 84% of chronicity rate. Acute non-A-E hepatitis patients were less likely to evolve toward chronicity, as compared with acute HCV cases (16% vs. 84%; P =.0001). Only 4 (16%) of the non-A-E patients were hepatitis G virus (HGV)-RNA-positive. Concerning risk factors for acquiring parenterally transmitted viruses, tattooing was the only one that could be associated with HCV transmission (P =.002). No risk factors could be identified for putative non-A-E virus transmission. Liver biopsies performed for chronic HCV patients showed a variable degree of inflammation, while the non-A-E patients presented less severe histological disease.
authors.affiliation: Hepatology Unit of Bahia, University Hospital of Bahía, Brazil.
authors.forename: R
authors.initials: R
authors.lastname: Paraná
authors.forename: L
authors.initials: L
authors.lastname: Vitvitski
authors.forename: Z
authors.initials: Z
authors.lastname: Andrade
authors.forename: C
authors.initials: C
authors.lastname: Trepo
authors.forename: H
authors.initials: H
authors.lastname: Cotrim
authors.forename: P
authors.initials: P
authors.lastname: Bertillon
authors.forename: F
authors.initials: F
authors.lastname: Silva
authors.forename: L
authors.initials: L
authors.lastname: Silva
authors.forename: I R
authors.initials: IR
authors.lastname: de Oliveira
authors.forename: L
authors.initials: L
authors.lastname: Lyra
mesh_terms: D000208:Acute Disease; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001663:Bilirubin / Q000097:blood; D001938:Brazil; D005260:Female; D018067:Flaviviridae / Q000302:isolation & purification; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000302:isolation & purification; D006526:Hepatitis C / Q000473:pathology / Q000503:physiopathology* / Q000635:transmission*; D016751:Hepatitis E / Q000473:pathology / Q000503:physiopathology* / Q000635:transmission*; D016752:Hepatitis E virus / Q000302:isolation & purification; D006525:Hepatitis, Viral, Human / Q000473:pathology / Q000503:physiopathology* / Q000635:transmission*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation; D008099:Liver / Q000473:pathology; D008297:Male; D012367:RNA, Viral / Q000097:blood; D012016:Reference Values; D012307:Risk Factors
chemical_list: D007074:Immunoglobulin G; D012367:RNA, Viral; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001663:Bilirubin