Seroepidemiologic studies of hepatitis C virus infection in a population of Okayama Prefecture screened for liver disease

Citation
S. Uesugi et al., Seroepidemiologic studies of hepatitis C virus infection in a population of Okayama Prefecture screened for liver disease, ACT MED OKA, 53(1), 1999, pp. 31-38
Citations number
35
Categorie Soggetti
Medical Research General Topics
Journal title
ACTA MEDICA OKAYAMA
ISSN journal
0386300X → ACNP
Volume
53
Issue
1
Year of publication
1999
Pages
31 - 38
Database
ISI
SICI code
0386-300X(199902)53:1<31:SSOHCV>2.0.ZU;2-3
Abstract
To better understand the spread of hepatitis C virus (HCV) infection, we st udied the association of HCV infection with similarly transmissible hepatit is B virus (HBV) infection and with hepatitis A virus (HAV) infection, whic h is supposed to be related to a nosocomial transmission of HCV. This was d one by studying the presence or absence of antibodies to these viruses, as well as hepatitis B surface antigen, in a population of 1,398 inhabitants w ith abnormal liver function tests or history of liver disease and/or blood transfusion. This group was drawn from a group of 7,905 examinees screened for liver disease in 26 districts of Okayama prefecture, Japan. The prevale nce of antibody-positive cases increased with age for those viruses. Small but significantly increased odds ratios were obtained among anti-HCV antibo dies (HCVAb), anti-hepatitis B core antibodies (HBcAb) and anti-hepatitis A antibodies (HAVAb). After adjusting odds ratios by logistic regression ana lysis, a significant association was present only between HCVAb and HBcAb. The distribution of age-adjusted prevalences (AAP) of HCVAb in 26 districts was significantly wider than those of HBcAb or HAVAb. The district-based A AP of HCVAb, but not of HBcAb and HAVAb, correlated significantly with the district-based prevalence of infectious hepatitis having a tendency of chro nicity reported in 1953-1955. Adjusted odds ratios calculated by logistic r egression analysis of the virus markers showed that HCVAb was significantly associated with a past history of blood transfusion. Thus, the spread of H CV infection is speculated to have been triggered by blood transfusion, par ticularly from paid donors initially, followed by transmission by nosocomia l or close person-to-person contact.