SEROEPIDEMIOLOGY OF HEPATITIS-C VIRUS-INFECTION IN JAPAN AND HCV INFECTION IN HEMODIALYSIS-PATIENTS

Citation
K. Yamaguchi et al., SEROEPIDEMIOLOGY OF HEPATITIS-C VIRUS-INFECTION IN JAPAN AND HCV INFECTION IN HEMODIALYSIS-PATIENTS, FEMS microbiology reviews, 14(3), 1994, pp. 253-258
Citations number
10
Categorie Soggetti
Microbiology
Journal title
ISSN journal
01686445
Volume
14
Issue
3
Year of publication
1994
Pages
253 - 258
Database
ISI
SICI code
0168-6445(1994)14:3<253:SOHVIJ>2.0.ZU;2-#
Abstract
Since January 1990, Japanese Red Cross Blood Centres have introduced h epatitis C virus screening with a first-generation ELISA. From April t o December 1992, approximately 0.98% among 10 905 489 blood donations screened by a second-generation assay were anti-HCV-positive in all Ja pan. Seropositivity of anti-HCV increased with the age and serum trans aminase value in both sexes. In blood donors having a history of trans fusion, the anti-HCV reactive rate was 7.4%. The results of the study made by the Japanese Red Cross Non-A, Non-B Hepatitis Research Group s how the effectiveness of implementation of HCV screening to prevent po sttransfusion hepatitis. Consecutive haemodialysis patients with chron ic renal failure are at risk for infection by a variety of blood-borne agents transmitted within dialysis units. Because of their immunocomp romised state, they frequently also have an unusual susceptibility to a variety of nosocomial infections, such as HBV, HCV, and HTLV-I. We t ested the prevalence of anti-HCV in 1423 (848 males and 575 females) h aemodialysis patients from 18 hospitals in Kumamoto Prefecture, Japan, using the Ortho first generation anti-HCV screening assay. There were 316 patients (22.2%) positive for HCV antibodies. The second-generati on test was positive in most haemodialysis patients who were reactive to the first-generation assay. The prevalence of HCV infection increas ed with the duration of haemodialysis, yet there was a high frequency of HCV seropositivity even without blood transfusion. Acquisition of H CV in dialysis patients could be explained by HCV infection within the unit other than by blood (all haemodialysis are done with disposable kits, syringes, and needles), by secondary HCV infection after the imm unodeficiency of haemodialysis, or by HCV infection of the kidney or g lomerular deposition of immune HCV/anti-HCV complexes leading to chron ic renal failure (as with HBV infection of the liver and kidney).