title: Immunosuppression may lead to progression of hepatitis C virus-associated liver disease in hemophiliacs coinfected with HIV.
abstract: OBJECTIVE
  The aim of this study was to examine the interaction between HIV and hepatitis C virus (HCV) in hemophiliacs coinfected with the viruses and to investigate the possible relationship between immunosuppression and liver failure.
  
  
  METHODS
  To identify risk factors for impending liver failure in hemophiliacs coinfected with HIV and HCV, we analyzed clinical and laboratory parameters, including CD4 count, aminotransferases (ALT, AST), cholinesterase, alkaline phosphatase, bilirubin, and gamma-glutamyltransferase, during 3 yr of follow-up (1990-1993) in four groups of patients: hemophiliacs with progressive immunodeficiency who were coinfected with HCV and HIV (group A, n = 49); hemophiliacs with stable immune function who were seropositive for HIV and HCV (group B, n = 95); hemophiliacs who were infected with HCV but not HIV (group C, n = 72); and homosexuals with progressive immunodeficiency who were infected with HIV but not HCV (group D, n = 24).
  
  
  RESULTS
  Univariate analysis of data for group A showed a significant rise in gamma-glutamyltransferase and alkaline phosphatase (p < 0.01) that was not seen in groups B, C, and D. In a multivariate Cox regression analysis, age (odds ratio, 1.054 per yr; 95% confidence interval, 1.014-1.096 per yr), decline in CD4 count (odds ratio, 1.063 per cell/microl; 95% confidence interval, 1.037-1.091 per cell/microl), and alkaline phosphatase level (odds ratio, 1.012 per U/L; 95% confidence interval, 1.002-1.021 per U/L) emerged as independent determinants of death.
  
  
  CONCLUSIONS
  Our data suggest that progressive immune dysfunction in hemophiliacs coinfected with HIV and HCV may influence progression of liver failure. In these patients cholestasis is an additional prognostic marker for survival that may reflect both exhausted immunity and impaired liver function.
authors.affiliation: Department of Internal Medicine, Institute for Experimental Hematology, University of Bonn, Germany.
authors.forename: J K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: U
authors.initials: U
authors.lastname: Spengler
authors.forename: T
authors.initials: T
authors.lastname: Sudhop
authors.forename: S
authors.initials: S
authors.lastname: Ewig
authors.forename: A
authors.initials: A
authors.lastname: Theisen
authors.forename: U
authors.initials: U
authors.lastname: Hammerstein
authors.forename: E
authors.initials: E
authors.lastname: Bierhoff
authors.forename: H P
authors.initials: HP
authors.lastname: Fischer
authors.forename: J
authors.initials: J
authors.lastname: Oldenburg
authors.forename: H H
authors.initials: HH
authors.lastname: Brackmann
authors.forename: T
authors.initials: T
authors.lastname: Sauerbruch
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications*; D000328:Adult; D015331:Cohort Studies; D018450:Disease Progression; D006467:Hemophilia A / Q000150:complications*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D007165:Immunosuppression Therapy / Q000009:adverse effects*; D008099:Liver / Q000473:pathology; D008107:Liver Diseases / Q000503:physiopathology* / Q000821:virology*; D017093:Liver Failure; D008297:Male; D012307:Risk Factors; D016019:Survival Analysis