title: Association of hepatitis C with markers of hemostasis in HIV-infected and uninfected women in the women's interagency HIV study (WIHS).
abstract: BACKGROUND
  Coinfection with HIV and hepatitis C virus (HCV) is common. HIV infection and treatment are associated with hypercoagulability; thrombosis in HCV is underinvestigated. Proposed markers of hemostasis in HIV include higher D-dimer, Factor VIII%, and plasminogen activator inhibitor-1 (PAI-1) antigen and lower total Protein S% (TPS) but have not been examined in HCV. We assessed the independent association of HCV with these 4 measures of hemostasis in a multicenter, prospective study of HIV: the Women's Interagency HIV Study.
  
  
  METHODS
  We randomly selected 450 HCV-infected (anti-HCV+ with detectable plasma HCV RNA) and 450 HCV-uninfected (anti-HCV-) women. HCV was the main exposure of interest in regression models.
  
  
  RESULTS
  Four hundred forty-three HCV+ and 425 HCV- women were included. HCV+ women had higher Factor VIII% (124.4% ± 3.9% vs. 101.8% ± 3.7%, P < 0.001) and lower TPS (75.7% ± 1.1% vs. 84.3% ± 1.1%, <0.001) than HCV- women, independent of HIV infection and viral load; there was little difference in PAI-1 or log10 D-dimer. After adjustment for confounders, these inferences remained. HIV infection was independently associated with higher Factor VIII% and log10 D-dimer and lower TPS.
  
  
  CONCLUSIONS
  HCV was independently associated with higher Factor VIII% and lower TPS consistent with hypercoagulability. Higher Factor VIII% and D-dimer and lower TPS were also strongly associated with HIV infection and levels of HIV viremia, independent of HCV infection. Further investigation is needed to determine if there is increased thrombotic risk from HCV. Studies examining hemostasis markers in HIV infection must also assess the contribution of HCV infection.
authors.affiliation: Division of General Internal Medicine, Mount Sinai School of Medicine, New York, NY, USA. elizabeth.kiefer@mountsinai.org
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Kiefer
authors.forename: Qiuhu
authors.initials: Q
authors.lastname: Shi
authors.forename: Donald R
authors.initials: DR
authors.lastname: Hoover
authors.forename: Robert
authors.initials: R
authors.lastname: Kaplan
authors.forename: Russell
authors.initials: R
authors.lastname: Tracy
authors.forename: Michael
authors.initials: M
authors.lastname: Augenbraun
authors.forename: Chenglong
authors.initials: C
authors.lastname: Liu
authors.forename: Marek
authors.initials: M
authors.lastname: Nowicki
authors.forename: Phyllis C
authors.initials: PC
authors.lastname: Tien
authors.forename: Mardge
authors.initials: M
authors.lastname: Cohen
authors.forename: Elizabeth T
authors.initials: ET
authors.lastname: Golub
authors.forename: Kathryn
authors.initials: K
authors.lastname: Anastos
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000032:analysis; D060085:Coinfection / Q000097:blood*; D003430:Cross-Sectional Studies; D005169:Factor VIII / Q000032:analysis; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D015658:HIV Infections / Q000097:blood*; D006487:Hemostasis / Q000502:physiology*; D006526:Hepatitis C / Q000097:blood*; D006801:Humans; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D017293:Protein S / Q000032:analysis; D012044:Regression Analysis; D014481:United States
chemical_list: D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D017293:Protein S; C036309:fibrin fragment D; D005169:Factor VIII