title: Hepatitis C virus infection is associated with endothelial dysfunction in HIV/hepatitis C virus coinfected patients.
abstract: OBJECTIVE
  To quantify serum levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in HIV/HCV coinfected patients to examine their association with several clinical and epidemiological characteristics and the therapeutic responsiveness to interferon (IFN)-alpha and ribavirin therapy (IFN-alpha + RBV).
  
  
  METHODS
  Retrospective study.
  
  
  METHODS
  We carried out a cross-sectional study with 183 IFN-alpha-naive patients on HAART, and 24 healthy controls. We also analyzed 30 out of 183 patients on IFN-alpha + RBV for the duration of 48 weeks.
  
  
  RESULTS
  HIV/HCV coinfected patients had higher levels of sICAM-1 and sVCAM-1 than the healthy control group (P < 0.05). Patients with HCV-genotype 1, advanced fibrosis (F>or=3) or moderate to severe activity grade (A>or=2) had the highest values of sICAM-1 and sVCAM-1. When we carried out a multivariate analysis, we found a significant positive relationship between both HCV-genotype 1 and advanced fibrosis (F>or=3) with sICAM-1 (R = 0.549; P < 0.001); and a significant positive relationship between HCV-genotype 1 and advanced fibrosis (F>or=3) with sVCAM-1 (R = 0.624; P < 0.001). We also found a positive relationship of sICAM-1 or sVCAM-1 levels with transaminases and alkaline phosphatase circulation levels (P < 0.05). Nonresponder patients had higher sICAM-1 and sVCAM-1 serum levels, and patients with sustained virologic response had significantly lower levels of sICAM-1 (P = 0.001) and sVCAM-1 (P = 0.019).
  
  
  CONCLUSIONS
  HIV and HCV coinfection induces alterations in sICAM-1 and sVCAM-1 serum levels, which were higher in patients with HCV-genotype 1 and advanced stage of HCV infection. However, response to IFN-alpha + RBV may reduce these cardiovascular risk markers.
authors.affiliation: Laboratory of Molecular Epidemiology of Infectious Diseases, National Centre of Microbiology, Instituto de Salud Carlos III, Majadahonda,Madrid, Spain.
authors.forename: Isabel Fernández
authors.initials: IF
authors.lastname: de Castro
authors.forename: Dariela
authors.initials: D
authors.lastname: Micheloud
authors.forename: Juan
authors.initials: J
authors.lastname: Berenguer
authors.forename: María
authors.initials: M
authors.lastname: Guzmán-Fulgencio
authors.forename: Pilar
authors.initials: P
authors.lastname: Catalán
authors.forename: Pilar
authors.initials: P
authors.lastname: Miralles
authors.forename: Emilio
authors.initials: E
authors.lastname: Alvarez
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: López
authors.forename: Jaime
authors.initials: J
authors.lastname: Cosín
authors.forename: Raquel
authors.initials: R
authors.lastname: Lorente
authors.forename: Ma Angeles
authors.initials: MA
authors.lastname: Muñoz-Fernández
authors.forename: Salvador
authors.initials: S
authors.lastname: Resino
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000209:etiology / Q000821:virology; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D012189:Retrospective Studies; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*; D019562:Viral Load
chemical_list: D015415:Biomarkers; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1