title: Platelet function and HIV: a case-control study.
abstract: OBJECTIVE
  Cardiovascular disease and myocardial infarction are of increasing concern in HIV-infected populations. Although platelets mediate arterial thrombosis, central to myocardial infarction, data on platelet function in HIV infection are lacking. We hypothesized that HIV-infected patients would have altered platelet reactivity.
  
  
  METHODS
  A case-control study of platelet reactivity in 20 HIV-infected (HIVpos) and 20 age and sex-matched HIV-negative (HIVneg) individuals.
  
  
  METHODS
  Time-dependent platelet aggregation was measured in response to increasing concentrations of platelet agonists: epinephrine, collagen, thrombin receptor-activating peptide and ADP using light absorbance.
  
  
  RESULTS
  In both groups, mean age was 34 years, and 65% were men. Sixteen out of 20 (80%) of the HIVpos patients were on antiretroviral therapy with 12 out of 20 (60%) patients having HIV RNA less than 50 copies/ml. There were significant between-group differences in platelet reactivity across all four agonists. Platelets from HIVpos patients were more reactive to epinephrine [mean (SD) log concentration required to induce 50% maximal aggregation, 1.9 (1.2) versus 3.0 (1.7) mumol/l in HIVneg individuals, P = 0.028], whereas less platelet aggregation was observed in response to submaximal concentrations of the other agonists [thrombin receptor-activating peptide 72.5 (14.5)% versus 82.2 (7.6)% at 10 mumol/l, P = 0.011; ADP 67.3 (12.1)% versus 75.2 (8.8)% at 10 mumol/l, P = 0.035; collagen 16.6 (25.1)% versus 35.4 (31.5)% at 71.25 microg/ml, P = 0.007].
  
  
  CONCLUSIONS
  Between-group differences in platelet responses to all agonists suggest multiple underlying defects in platelet function in HIV infection. Further research is required to determine the contribution of antiretroviral therapy and relationships between platelet function and the increased cardiovascular disease observed in HIV-infected populations.
authors.affiliation: School of Medicine and Medical Sciences, University College Dublin, Ireland. claudette.satchell@ucd.ie
authors.forename: Claudette S
authors.initials: CS
authors.lastname: Satchell
authors.forename: Aoife G
authors.initials: AG
authors.lastname: Cotter
authors.forename: Eileen F
authors.initials: EF
authors.lastname: O'Connor
authors.forename: Aaron J
authors.initials: AJ
authors.lastname: Peace
authors.forename: Anthony F
authors.initials: AF
authors.lastname: Tedesco
authors.forename: Andrew
authors.initials: A
authors.lastname: Clare
authors.forename: John S
authors.initials: JS
authors.lastname: Lambert
authors.forename: Gerard J
authors.initials: GJ
authors.lastname: Sheehan
authors.forename: Dermot
authors.initials: D
authors.lastname: Kenny
authors.forename: Patrick W G
authors.initials: PW
authors.lastname: Mallon
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects; D001792:Blood Platelets / Q000187:drug effects*; D016022:Case-Control Studies; D005260:Female; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D010979:Platelet Function Tests; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D010975:Platelet Aggregation Inhibitors