Skip Navigation LinksHome > March 13, 2010 - Volume 24 - Issue 5 > Platelet function and HIV: a case–control study
doi: 10.1097/QAD.0b013e328336098c
Basic Science

Platelet function and HIV: a case–control study

Satchell, Claudette Sa; Cotter, Aoife Gb; O'Connor, Eileen Fb; Peace, Aaron Jc; Tedesco, Anthony Fc; Clare, Andrewb; Lambert, John Sb; Sheehan, Gerard Jb; Kenny, Dermotc; Mallon, Patrick WGa,b

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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.

Design: 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) μmol/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 μmol/l, P = 0.011; ADP 67.3 (12.1)% versus 75.2 (8.8)% at 10 μmol/l, P = 0.035; collagen 16.6 (25.1)% versus 35.4 (31.5)% at 71.25 μg/ml, P = 0.007].

Conclusion: 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.

© 2010 Lippincott Williams & Wilkins, Inc.


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