Authors
Satchell, Claudette SCotter, Aoife G
O'Connor, Eileen F
Peace, Aaron J
Tedesco, Anthony F
Clare, Andrew
Lambert, John S
Sheehan, Gerard J
Kenny, Dermot
Mallon, Patrick W G
Affiliation
School of Medicine and Medical Sciences, University College Dublin, Ireland. claudette.satchell@ucd.ieIssue Date
2010-03-13Keywords
HIV INFECTIONMeSH
AdultAntiretroviral Therapy, Highly Active
Blood Platelets
Case-Control Studies
Female
HIV Infections
Humans
Male
Myocardial Infarction
Platelet Aggregation
Platelet Aggregation Inhibitors
Platelet Function Tests
Prospective Studies
Risk Factors
Metadata
Show full item recordCitation
Platelet function and HIV: a case-control study. 2010, 24 (5):649-57 AIDSJournal
AIDS (London, England)DOI
10.1097/QAD.0b013e328336098cPubMed ID
20177361Additional Links
http://www.ncbi.nlm.nih.gov/pubmed?term=20177361Abstract
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.A case-control study of platelet reactivity in 20 HIV-infected (HIVpos) and 20 age and sex-matched HIV-negative (HIVneg) individuals.
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.
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].
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.
Item Type
ArticleLanguage
enISSN
1473-5571ae974a485f413a2113503eed53cd6c53
10.1097/QAD.0b013e328336098c