Show simple item record

dc.contributor.authorSatchell, Claudette S
dc.contributor.authorCotter, Aoife G
dc.contributor.authorO'Connor, Eileen F
dc.contributor.authorPeace, Aaron J
dc.contributor.authorTedesco, Anthony F
dc.contributor.authorClare, Andrew
dc.contributor.authorLambert, John S
dc.contributor.authorSheehan, Gerard J
dc.contributor.authorKenny, Dermot
dc.contributor.authorMallon, Patrick W G
dc.date.accessioned2011-11-18T11:41:14Z
dc.date.available2011-11-18T11:41:14Z
dc.date.issued2010-03-13
dc.identifier.citationPlatelet function and HIV: a case-control study. 2010, 24 (5):649-57 AIDSen
dc.identifier.issn1473-5571
dc.identifier.pmid20177361
dc.identifier.doi10.1097/QAD.0b013e328336098c
dc.identifier.urihttp://hdl.handle.net/10147/189931
dc.description.abstractCardiovascular 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.
dc.description.abstractA case-control study of platelet reactivity in 20 HIV-infected (HIVpos) and 20 age and sex-matched HIV-negative (HIVneg) individuals.
dc.description.abstractTime-dependent platelet aggregation was measured in response to increasing concentrations of platelet agonists: epinephrine, collagen, thrombin receptor-activating peptide and ADP using light absorbance.
dc.description.abstractIn 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].
dc.description.abstractBetween-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.
dc.language.isoenen
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed?term=20177361en
dc.subjectHIV INFECTIONen
dc.subject.meshAdult
dc.subject.meshAntiretroviral Therapy, Highly Active
dc.subject.meshBlood Platelets
dc.subject.meshCase-Control Studies
dc.subject.meshFemale
dc.subject.meshHIV Infections
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMyocardial Infarction
dc.subject.meshPlatelet Aggregation
dc.subject.meshPlatelet Aggregation Inhibitors
dc.subject.meshPlatelet Function Tests
dc.subject.meshProspective Studies
dc.subject.meshRisk Factors
dc.titlePlatelet function and HIV: a case-control study.en
dc.typeArticleen
dc.contributor.departmentSchool of Medicine and Medical Sciences, University College Dublin, Ireland. claudette.satchell@ucd.ieen
dc.identifier.journalAIDS (London, England)en
dc.description.provinceLeinster
html.description.abstractCardiovascular 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.
html.description.abstractA case-control study of platelet reactivity in 20 HIV-infected (HIVpos) and 20 age and sex-matched HIV-negative (HIVneg) individuals.
html.description.abstractTime-dependent platelet aggregation was measured in response to increasing concentrations of platelet agonists: epinephrine, collagen, thrombin receptor-activating peptide and ADP using light absorbance.
html.description.abstractIn 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].
html.description.abstractBetween-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.


This item appears in the following Collection(s)

Show simple item record