Arachidonic acid-stimulated platelet tests: Identification of patients less sensitive to aspirin treatment. (17th November 2015)

• Record Type: Journal Article
• Authors: Temperilli, Flavia; Rina, Aldona; Massimi, Isabella; Montemari, Anna Lisa; Guarino, Maria Luisa; Zicari, Alessandra; Pulcinelli, Fabio M.
• Is Part Of: Platelets. Volume 26:Number 8(2015:Dec.)
• Page Start: 783
• Page End: 787
• Publication Date: 2015-11-17
• Subjects: Arachidonic acid -- aspirin -- COX-1 -- platelet aggregation -- thromboxane B2; Blood platelets -- Periodicals; Blood Platelets -- Periodicals; 615.39
• DOI: 10.3109/09537104.2014.1003291
• Languages: English
• ISSNs: 0953-7104

Abstract

Abstract: Serum thromboxane-B2 (TxB2), together with arachidonic acid (AA)-induced platelet aggregation, are, at the moment, the most used tests to identify patients displaying high on-aspirin treatment platelet reactivity (HAPR). Both tests are specific for aspirin action on cyclooxygenase-1. While the correlation between serum TxB2 assay and clinical outcome is established, data are conflicting with regard to aspirin treatment and a possible association with AA-stimulated platelet markers and clinical outcome. To understand such discrepancy, we performed a retrospective study to compare both assays. We collected data from 132 patients receiving a daily dose of aspirin (100 mg/day) and data from 48 patients receiving aspirin on alternate days. All Patients who received a daily dose of aspirin were studied for AA-induced platelet aggregation together with serum TxB2 levels and AA-induced TxB2 formation was also studied in 71 patients out of entire population. Consistent with recommendations in the literature, we defined HAPR by setting a cut-off point at 3.1 ng/ml for serum levels of thromboxane B2 and 20% for AA-induced platelet aggregation. According to this cut-off point, we divided our overall population into two groups: (1) TxB2 < 3.1 ng/ml and (2) TxB2 > 3.1 ng/ml. We found low agreement between such tests to identify patients displaying HAPR. Our results show that AA-induced platelet aggregation >20% identify a smaller number of HAPR patients in comparison with TxB2. A good correlation between serum TxB2 and arachidonic acid-induced TxB2 production was found ( r = 0.76619).