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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Pharmacogenomics of anti-platelet therapy focused on peripheral blood cells of coronary arterial disease patients

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Luchessi, Andre Ducati [1] ; Silbiger, Vivian Noguiea [1, 2] ; Crespo Hirata, Rosario Dominguez [1] ; Lima-Neto, Lidio Goncalves [1] ; Cavichioli, Debora [1] ; Iniguez, Andres [3] ; Bravo, Marisol [3] ; Bastos, Guillermo [3] ; Morais Rego Sousa, Amanda Guerra [4] ; Brion, Maria [5] ; Carracedo, Angel [5] ; Hirata, Mario Hiroyuki [1]
Total Authors: 12
[1] Univ Sao Paulo, Sch Pharmaceut Sci, BR-05508900 Sao Paulo - Brazil
[2] Univ Fed Rio Grande do Norte, Sch Pharm, BR-59072970 Natal, RN - Brazil
[3] Meixoeiro Hosp, Vigo - Spain
[4] Dante Pazzanese Inst Cardiol, Sao Paulo - Brazil
[5] Univ Santiago de Compostela, CIBERER, Fdn Genom Med, Grp Genom Med, Santiago De Compostela - Spain
Total Affiliations: 5
Document type: Journal article
Source: Clinica Chimica Acta; v. 425, p. 9-17, OCT 21 2013.
Web of Science Citations: 5

Background: To investigate genes differentially expressed in peripheral blood cells (PBCs) from patients with coronary arterial disease (CAD) under double anti-platelet therapy. Methods: Twenty-six CAD patients that were submitted to percutaneous coronary intervention (PCI) were selected to participate in this study. These patients took 100 mg/day of acetylsalicylic acid (ASA) and 75 mg/day of clopidogrel. Blood samples were collected before PCI to evaluate platelet reactivity using VerifyNow ASA and P2Y12 assays (Accumetrics). The patients were stratified into 4 quartiles based on ASA reaction units (ARUs) and P2Y12 reaction units (PRUs). Quartile 1 (Q1) patients were classified as responders and quartile 4 (Q4) patients as non-responders. Global mRNA expression from Q1 to Q4 was analyzed by microarray using the GeneChip Exon 1.0 ST array (Affymetrix) and was confirmed by RT-qPCR. Results: Patients with ARU or PRU values within the first quartile (Q1, ARU < 390 and PRU < 151) were considered responders, while those who had ARU or PRU within the fourth quartile (Q4, ARU > 467 and PRU > 260) were considered nonresponders. The risk factors associated for CAD showed expected frequencies and no difference was found between Q1 and Q4. Microarray analysis identified 117 genes differentially expressed for ASA and 29 for clopidogrel between Q1 and Q4 groups (p < 0.01, FC > 1.2). Conclusion: The variation in response to ASA may be related with an increased expression of IGF1 and IGF1R, as well as a response to clopidogrel can be affected by pharmacokinetic change related to the reverse transport pathway by increased expression of ABCC3. (C) 2013 Elsevier B.V. All rights reserved. (AU)

FAPESP's process: 09/10862-4 - Analysis pharmacogenomics: coronary syndromes in patients who underwent double antiplatelet aggregation, with an indication for implantation of stent
Grantee:Amanda Guerra de Moraes Rego Souza
Support Opportunities: Regular Research Grants