Nongnuch SirachainanPiyathida WijarnAmpaiwan ChuansumritPraguywan KadegasemPakawan WongwerawattanakoonAnucha SoisamrongMahidol University2018-11-232018-11-232015-05-01Thrombosis Research. Vol.135, No.5 (2015), 916-92218792472004938482-s2.0-84928613822https://repository.li.mahidol.ac.th/handle/20.500.14594/36443© 2015 Elsevier Ltd. All rights reserved. Aspirin is now recommended for splenectomized thalassemia patients with high platelet counts. However, aspirin resistance defined by arachinodic acid (ACA) induced platelet aggregation 20%, has never been reported in this group of patients. In this study, twenty-four splenectomized thalassemia patients (15.7 ± 4.1 years), with platelet counts 800x109/L, and 21 non-splenectomized severe thalassemia patients (14.3 ± 3.2 years), were enrolled. After taking aspirin (2 mg/kg/day), seven patients (29.2%) displayed aspirin resistance. Serum thromboxane B2(TXB2) levels in the aspirin responsive group decreased significantly [52.6(8.8-174.6) vs 4.0(1.6-7.3) mcg/mL, p < 0.001], while no change was demonstrated in the aspirin resistant group. Having increased aspirin to 4 mg/kg/day, three of the seven aspirin resistant patients responded, while one developed upper GI bleeding from esophageal varices and was withdrawn from the study. For the three remaining patients, their doses were increased to the maximum of 300 mg/day, and two of the three responded. Thrombin antithrombin complex and D-dimer levels were significantly decreased after taking aspirin (2 mg/kg/day), although D-dimer level was still significantly higher than that in non-splenectomized group. Therefore, aspirin dosage can be adjusted individually to reach maximum effect of platelet inhibition. In addition, aspirin can reduce the levels of coagulation markers.Mahidol UniversityMedicineArticleSCOPUS10.1016/j.thromres.2015.03.003