Inhibition of thromboxane biosynthesis by triflusal in type 2 diabetes mellitus.

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RESEARCH PRODUCT

Inhibition of thromboxane biosynthesis by triflusal in type 2 diabetes mellitus.

Giovanni Davì M. Di Nicola Angela Falco Gino Avellone C. Di Febbo Ester Vitacolonna Giovanni Ciabattoni Antonio Pinto F. Salvati Enzo Ballone

subject

Adult Male medicine.medical_specialty Thromboxane aspirin Radioimmunoassay chemistry.chemical_compound Thromboxane A2 Von Willebrand factor Double-Blind Method Internal medicine type 2 diabetes triellitus von Willebrand Factor medicine platelet activation Humans Platelet Platelet activation Aged Retrospective Studies Aspirin biology Dose-Response Relationship Drug Middle Aged Salicylates Thromboxane B2 Thromboxane B2 triflusal P-Selectin Endocrinology chemistry Diabetes Mellitus Type 2 biology.protein Triflusal Female Cardiology and Cardiovascular Medicine Biomarkers Platelet Aggregation Inhibitors medicine.drug Follow-Up Studies

description

Abstract Triflusal is an antiplatelet drug related to aspirin, with different pharmacological properties and a lower haemorrhagic risk. We aimed at comparing their effects on platelet and endothelial activation in type 2 diabetes mellitus (T2DM). In a randomized, double-blind, parallel group study, we compared the effects of three daily regimens (300, 600, and 900mg) of triflusal, and aspirin (100mg/day) on urinary 11-dehydro-thromboxane (TX)B 2 , index of in vivo platelet activation, ex vivo platelet function using the analyzer PFA-100, plasma von Willebrand factor (vWF), P-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and serum nitrite and nitrate (NO 2 − +NO 3 − ) in 60 T2DM patients. Triflusal induced a dose-dependent reduction in 11-dehydro-TXB 2 and a prolongation of closure time in the presence of collagen plus epinephrine (Coll/Epi-CT). The effects of the highest triflusal dose were not different from those of aspirin. The closure time in the presence of collagen plus ADP (Coll/ADP-CT), ICAM-1, VCAM-1, and NO 2 − +NO 3 − were not modified either by triflusal or aspirin. Plasma P-selectin and vWF were reduced by triflusal but not by aspirin. In T2DM triflusal causes a profound inhibition of platelet TXA 2 biosynthesis in vivo, acting on different targets involved in the platelet–endothelial cell interactions.

year	journal	country	edition	language
2004-09-09

10.1016/j.atherosclerosis.2005.03.014 http://hdl.handle.net/10447/2036