Platelet thromboxane (11-dehydro-Thromboxane B2) and aspirin response in patients with diabetes and coronary artery disease

A schematic representation of the arachidonic/thromboxane metabolic pathway: Arachidonic acid generated from membrane phospholipids by phospholipase A2 and phospholipase C undergoes additional enzymatic transformation by cyclooxygenases (COX-1 and COX-2) into prostaglandin and thromboxane metabolites. In platelets, Arachidonic acid (AA) is metabolized by COX-1 into prostaglandins PGG2, PGH2 and by thromboxane synthase into the bioactive thromboxane A2 (TXA2), which is a potent activator of platelet aggregation with a short half-life. TXA2 is quickly inactivated into a more stable thromboxane B2 (TXB2) and converted in the liver into an 11-dehydro-thromboxane B2 (11dhTXB2) metabolite excreted in the urine. Aspirin (ASA) irreversibly inhibits platelet COX-1 leading to decreased thromboxane-mediated platelet activation. TXA2 and 11dhTXB2 can be generated by COX-2 present in various inflammatory cells, pathway not affected by ASA.

Publication

Platelet thromboxane (11-dehydro-Thromboxane B2) and aspirin response in patients with diabetes and coronary artery disease. (2014) Luis R Lopez, et al. World J Diabetes. 2014 Apr 15;5(2):115-127. Figure: F1. Drosophila melanogaster

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