Low-Dose Aspirin, Coxibs, and other NSAIDS: A Clinical Mosaic Emerges

Assessing the relationship between inhibition of platelet COX-1 activity and thromboxane biosynthesis in man. In human platelets (left), the maximal capacity for COX-dependent prostanoid synthesis ex vivo (here, measured as TXB₂ produced during whole blood clotting) is three orders of magnitude greater than the basal in vivo biosynthetic rate of thromboxane (middle panel, calculated according to excretion of liver-metabolized products in urine; designated as 11-dehydro-TXB2 & other metabolites). Following aspirin administration, the relationship between inhibition of platelet cyclooxygenase activity measured ex vivo (serum TXB₂), and inhibition of thromboxane biosynthesis in vivo (urinary 11-dehydro-TXB₂) is non-linear, with substantial inhibition of the latter only occurring at complete suppression of the former (right panel). [ See (8, 10) and references therein.]