Urinary Prostanoid Metabolites and Serum Thromboxane Following Recovery from Cyclooxygenase Inhibition with Aspirin

Summary: A previous study that measured urinary nary 11-dehydro-TXB2, 114.4 ± 13.8%, and urinary thromboxane B2 (TXB2) and 6-keto-PGF1α after with- TXB2, 106.0 ± 12 % (all not significant compared with drawal of aspirin found evidence of a rebound in urinary control). The urinary 6-keto-PGF1α level 14 days after prostanoid excretion above control levels 14 days after aspirin withdrawal was 96.9 ± 17.8 % of control (NS). aspirin administration ceased. This study aimed to con- Twenty-one days after aspirin withdrawal, TXB2 metab-firm these findings using a wider range of prostanoid me- olites as a percentage of control were, respectively, se-tabolites. The subjects were 17 young, healthy volunteers rum TXB2, 154 ± 39%; urinary TXB2, 114 ± 11 % (both who had taken 100 mg of enteric-coated aspirin daily for NS compared with control; and urinary 11-dehydro-7 days followed by 650 mg of enteric-coated aspirin for a TXB2, 127.2 ± 11.9 % (p = 0.037 compared with control). further 7 days as part of another study. They showed Urinary 6-keto-PGF1α 21 days after aspirin withdrawal signs of the expected inhibition of TXB2 metabolites at was 159.9 ± 46.2 % of control (NS). Overall there would the end of aspirin treatment. After 650 mg aspirin, serum appear to be a trend to increased production of prostanoid generation of TXB2 by clotting blood was 0.77 ± 0.2 % of metabolites 14 and 21 days after aspirin withdrawal, but it control (p < 0.0001), urinary 11-dehydro-TXB2was 21.8 reached statistical significance only for 11-dehydro-TXB2 ± 2.8 % of control (p < 0.0001), and urinary TXB2 was at 21 days ’ withdrawal. As platelets are the major sourc