Does Non-Acetylated Salicylate Inhibit Thromboxane Biosynthesis in Human Platelets?

Abstract

Ingestion of aspirin (acetyl salicylic acid: ASA) may promote bleeding complications due to inhibition of thromboxane biosynthesis, which results in the prolongation of bleeding time. The effect is believed to be achieved by the irreversible acetylation of the enzyme cyclooxygenase by aspirin.¹ This alteration in platelet function by aspirin prohibits its use in patients with bleeding disorders such as haemophiliacs. Choline magnesium trisalicylate (CMT; Napp Laboratories Ltd) is a non-acetylated salicylate with analgesic and anti-inflammatory effects similar to that of aspirin.² However, despite a comparable salicylate absorption from the two drugs, CMT is found to have no inhibitory action in platelet aggregation³ and to cause less gastric mucosal damage⁴ and gastrointestinal blood loss than aspirin. to investigate the role of the acetyl moiety in the inhibition of platelet thromboxane biosynthesis, we studied the effect of CMT and ASA on bleeding time, serum thromboxane B₂ (TxB₂) and thromboxane (Tx) generation in healthy volunteers.