Acetaminophen and meloxicam inhibit platelet aggregation and coagulation in blood samples from humans

Acetaminophen (Ace) and meloxicam (Mel) are the two types of analgesic and antipyretic medications. This study investigated the dose responses of acetaminophen and meloxicamon platelet aggregation and coagulation function in human blood samples. Blood samples were collected from six healthy humans and processed to make plateletadjusted (100×10³ cells/ml) blood samples. Acetaminophen (Tylenol, Q-PAP, 100mg/ml) was added at the doses of 0μg/ml (control), 214 μg/ml (the standard dose, 1×), 4×, 8×, 10×, 12×, 16×, and 20×. Similarly, meloxicam (Metacam, 5mg/ml) was added at doses of 0 μg/ml (control), 2.85 μg/ml (the standard dose, 1×), 4×, 8×, 10×, 12×, 16×, and 20×. Fifteen minutes after the addition of acetaminophen and/or meloxicam, platelet aggregation was stimulated with collagen (2μg/ml) or arachidonic acid (0.5 mmol/l) and assessed using a Chrono-Log 700 aggregometer. Coagulation function was assessed by prothrombin time (PT), activated partial thromboplastin time (aPTT), and using Rotem thrombelastogram. A robust inhibition by acetaminophen and/or meloxicam was observed in arachidonic acidstimulated platelet aggregation starting at 1× dose. Collagen-stimulated platelet aggregation was inhibited by ACE starting at 1× (78±10% of control), and by meloxicam starting at 4× (72±5% of control, both P<0.05). The inhibitions by acetaminophen and meloxicam combined were similar to those by acetaminophen or meloxicam. aPTT was prolonged by meloxicam starting at 4×. No changes were observed in PT or any of Rotem measurements by acetaminophen and/or meloxicam. Acetaminophen and meloxicam compromised platelet aggregation and aPTT. Further effort is warranted to characterize the effects of acetaminophen and meloxicam on bleeding in vivo.