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 meloxicam on platelet aggregation and coagulation function in human blood samples. Blood samples were collected from six healthy humans and processed to make platelet-adjusted (100T103 cells/ml) blood samples. Acetaminophen (Tylenol, Q-PAP, 100 mg/ml) was added at the doses of 0mg/ml (control), 214mg/ml (the standard dose, 1T), 4T, 8T, 10T, 12T, 16T, and 20T. Similarly, meloxicam (Metacam, 5 mg/ml) was added at doses of 0mg/ml (control), 2.85mg/ml (the standard dose, 1T), 4T, 8T, 10T, 12T, 16T, and 20T. Fifteen minutes after the addition of acetaminophen and/or meloxicam, platelet aggregation was stimulated with collagen (2mg/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 acid-stimulated platelet aggregation starting at 1T dose. Collagen-stimulated platelet aggregation was inhibited by ACE starting at 1T (78W10% of control), and by meloxicam starting at 4T (72W5% of control, both P0.05). The inhibitions by acetaminophen and meloxicam combined were similar to those by acetaminophen or meloxicam. aPTT was prolonged by meloxicam starting at 4T. 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.
Published in Blood Coagulation and Fibrinolysis, v25 n8 p831-837, 2014. Prepared in collaboration with Rice University, Houston, TX.