Abstract
Auranofin (Aur), a new oral gold compound valuable in treatment of patients with rheumatoid arthritis, is known to have an inhibitory effect on ADP- and epinephrine-induced platelet aggregation in vitro. This may be of clinical importance as platelets participate in thrombus formation and are believed to act as proinflammatory cells in the diseased synovial tissue of rheumatoid arthritis. In the present in vitro study it was confirmed that Aur inhibits both ADP- and adrenaline-induced platelet aggregation in a dose- and time-dependent manner. In addition, a time- and dose-dependent decrease in platelet release of serotonin as well as a pronounced increase in the production of cyclic-AMP was found to result from Aur incubation. Aur's inhibitory effect on platelets is probably mediated through cyclic-AMP stimulation. Future studies of Aur's platelet inhibitory effect should investigate the mechanisms by which cyclic-AMP formation is increased, since this may be of importance also for Aur's action on other cell types.
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Winther, K., Oxholm, P. & Sengeløv, H. Effect of auranofin on human platelet aggregation, release of serotonin, and cyclic-AMP formation. Inflammation 12, 107–112 (1988). https://doi.org/10.1007/BF00915896
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DOI: https://doi.org/10.1007/BF00915896