Abstract
Sulphinpyrazone normalises the shortened platelet survival associated with gout or artificial heart valves and has shown benefit in secondary prevention of myocardial infarction. The compound is metabolised in all species but in variable amounts to a sulphide metabolite which is a potent cyclo-oxygenase inhibitor. At the plasma concentration found in man, the metabolite inhibits prostaglandin synthesis-dependent platelet behaviour and this is therefore the likely mechanism of action of sulphinpyrazone. The compound has some additional effects which may be important.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
