I wouldn't read too terribly much into this -- other than to say that similar agents still on the market ought to be designing protocols to monitor this lipid.
Here is an interesting story -- out of the Sacramento Business Journal, tonight -- do go read it all:
. . . .Using a method to profile rodent blood, scientists discovered that Vioxx causes a dramatic increase in a bio-marker that could be a major contributor of heart attacks and strokes. . . .
The study shows that significant concentrations of a lipid known as 20-HETE contributes to Vioxx-related heart problems. . . .
This suggests cardiovascular risk associated with Vioxx is not unique to this drug but is likely shared by others in this drug class — and that it may be possible to predict patients who are at risk by monitoring their 20-HETE levels. . . .
The research took place in laboratories run by Hammock, cell biologist Nipavan Chiamvimonvat at the UC Davis Division of Cardiovascular Medicine and physiologist Yi Zhu at Peking University. The study will be published this week in Proceedings of the National Academy of Sciences. . . .
Actually, with Vioxx® long-since withdrawn, this finding probably has more relevance for other agents in its class (Avandia anyone?). Still, it could lead to a next-gen version, designed to avoid the 20-HETE elevation, and associated elevated CV risks.
1 comment:
The proposed mechanism is not new. It was proposed and known by Merck as long ago as the mid-1990s before the CV risks were even seen in patients. It's only after drug classes are nearing the end of their lifespans that academicians begin to look into the likely causes for severe toxicities.
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