Evidence is growing that we can use whole blood and plasma/urine markers…
…to indicate aspirin response. In my July 16, 2007 post I mentioned a presentation I’ll be giving on Friday at the ASCLS/AACC annual meeting in San Diego. I’ll be describing platelet adhesion molecules and their relationship to cardiovascular disease. That is not the end of the story.
Dave McGlasson, MT (ASCP) is making two presentations. On Wednesday, July 18, 2007 he will stand by his AACC poster, “Comparison of metabolic platelet responses to single and seven-day aspirin reveals dosage effect.” On Friday he will give an ASCLS platform presentation, “Laboratory testing to detect aspirin sensitivity and resistance.”
Dave will be describing assays that detect “aspirin resistance,” a laboratory phenomenon that may predict inadequate clinical response to aspirin therapy. There are several whole blood-based platelet aggregometry tests and one immunoassay for a metabolite of platelet activation, 11-dehydro thromboxane B2 (UDHT).
We all know aspirin suppresses platelet activation, reflected in suppression of the aggregometry response to collagen and arachidonic acid. Further, many realize that some 15-20% of patient platelets aggregate normally despite aspirin. These are thought to be “aspirin resistant.”
Whether aspirin resistance is a clinical phenomenon as well as a laboratory finding is up for debate. However, there are some case-control retrospective studies that relate inadequate aspirin response to elevated cardiovascular risk.
Dave’s talk will reveal yet another emergent platelet-related assay likely to engage laboratory scientists in the near future. Geo.