From Kelly Townsend at Tricore Labs: We have a patient whose platelets clump in every anticoagulant we’ve tried. He has normal prothrombin time, partial thromboplastin time, fibrinogen, and von Willebrand disease panel results, but oozes after even minor procedures. The clinicians want to evaluate platelet function, but we are hesitant because of his platelet clumping. Any suggestions for obtaining accurate platelet function analyzer (PFA-100) and/or platelet aggregation results in a platelet clumper? We use the Chrono-log Lumiaggregometer (whole blood).
Category: Platelet Function Testing
A second great question from our Rutgers graduate hemostasis course participants, this one from Brandy Gunsolus, Healthplex Family Clinic in Shreveport, LA, and Jene Shafer from Orange Regional Hospital, Middletown, NY. We are studying the new cell-based model of coagulation and they ask whether the storage lesion of platelet concentrates affects their ability to be activated in vivo upon administration. The cell-based model relies on collagen and thrombin-activated (COAT) platelets; they wonder if stored platelets are able to be activated as effectively as patient’s own platelets. I have found no studies examining this question.
From Gnaesh Lyer, Florida Hospital: Have you done any correlation studies for Plavix and aspirin if the tubes are sent by tube system from floors rather than hand delivering the tubes? Does the results vary a lot or with in acceptable range? Thanks.
Hello, Gnaesh Lyer, and thank you for your question. I know of no studies that examine the effect of specimen tube system agitation affecting platelet function assay results, and have forwarded your question to several colleagues to learn if anyone has unpublished data on the subject. Perhaps one of our participants may have a comment to add.
From Jeanine Walenga, PhD, Loyola University Medical Center, Maywood, IL: When we perform the test for heparin-induced thrombocytopenia with thrombosis (HIT) using platelet aggregation, we use a reagent to remove heparin contaminant from the patient sample–ecteola cellulose. If there is a positive baseline (spontaneous aggregation with no heparin reagent added) we assume that there may be heparin in the patient sample. Se we treat the sample with ecteola cellulose, centrifuge, then retest the sample in the HIT aggregation assay. We just learned that the company Inotech Biosystems International, Inc. will not supply the ecteola cellulose until they find another manufacturer. Is there another source, preferably a clinical kit (not Sigma)? If Sigma is the only source, does someone have a clinical protocol? Thanks.
Here is a recent note from Lauren Smith Helfgott, applications specialist at Chrono-log Corporation:
“Hello, George. A clinician and I were recently discussing platelet aspirin-like defect (secretion disorder). He came across slides 28 and 30 from the Fritsma Factor audio module Platelet Function Testing Part 2 and sent them over. The tracings are labeled ‘aspirin or aspirin-like (secretion) disorder,’ and are attributed to Edward Masel, University of Rochester Medical Center, Rochester NY, dated 3/22/06. According to our communications with Ed, these tracings are actually from a patient with an acquired secretion defect due to platelet antibodies. We just wanted you to be aware that this patient had a platelet secretion defect as a result of antibodies; not an inherited secretion disorder.”
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Another interesting discussion from our UMDNJ graduate Hemostasis course:
(Original post February 1, 2012, re-posted January 15, 2013 to encourage comments)
About 6 years back, I caught wind of a discussion regarding platelet substitutes, which I found quite intriguing. I did some digging as a result of this discussion and am amazed by the potential of such technologies. It appears that platelet rich plasma (PRP) gel has been around for some time, more than two decades according to Carter, et al. (2011). Do you know how often and in what circumstances such a technology as PRP gel is utilized?
I am reconstructing previous Fritsma Factor posts subsequent to the crashes we experienced in November and December and came across an April 12, 2012 communication from an individual who has non-symptomatic thrombocytopenia with giant platelets. I suggested this could be one of the MYH9 mutations such as May-Hegglin anomaly. I post this link now, hoping to attract comments from some platelet experts. Please respond if you have more information on this interesting case.