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Bleeding Diathesis Discussion Part 1

We received several responses to Dr. Ari Elman’s 12/20/17 Undiagnosed Bleeding Diathesis post. This post begins a summary of possibilities.

From George Fritsma, moderator, given that the patient’s platelets fail to secrete in response to ADP, epinephrine, and arachidonic acid, could this be an acquired platelet activation pathway enzyme deficiency? Could she have developed an autoantibody, for instance, to the ADP receptor, P2Y12, or another platelet activation component? The argument against this theory is that it doesn’t account for the consistent finding of delayed bleeding, but it is supported by the platelet-type bleeding pattern.

Dave McGlasson (by phone) postulated an acquired Glanzmann thrombasthenia, perhaps an autoantobody specific to a component of the platelet membrane glycoprotein IIb/IIIa receptor. This is similar to George’s suggestion, and does not account for delayed bleeding. Dr. Elman had ruled out an antibody in his diagnostic effort, however, as others speculate, there may exist a hitherto unidentified autoantibody.

Dr. Huy Pham, Keck School of Medicine, University of Southern California, Los Angeles, wrote: “It seems to me that the patient has delayed bleeding and usually responded with antifibrinolytic agent. What does her urinalysis show? Does she have any blood in the urine? A very wild guess for some kind of bladder problem producing uPA. It also seems that she has problems with wound healing. Could this be vitamin C deficiency or some type of collagen disorders? This is a complex case!  Thank you for sharing!”

Dr. Emmanuel Favaloro, Department of Haematology, Institute of Clinical Pathology and Medical Research, New South Wales, wrote, “Have you discounted Quebec Platelet disorder?” QPD accounts for the delayed platelet-type bleeding symptoms, but as an inherited disorder its symptoms should have appeared early in the patient’s life and in the patient’s first-degree relatives.


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