Intermediate syndrome of platelet dysfunction

Abstract

We studied eight patients with intermittent bleeding episodes usually following trauma and associated with the ingestion of medicine known to interfere with platelet function. All patients had a normal or minimally prolonged baseline bleeding time. All had a normal platelet count, glass bead retention test, and platelet serotonin content and a variable pattern of abnormalities in prothrombin consumption and platelet factor 3 availability. However, all showed abnormal platelet aggregation reactions using epinephrine, adenosine diphosphate, and collagen. Following the administration of 975 mg aspirin, our patients' bleeding times became prolonged to a greater extent than the bleeding times of normal controls (range 13 to greater than 20 min). Review of the literature showed approximately 5% of “normal” controls had findings similar to those we report. We believe we are describing a group of individuals with an intermediate form of platelet dysfunction. Although their bleeding diathesis is not as severe as that of patients with platelet dysfunction syndromes previoulsy described, they do bleed significantly when subjected to trauma following the ingestion of drugs such as aspirin. We propose that this defect is common and should be screened for. The aspirin tolerance test is a simple test for detecting these patients.

Interaction between the LMWH reviparin and aspirin in healthy volunteers

“…In all of these studies ASA appeared to be associated with a modest increase in bleeding time only in some of the subjects, suggesting variability in response to ASA. On the other hand, variations in the performance of bleeding time assessment (direction of skin cuts and depth of incisions) might explain differences in bleeding time results throughout the studies [18–20]. Finally different treatment allocations and varying doses of ASA and heparins administered throughout the studies have to be considered.…”

Congenital Disorders Affecting Platelets

“…Current evidence suggests that these "aspirin-like" defects represent a hetero geneous group of disorders, at least some of which differ from the defect produced by aspirin. For example, ultrastructural abnormalities were described in one patient [280], while in others aspirin worsened the hemostatic defect [59]. Stuart has suggested that a variety of enzymatic and membrane defects, as yet unidentified, may fit into this general category of aspirin-like defects [248].…”