A study of aspirin induced changes in bleeding time, platelet aggregation, and sonoclot® coagulation analysis in humans

• Published in: Annals of clinical and laboratory science Vol. 21; no. 5; pp. 315 - 327
• Main Authors: SAMRA, S. K, HARRISON, R. L, BEE, D. E, VALERO, V
• Format: Conference Proceeding Journal Article
• Language: English
• Published: Philadelphia, PA Institute for Clinical Science 01.09.1991
• Subjects: Adult; Aspirin - adverse effects; Biological and medical sciences; Bleeding Time; Blood Coagulation - drug effects; Blood Coagulation Disorders - blood; Evaluation Studies as Topic; Female; Hematologic and hematopoietic diseases; Humans; Male; Medical sciences; Middle Aged; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors - pharmacology; Platelet Function Tests - instrumentation; Human; Exploration; Platelet; Hemopathy; Bleeding time
• ISSN: 0091-7370; 1550-8080

The purpose of this study was to determine whether or not a newer test of platelet function, Sonoclot coagulation analysis, can identify the patients who develop significant prolongation of bleeding time after aspirin ingestion. Template bleeding time, platelet aggregation in response to arachidonic acid, collagen, epinephrine, adenosine diphosphate, and ristocetin, and Sonoclot coagulation analysis were performed before and after ingestion of aspirin in 22 adult volunteers. Mean bleeding time increased from 5.32 +/- 2.16 min to 7.34 +/- 2.1 min, but remained within normal range (2.5 to 9 min). There was marked intersubject variability in the effect of aspirin on bleeding time, and difference between men and women was not significant. There was significant decrease in platelet aggregation in response to arachidonic acid, collagen and epinephrine. Sonoclot coagulation analysis did not show significant effect of aspirin administration. There was no correlation among changes in bleeding time, platelet aggregation, and Sonoclot coagulation analysis. Five patients with known platelet function disorders and prolonged bleeding times (mean = 18.5 min, range 14 to 22) without any other coagulation abnormalities were also studied. In four of these patients who had normal platelet count, Sonoclot graphs were morphologically similar to those in the volunteers with normal bleeding times, but in one patient with thrombocytopenia, morphology was altered. It is our conclusion that Sonoclot coagulation analysis is unlikely to identify patients with prolonged bleeding time in whom platelet count and other coagulation factors are normal.