Thrombocytopathia Due to Abnormalities in Platelet Release Reaction—Studies on Six Unrelated Patients

Harvey J. Weiss, John Rogers


The prolonged bleeding time in six unrelated patients ages 24-63, was attributed to impaired platelet aggregation; this could be accounted for by the decreased release of platelet adenosine diphosphate (ADP) that was obtained in all patients. As a consequence of this "platelet release abnormality," collagen-induced platelet aggregation was impaired, the second wave of epinephrine-induced aggregation was decreased (although not invariably absent), and the normal initial wave of ADP-induced aggregation was followed by rapid disaggregation at 37°C. In four patients, the abnormality in collagen-induced aggregation and ADP release appeared to be different than the defect produced by aspirin, whereas two patients appeared to have an "aspirinlike defect." The platelets of all patients adhered normally to connective tissue fibers but were poorly retained in glass bead filters. Other abnormalities included impaired kaolin-induced platelet factor 3 availability in four patients, large platelets (which aggregated normally with bovine fibrinogen) in two, and small platelets in one patient. The general term thrombocytopathia is suggested to describe abnormalities in platelet function; where a specific defect in the release reaction has been demonstrated, "platelet release abnormality" is suggested as an appropriate, specific term.

  • Submitted April 20, 1971.
  • Revision received August 16, 1971.
  • Accepted August 20, 1971.