Summary
33 patients with myeloproliferative disorder were studied and in 28 (84%) various
anomalies of platelet function were observed. Single, or more commonly, multiple platelet
aggregation defects and impaired release of platelet ADP and platelet factor 3 activity
were the chief anomalies noted, whether thrombocytosis was present or not. The effect
of myelosuppressive therapy upon the defects demonstrated varied from patient to patient,
and from one anomaly to another. Reducing the high platelet count to normal levels
does not seem to be sufficient to eradicate qualitative platelet defects.