Abnormalities of platelet function in patients with polycythemia vera.

Summary The exact mechanism(s) of thrombosis and hemorrhage in polycythemia vera has not yet been delineated. Platelet function studies were performed by examining platelet aggregation in 47 polycythemia vera patients (62 studies) with low (“spent”), normal, or elevated hematocrits and with varying platelet counts. Adenosine diphosphate, epinephrine, collagen, and thrombin were used as aggregating agents. Eighty-one % of the 62 studies were abnormal. The frequency of abnormal tests increased from those with normal hematocrits and platelet counts (75%) through to those with elevated hematocrits and platelet counts (100%). One hundred % of the studies in spent polycythemia vera were abnormal. Abnormal bleeding times and thrombohemorrhagic complications did not correlate with each other or with abnormal aggregation, hematocrits, or platelet counts. Repeat studies following therapy showed improvement in 10 of 13 patients. The incidence of abnormal aggregation in polycythemia vera is high; however, the significance of this finding in the pathogenesis of thrombosis and hemorrhage remains obscure.