In 3 patients with dysproteinaemia the defects in haemostasis were investigated: Waldenström’s macroglobulinaemia, macroglobulinaemia associated with undifferentiated malignancy in the marrow, diffuse hypergammaglobulinaemia associated with drug sensitive purpura. Platelet factor 3 release, reduction of its total contents and poor platelet adhesion were found in all 3 patients. Platelet aggregation was absent in 2 patients who had macroglobulinaemia with monoclonal spike. It is suggested that the platelet factor 3 assay may be of value in the investigation of these changes in relation to dysproteinaemias.

The present paper describes 3 cases of classical thrombasthenia and 3 cases of combined platelet factor 3 defi- 3 ciency and absence of platelet aggregation. The bleeding time and the clot retraction in the latter 3 patients were They, however, did not differ in clinical presentation of classical thrombasthenia. These cases have been designated as thrombopathic thrombasthenia. The possibility of an in vivo platelet activation leading to variable amounts of platelet factor 3 release in thrombasthenia has been raised. Mechanism of PF3 release in vivo in thrombasthenia, however, is not known and needs further study.

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