Summary
1. The antibotic, Ristocetin, causes precipitation of fibrinogen from platelet poor
plasma, as well as platelet aggregation.
2. The precise mechanism of Ristocetin’s effect on platelets has not been elucidated,
but it has been shown to initiate ADP release, which may contribute in part to its
aggregating ability.
3. Ristocetin has been shown to produce aggregation in platelet rich plasma from thrombasthenic
patients.
4. Three patients with Von Willebrand’s disease were examined. In 2, Ristocetin caused
no platelet aggregation whatsoever, whilst the third aggregated normally. It is suggested,
on this basis, that Von Willebrand’s disease may be subdivided into two types and
that Ristocetin could prove to be a valuable technique for further study of this group
of disorders.
