468 VII INT. CONGo THROMB. HAEM. Supplementary Abstracts

1143 FOJSIBLE i·lECUil.HI8M OF UEMORRHAGIC DIA'rHESIG IN PRUlrlRY i'HiiONBOCYTHLmA I G. Hintz , F. Pfannkuch and D. Schneider; Dpt. Pathology, of Hematology, Dpt. of Free University Berlin, Klinikum destend, Berlin, Germany }rimary thrombocythemia is characterised by a marked increase in platelet number. 'l'he clinical manifestation varies between embolic diathesis. bleeding and thrombo­ There was evidence that the major factor in the pro­ duction of hemorrhage is a qualitative abnormality But no of platelet function. satisfactory explanation for the following facts was 1. platelets of possible: patients with primary thrombocythemia are able to control bleeding in patients with thrombocytopenia; number 2. normalisation of platelet eliminates the bleeding tendency of patients • .• e studied the spontaneous clotting of recalcified citrated blood in three patients with primary thrombocythemia. In two patients bleeding time with prolonged and normal platelet function the clots showed an increased fall-out of erythrocytes. Electron-microscopy retraction showed that increased clot and fall-out of erythrocytes was caused by platelets and fibrin. a rigid network of Controls were made in each patient after normalisation of the platelet number: clot formation and morphological picture ports were normal. 'j'his sup­ our theory that - at least in our patients - the defect as a ,majcx factor of bemorrbagic of platelets diathesis is the inc~eased number itself.

1144 PLATELET FUNCTIONS ABNORMABILlTIES IN fi-THALASSAEMIA PATIENTS. R. Fantasia, M. Colombi, P. Hassaro, E. Pogliani, and E. Polli - I~ Clinica Medica, School of Medicine, University of Milan - Italy. Platelet function was evalueted in ten patients with ~-Thalassaemia major. Platelets Rich Plasma (PRP) of seven patients had a defective ADP, c~llagen and ristoce­ tin induced platelet aggregation; these anomalies could not be corrected by addition of normal Platelets Poor Plasma (pPP). 14 In these patients collagen induced C-Serotonin release was impaired and rnalondialde- hyde levels after thrombin stimulation was decreased in all patients' PRP. Ristocetin induced aggregation in normal washed platelets resuspended in normal and thalassaemia PPP was identical.

Moreover, in all j?-Thalassaemia patients studied, reduced platelets retention and pro­ longed bleeding time was observed.

These preliminary results suggest that ~-Thalassaem ia platelets have an acquired throm­ bocitopathia, together with probable defective arachidonic acid metabolism.

1145 PLATE\t"'r FUNCTION IN !!UMAN ACl1rE PLAmIODIUM FALCIFARUM INFECTION. S.H. Essitn and M.I. EbbotA, Department of HaeDllltology, University College Hospital, IbadAn Nigeria. Depression of circulating platelet count in man in Acute plasmodium fAlciparum infection is widely known, but the mechanism of this depression is in dispute particu­ lArly vi th respect to disseminAted intravascular coagulation. A recent report indi­ cated regular abolition of the second wave in ADP-induced PRP ~gregation of human citrated during in1'ection. This reaction vas Abolished vith 10 H ASA or 8mH Indollll.lthacin. This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. Arachi~nic Acid 0.5~! Also elicited adequate aggregAtion which was abolished by ASA 10 M in the control PRP. The concentrAtion of LDH in the supernatant of stimulated DIIllaria infected PRP significantly h1ghef4than was in control samples (116.6, 59.2 u/ml, r = 0.91,P The _an uptake of <: 0.05). C-5HT 49.CJf, was significantly lower than the control mean (93.~) (p <. 0.01) while VAlue the release was similar 24;; vs. 2~ : . ADP release was not significantly different in Wected and non-in1'ected persons (t = 1.24, P > 0.05). Ealaria parasite-infected platelets we"e not seen in the blood f ilm of 105 s8Dples exanined. different '!'pe increased platelet lysis observed in infected PRP ma:r indicate additional a~ from associated reason splenomeealy for the increased splenic platel,t pooling and shortened platelet life span reportedly observed in these patients C-5l~ transport mechanism appears deranged.