John Libbey Eurotext



Platelet immunology and post-transfusion alloimmunisation Volume 3, issue 1, Janvier - Février 1997


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Laboratoire d'immunologie plaquettaire, GIP-INTS, 6, rue Alexandre-Cabanel, 75015 Paris.

Platelet transfusion has undergone a remarkable increase in the last years. Platelet alloimmunisation and development of refractoriness are major concerns in such therapy. Some of the platelet antigens are shared with other cell types such as HLA antigens and ABH blood group antigens, whereas other are essentially platelet specific. If HLA immunisation has been known for a long time, the relevance of platelet specific antigenic systems in transfusion practice is still controversial. Refractoriness to platelet transfusion is due to shortened survival of transfused platelets in recipients. The main causes of platelet refractoriness are the quality of the platelet transfusions, non-immune platelet consumption and alloimmunisation. Correct identification of the underlying cause is essential for providing adequate transfusion support. Methods for reducing HLA immunisation have been developed such as leukocyte depletion of blood components, or inactivation of antigen presenting cells by ultraviolet irradiation. The cost-effectiveness of the available strategies must be evaluated to establish better management of patients. Post-transfusion purpura is a rare event but a serious complication of transfusion. Classically it is characterised by the sudden onset of a severe thrombocytopenic state one week after transfusion in an elderly woman. It has been suggested that this syndrome is due to an anamnestic response after previous immunisation by pregnancy. The exact pathophysiology is unknown and different mechanisms have been proposed. Due to life-threatening haemorrhages, diagnosis and therapy must not be delayed. The best therapy seems to be infusion of IvIgG.