Platelet abnormalities in experimental malaria: a review

ABSTRACT

Several abnormalities of platelet haemostatic function that have been previously described; are summarized in this article. These include hypersensitivity to agonists such as adenosine diphosphate (ADP); adrenaline and arachidonic acid; increased loss of platelet lactate dehydrogenase (LDH); and enhanced platelet production of thromboxane A2 (TXA2) found with enhanced but delayed prostacyclin (PGI2) production. Other features include marked reduction (by 36-62) of total platelet sialic acid associated with shortened platelet life span. It was also observed that platelets thathad interacted even for only one minute with Plasmodium falciparum-infected erythrocytes in culture; when challenged immediately afterwards with optimal concentration of ADP; had lost the usual platelet refractoriness after interaction with sub-optimal ADP concentration. The significance of this novel finding has not been investigated further. These platelet changes which were also observed in the human disease; suggest that a hypercoagulable state associated with platelet activation exists in acute P. falciparum infection in man; a feature that was not previously described and appreciated. Its significance has not been investigated. However; it explains the relative rarity of bleeding complication that is sometimes described in the disease in man. Some of the changesdescribed also suggest that additional mechanism(s) of platelet destruction in addition to those previously postulated; may occur in the infection. They also suggest that other therapeutic modalities may be available