Immune-mediated thrombocytopenia of malaria.

J G Kelton; J Keystone; J Moore; G Denomme; E Tozman; M Glynn; P B Neame; J Gauldie; J Jensen

doi:10.1172/JCI110836

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Published in Volume 71, Issue 4 on April 1, 1983
J Clin Invest. 1983;71(4):832–836. https://doi.org/10.1172/JCI110836.
© 1983 The American Society for Clinical Investigation

Published April 1, 1983 - Version history

Thrombocytopenia frequently complicates malarial infections but the mechanism has not been elucidated. We studied 28 patients with malarial infections and noted that 16 of 17 thrombocytopenic patients had elevated levels of platelet-associated IgG (PAIgG). In all thrombocytopenic patients studied, the level of PAIgG returned to normal as the platelet count rose to normal levels. To study the mechanism of the elevated platelet-bound IgG, IgG and F(ab')2 from patients with recurrent Plasmodium falciparum infections was purified and radiolabeled. Labeled and unlabeled P. falciparum antigen was also prepared. IgG did not nonspecifically bind to malaria-damaged platelets. Binding studies with 3H-malarial antigen demonstrated platelets have saturable binding sites for malarial antigen. Increasing concentrations of malarial antigen displaced the 125I-IgG antimalarial antibody from the platelets. The binding of 125I-IgG and 125I-F(ab')2 was similar and this excluded significant immune complex binding. The thrombocytopenia that complicates at least some malarial infections is caused by immune mechanisms; specific IgG binds to platelet-bound malaria antigen through the Fab portion of the immunoglobulin molecule.

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