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Mechanisms of Thrombocytopenia in Malignant Tertian Malaria

Br Med J 1973; 2 doi: https://doi.org/10.1136/bmj.2.5865.515 (Published 02 June 1973) Cite this as: Br Med J 1973;2:515
  1. R. B. Skudowitz,
  2. J. Katz,
  3. A. Lurie,
  4. J. Levin,
  5. J. Metz

    Abstract

    The mechanism of thrombocytopenia in six patients with falciparum malaria has been studied. All the patients recovered after antimalarial therapy, and cerebral malaria was not a feature. Radioactive-labelled platelets and fibrinogen were injected into the patients during the phase of thrombocytopenia. In all cases recovery of injected platelets was notably subnormal, indicating excessive splenic pooling of platelets. Platelet life span was moderately shortened in all patients, and platelet turnover increased approximately two-fold. Fibrinogen catabolism was moderately increased in all patients, but coagulation tests failed to reveal evidence of disseminated intravascular coagulation. The results suggest that in uncomplicated cases of malaria thrombocytopenia is the result of splenic pooling of platelets aggravated by a moderate decrease in platelet life span. In such cases thrombocytopenia is thus not the result of disseminated intravascular coagulation (D.I.C.), and heparin therapy is not indicated unless there is unequivocal ancillary evidence of D.I.C.