Mechanisms of thrombocytopenia in malignant tertian malaria

Br Med J. 1973 Jun 2;2(5865):515-8. doi: 10.1136/bmj.2.5865.515.

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.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Antigens
  • Blood Coagulation Tests
  • Blood Platelets
  • Chromium Isotopes
  • Disseminated Intravascular Coagulation / drug therapy
  • Factor V
  • Factor VIII
  • Fibrinogen / metabolism
  • Half-Life
  • Heparin / therapeutic use
  • Humans
  • Iodine Radioisotopes
  • Malaria / blood
  • Malaria / complications*
  • Malaria / drug therapy
  • Malaria / immunology
  • Middle Aged
  • Prothrombin Time
  • Spleen
  • Thrombocytopenia / drug therapy
  • Thrombocytopenia / etiology*
  • Time Factors

Substances

  • Antigens
  • Chromium Isotopes
  • Iodine Radioisotopes
  • Factor V
  • Factor VIII
  • Fibrinogen
  • Heparin