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Anemia is an important complication of P. falciparum malaria infection. This paper describes recent studies that have attempted to define some of the pathophysiological mechanisms involved in different forms of infection and at different stages of the illness. After an acute infection there is a steady fall in the haemoglobin level with an inappropriate reticulocyte response. Current evidence indicates that this form of anaemia may result from a combination of acute sequestration of iron in the reticuloendothelial system associated with a shortened red cell survival. Recent studies indicate that there may be a dyserythropietic component as well. The mechanism for the shortened red cell survival is uncertain; although it may be due in part to sequestration of parasitized cells, the haemoglobin level continues to fall for several weeks after the acute episode and other factors must be involved. The role of immune haemolysis appears to be relatively small. It is becoming apparent that severe dyserythropoiesis with minimal haemolysis plays a major role in the anaemias of Plasmodium falciparum infection, particularly in immune individuals. This phenomenon has been studied by both light and electron microscopy and by assessing the in vitro kinetics of erythroid precursor proliferation. The results indicate a major defect in erythroid maturation with a significant degree of erythrophagocytosis. Although these studies have provided a clearer picture of the pathophysiology of anaemia at different phases of P. falciparum infection, there is still little indication of how the basic changes in red cell production and survival are mediated.

Type

Journal article

Journal

Ciba Found Symp

Volume

94

Pages

74 - 97