Reduced erythrocyte survival following clearance of malarial parasitaemia in Thai patients

Summary. Erythrocyte survival times were measured in healthy Thai controls and in patients following clearance of asexual P. falciparum or P. vivax parasitaemia. In five controls the mean cell life (MCL) of compatible donor erythrocytes was 89.6 d (mean range 73–101 d) compared with a mean MCL of 56.8 d (range 30–66 d) for autologous erythrocytes in 12 falciparum patients. In one of these patients the survival curve was biphasic with a rapid loss of some labelled cells. The survival of compatible donor erythrocytes was also studied in 10 patients and two types of survival curve could be distinguished. In five patients the cells had a mean MCL of 64.4 d (range 42–90 d). In the others survival curves were curvilinear, suggesting a complex mechanism of cell clearance or the presence of more than one cell population. There was initially a more rapid rate of destruction. In P. vivax malaria the MCL of autologous erythrocytes in seven patients was a mean of 67.2 d (range 34.74 d) and that of compatible donor cells in six patients was 66.8 d (range 54–76 d). In all except one of these patients both autologous and donor cell survival curves could be fitted to straight lines. No increase in cell‐bound IgG or C3 was evident in 12 patients tested. The differences between the mean MCL in all the groups of patients and the controls were statistically significant at the 5% level. This indicates an increased rate of erythrocyte destruction following clearance of P. falciparum or P. vivax parasites which is not antibody or complement mediated. The mechanism is unknown, but appears to be extrinsic to the erythrocytes themselves and may result from nonspecific activation of the reticuloendothelial function associated with the parasitic infection.

[1]  H. Karle Destruction of erythrocytes during experimental fever. Quantitative aspects. , 2009, Acta medica Scandinavica.

[2]  G. Strickland,et al.  IgM antibodies to red cells and autoimmune anemia in patients with malaria. , 1973, The American journal of tropical medicine and hygiene.

[3]  R. J. Howard,et al.  Accelerated clearance of uninfected red cells from Plasmodium berghei-infected mouse blood in normal mice. , 1979, The Australian journal of experimental biology and medical science.

[4]  C. Reynafarje,et al.  The hemolytic anemia of human bartonellosis. , 1961, Blood.

[5]  B. Blumberg,et al.  Alterations in haptoglobin levels. , 1963, JAMA.

[6]  T. Quinn,et al.  Relationship of alterations in splenic clearance function and microcirculation to host defense in acute rodent malaria. , 1981, The Journal of clinical investigation.

[7]  R. A. Dudley,et al.  Recommended Methods for Radioisotope Red‐Cell Survival Studies * A REPORT BY THE ICSH PANEL ON DIAGNOSTIC APPLICATIONS OF RADIOISOTOPES IN HAEMATOLOGY , 1971, Blood.

[8]  W. H. Taliaferro,et al.  The Histopathology of Malaria with Special Reference to the Function and Origin of the Macrophages in Defence. , 1937 .

[9]  S. Spitz The pathology of acute falciparum malaria. , 1946, Military surgeon.

[10]  H. I. Glass,et al.  Elution Correction in 51Cr Red Cell Survival Studies , 1974, British journal of haematology.

[11]  S. Lee,et al.  Macrophage plasma membrane and secretory properties in murine malaria. Effects of Plasmodium yoelii blood-stage infection on macrophages in liver, spleen, and blood , 1986, The Journal of experimental medicine.

[12]  P. Mollison Measurement of survival and destruction of red cells in haemolytic syndromes. , 1959, British medical bulletin.

[13]  D. Wyler The spleen in malaria. , 2008, Ciba Foundation symposium.

[14]  N. White,et al.  Dynamic alteration in splenic function during acute falciparum malaria. , 1987, The New England journal of medicine.

[15]  H. Karle,et al.  Effect on Red Cells of a Small Rise in Temperature: in Vitro Studies , 1969, British journal of haematology.

[16]  S. Kahn,et al.  Platelet and Fibrinogen Kinetics with [75Se]‐Selenomethionine in Patients with Myeloproliferative Disorders , 1972, British journal of haematology.

[17]  F D SCHOFIELD,et al.  Changes in Haemoglobin Values and Hepatosplenomegaly Produced by Control of Holoendemic Malaria , 1964, British medical journal.

[18]  C. M. Gupta,et al.  A new look at nonparasitized red cells of malaria-infected monkeys , 1982, Nature.

[19]  F. Stohlman,et al.  Malaria in man. Infection by Plasmodium vivax and the B strain of Plasmodium cynomolgi. , 1963, JAMA.

[20]  D. Weatherall,et al.  The Anaemia of P. falciparum Malaria , 1980, British journal of haematology.

[21]  M. Adner,et al.  Coombs'-positive hemolytic disease in malaria. , 1968, Annals of internal medicine.

[22]  J. Atkinson,et al.  Pathophysiology of Immune Hemolytic Anemia , 1977 .

[23]  J. Brown,et al.  Direct Coombs antiglobulin reactions in Gambian children with Plasmodium falciparum malaria. I. Incidence and class specificity. , 1979, Clinical and experimental immunology.

[24]  D. Weatherall,et al.  The importance of anaemia in cerebral and uncomplicated falciparum malaria: role of complications, dyserythropoiesis and iron sequestration. , 1986, The Quarterly journal of medicine.

[25]  D. Warrell,et al.  Evidence against immune haemolysis in falciparum malaria in Thailand , 1986, British journal of haematology.

[26]  H. Gilles,et al.  Malaria, anaemia and pregnancy. , 1969, Annals of tropical medicine and parasitology.

[27]  A. Zuckerman Recent studies on factors involved in malarial anemia. , 1966, Military medicine.