Bone marrow suppression and severe anaemia associated with persistent Plasmodium falciparum infection in African children with microscopically undetectable parasitaemia
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* Corresponding author: Jorgen AL Kurtzhals j.kurtzhals@dadlnet.dk
1 Centre for Medical Parasitology, Department of Clinical Microbiology 7602, Copenhagen University Hospital, 2100 Copenhagen, Denmark
2 Department of Child Health, Korle-Bu Teaching Hospital, Accra, Ghana
3 Immunology Unit, Noguchi Memorial Institute for Medical Research, Legon, Ghana
Malaria Journal 2005, 4:56 doi:10.1186/1475-2875-4-56
Published: 1 December 2005Abstract
Background
Severe anaemia can develop in the aftermath of Plasmodium falciparum malaria because of protracted bone marrow suppression, possibly due to residual subpatent parasites.
Materials and methods
Blood was collected from patients with recent malaria and negative malaria microscopy. Detection of the Plasmodium antigens, lactate dehydrogenase (Optimal®), aldolase and histidine rich protein 2 (Now malaria®) were used to differentiate between patients with (1) no malaria, (2) recent cleared malaria, (3) persistent P. falciparum infection. Red cell distribution width (RDW), plasma levels of soluble transferrin receptor (sTfR) and erythropoietin (EPO) were measured as markers of erythropoiesis. Interleukin (IL) 10 and tumour necrosis factor (TNF)α were used as inflammation markers.
Results
EPO was correlated with haemoglobin, irrespective of malaria (R = -0.36, P < 0.001). Persistent P. falciparum infection, but not recent malaria without residual parasites, was associated with bone marrow suppression i.e., low RDW (P < 0.001 vs. P = 0.56) and sTfR (P = 0.02 vs. P = 0.36). TNF-α and IL-10 levels were not associated with bone marrow suppression.
Conclusion
In the treatment of malaria, complete eradication of parasites may prevent subsequent development of anaemia. Severely anaemic children may benefit from antimalarial treatment if antigen tests are positive, even when no parasites can be demonstrated by microscopy.