Abstract
BackgroundSevere anaemia can develop in the aftermath of Plasmodium falciparum malaria because of protracted bone marrow suppression, possibly due to residual subpatent parasites.Materials and methodsBlood 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.ResultsEPO 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.ConclusionIn 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.
Highlights
Anaemia is a common, life-threatening complication of Plasmodium falciparum malaria in African infants and young children
Anaemic children may benefit from antimalarial treatment if antigen tests are positive, even when no parasites can be demonstrated by microscopy
Forty eight patients were enrolled into group 1: 24 with severe anaemia and 24 with Hb ≥ 8 g/dl
Summary
Life-threatening complication of Plasmodium falciparum malaria in African infants and young children. The anaemia develops when accelerated removal of erythrocytes is not compensated by the bone marrow. Bone marrow suppression is generally present in all malaria patients [1] and has been described in asymptomatic P. falciparum infection [2]. Malaria Journal 2005, 4:56 http://www.malariajournal.com/content/4/1/56 must be explained by the amount of erythrocyte destruction during the period until return of normal bone marrow function. The anaemia may either develop rapidly with severe, acute haemolysis, or take a slow smouldering course, with a relatively slow rate of erythrocyte destruction in the presence of persistent bone marrow suppression [3]. Data on the duration of bone marrow suppression after a malaria attack are conflicting. Severe anaemia can develop in the aftermath of Plasmodium falciparum malaria because of protracted bone marrow suppression, possibly due to residual subpatent parasites
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
