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Published on: July 17, 2014
Anaemia in acute, Plasmodium falciparum malaria in children from Orissa state, India
Insights
Acute Plasmodium falciparum malaria causes severe anemia primarily through hemolysis in Indian children. Pre-existing iron deficiency worsens anemia, while bone marrow suppression plays a minor role.
Area of Science:
- Hematology
- Infectious Diseases
- Pediatrics
Background:
- Anemia is a significant complication of acute Plasmodium falciparum malaria.
- The contributing factors to malaria-associated anemia, including hemolysis, bone marrow suppression, and iron deficiency, require further elucidation.
Purpose of the Study:
- To assess the severity of anemia in Indian children with acute falciparum malaria.
- To determine the roles of hemolysis, bone marrow suppression, and pre-existent iron deficiency in malaria-associated anemia.
Main Methods:
- Investigated hemoglobin, bilirubin, haptoglobin, iron, transferrin, red cell morphology, and reticulocyte response in 102 children with malaria and 50 controls.
- Conducted bone marrow biopsies with iron staining in 23 severe anemia cases.
Main Results:
- Malaria patients exhibited signs of hemolysis, including elevated unconjugated bilirubin and decreased haptoglobin and hemoglobin levels.
- Hemoglobin levels correlated with haptoglobin and unconjugated bilirubin.
- Bone marrow showed erythroid hyperplasia, with iron deficiency noted in 17 of 23 severe anemia cases.
Conclusions:
- Hemolysis is the primary driver of anemia in acute falciparum malaria, exceeding parasite-induced erythrocyte destruction.
- Bone marrow suppression has a minimal impact on anemia severity.
- Pre-existing iron deficiency exacerbates the severity of anemia in malaria patients.
Abstract:
The severity of anaemia associated with acute, Plasmodium falciparum malaria and the extent to which haemolysis, bone-marrow suppression, and pre-existent iron deficiency contribute to the anaemia were assessed in 102 Indian children aged 2-12 years. Blood haemoglobin (Hb), plasma unconjugated bilirubin and haptoglobin, serum iron and transferrin concentrations and transferrin saturation, red cell morphology and reticulocyte response were investigated in the patients and in 50 control children. Twenty-three patients with severe anaemia (< 70 g Hb/litre) were investigated further, by bone-marrow biopsy followed by iron staining of sections or touch smears of the biopsy material. There was evidence of haemolysis in the malaria cases: in the peripheral blood smears and the significantly higher plasma concentrations of unconjugated bilirubin, lower plasma concentrations of haptoglobin and lower blood concentrations of Hb than those seen in the controls. Haemoglobin concentration correlated directly with haptoglobin (r = 0.489; P < 0.001) and inversely with unconjugated bilirubin in malaria patients (r = -0.526; P < 0.001) but not in controls (r = -0.140 and -0.061, respectively). Parasitaemia (parasites/microliter) was not significantly correlated with Hb, haptoglobin or unconjugated bilirubin. Compared with the earlier samples, follow-up samples from the patients, collected 2 weeks after discharge from hospital and antimalarial therapy, showed significant increase in Hb, haematocrit, haptoglobin and decreases in both total and unconjugated bilirubin. There was evidence of hypercellularity and mild-moderate erythroid hyperplasia, mainly of normoblastic maturation with adequate reticulocyte response, in the bone-marrow samples from the cases of severe anaemia; dyserythropoiesis was only noticed in one case and no stainable iron was detectable in 17 of the 23 cases. These observations indicate that haemolysis is the prime cause of the anaemia seen in acute falciparum malaria, although destruction of parasitised erythrocytes is not the sole cause of the haemolytic process. Bone-marrow suppression appears to have an insignificant role but pre-existent iron deficiency aggravates the severity of the anaemia.
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