Can Plasmodium falciparum Induce Homocysteinemia in Malaria Patients?

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Résumé

Background: Plasmodium falciparum has developed elaborate strategies to survive in the hostile intracellular environment of the infected host cell, including resistance to oxidative stress. Cysteine is a metabolic product of homocysteine and a precursor of the antioxidant glutathione used by Plasmodium falciparum to escape harmful oxidation. Objectives: In the present study we aimed to assess whether Plasmodium falciparum can induce homocysteinemia in malaria patients of Burkina Faso. Methods: Eighty-five (85) individuals including 25 affected by severe malaria, 44 by simple malaria, and 12 negative controls for P. falciparum infection were included in the present study. An enzymatic assay of plasma homocysteinemia was performed using the Homocysteine Enzymatic Assay reagent (ref 05385415 190) on the Roche/ Hitachi Cobas c. Results: The results of the present study show that the mean plasma homocysteine concentrations were 15.1 ± 8.4 μmol/L among patients with severe malaria, 14.0 ± 6.0 μmol/L in patients with uncomplicated malaria, and 12.6 ± 4.1 μmol/L in negative controls for malaria parasite. Conclusions: Our findings suggest high homocysteinemia in malaria patients, especially in those with severe malaria. Monitoring homocysteinemia in the latter group will be useful to avoid complications when an elevated plasma level of homocysteine is a known risk factor for cardiovascular diseases.

Mots-clés

Plasmodium falciparum, hyperhomocysteinemia, malaria, severe malaria, uncomplicated malaria, cysteine metabolism, glutathione, oxidative stress, cardiovascular risk, plasma homocysteine