Folate metabolism pathway and Plasmodium falciparum malaria infection in pregnancy

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Abstract

Malaria induced by Plasmodium falciparum is a major cause of mortality. P. falciparum has the ability to use host plasma folate as its primary folate source. Folate is a cofactor needed for both malaria parasite growth and host erythrocyte production. This review examines the possible impairment of the folate-mediated one-carbon metabolism pathway as a result of P. falciparum malaria infection during pregnancy. Folate deficiency during malaria infection is presented, with an emphasis on the controversy regarding the decrease of plasma or erythrocyte folate secondary to malaria. Maternal folate deficiency increases the risk of adverse pregnancy outcomes. Functional folate deficiency and/or increased plasma homocysteine levels during pregnancy of infected women in areas endemic for malaria is a probable scenario accentuating the impairment of placenta function leading to the occurrence of neural tube defects, low birth weights, and intrauterine growth retardations. Potential questions that may be answered in future investigations using an appropriate protocol to study pregnant women with malaria are also addressed. © 2011 International Life Sciences Institute.

Author-supplied keywords

  • *folate metabolism
  • *folic acid/ec [Endogenous Compound]
  • *malaria falciparum
  • *pregnancy
  • Plasmodium falciparum
  • article
  • carbon metabolism
  • endemic disease
  • erythrocyte
  • folic acid blood level
  • folic acid deficiency/et [Etiology]
  • homocysteine/ec [Endogenous Compound]
  • human
  • intrauterine growth retardation/co [Complication]
  • low birth weight/co [Complication]
  • neural tube defect/co [Complication]
  • nonhuman
  • placenta function
  • pregnancy outcome

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Authors

  • Chango A.

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