Paul Arthur sadly died during the course of this study.
Maternal vitamin A supplementation and immunity to malaria in pregnancy in Ghanaian primigravids
Version of Record online: 1 DEC 2005
Tropical Medicine & International Health
Volume 10, Issue 12, pages 1286–1297, December 2005
How to Cite
Cox, S. E., Staalsoe, T., Arthur, P., Bulmer, J. N., Tagbor, H., Hviid, L., Frost, C., Riley, E. M. and Kirkwood, B. R. (2005), Maternal vitamin A supplementation and immunity to malaria in pregnancy in Ghanaian primigravids. Tropical Medicine & International Health, 10: 1286–1297. doi: 10.1111/j.1365-3156.2005.01515.x
- Issue online: 1 DEC 2005
- Version of Record online: 1 DEC 2005
- vitamin A;
- antibodies VSA
Background Vitamin A supplementation is believed to enhance immune responses to infection but few studies have assessed its effects on anti-malarial immunity, especially during pregnancy when women are at increased risk from both vitamin A deficiency and pregnancy-associated malaria. The pathological effects of malaria in pregnancy are believed to be due to the sequestration of parasites in the placenta mediated via binding of variant surface antigens (VSA) expressed on the surface of P. falciparum infected red blood cells to placental chondroitin sulphate A (CSA).
Methods We conducted a randomized double-blind controlled trial of vitamin A supplementation in 98 primigravid Ghanaian women to investigate the effects of vitamin A supplementation on levels of IgG antibodies binding to VSA of a clinical, P. falciparum placental isolate and to two isolates selected (or not) for adherence to CSA in vitro (anti-VSACSA IgG or anti-VSA IgG). Placental malarial infection was determined by placental blood smear and histology.
Results Vitamin A supplementation was non-significantly associated with a decreased risk of active or chronic-active placental malarial infection compared to past, resolved infection at delivery, as determined by histology (OR = 0.42, P = 0.13 – adjusted for level of education). After adjustment for differences in baseline values, levels of anti-VSACSA IgG to a placental, CSA-adherent isolate (EJ-24) but not to two isolates selected for CSA-adhesion in vitro (FCR3CSA and BusuaCSA), were significantly lower in women receiving vitamin A supplementation than in women receiving placebo (P = 0.002). There was no apparent effect of vitamin A supplementation to levels of Ab to non-CSA-adherent parasite isolates.
Conclusions The data suggest that the reduction in the levels of anti-VSACSA antibodies to the known placental malaria isolate may reflect reduced intensity or duration of placental parasitaemia in women receiving vitamin A supplementation. These observations are of potential public health significance and deserve further investigation.