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Edward Kabyemela, Michal Fried, Jonathan Kurtis, Patrick Duffy, Reply to Lowe and Pasvol, The Journal of Infectious Diseases, Volume 199, Issue 1, 1 January 2009, Pages 152–154, https://doi.org/10.1086/594376
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To the Editors—Drs. Lowe and Pasvol highlight the complexity of diagnosing iron deficiency with existing tools, particularly in the presence of ongoing inflammation. We agree that this field of inquiry would benefit if improved biomarkers and diagnostics for iron status were developed. However, the available data from our study and numerous other studies indicate that iron status is an important determinant of malaria risk during pregnancy.
Regarding our own data, our findings are robust when the data are stratified by any of several definitions of iron deficiency, as well as when stratified by the definition we adopted for our published study. When we define iron deficiency by different levels of ferritin (e.g., ferritin <12 µg/mL [1] or ferritin <30 µg/mL [2]), by ferritin levels corrected for inflammation with C-reactive protein (CRP) measurements (ferritin <12 ng/mL when CRP <6 ng/mL or ferritin ≤50 ng/mL when CRP ≥6 ng/mL [3]), or by ratio of soluble transferrin receptor to ferritin levels (sTfR/log ferritin >2 [4]), we find that both the risk of placental malaria and the severity of placental malaria (table 1) are reduced in the presence of iron deficiency. By any of the criteria, the effect of iron deficiency on reducing the risk of placental malaria is greater in primigravidae than multigravidae.
