Assessment and interpretation of micronutrient status during pregnancy

Abstract

Accurate assessment of maternal micronutrient status is critical to the prevention of suboptimal micronutrient status and anaemia during pregnancy. Measurement of Fe, folate and vitamin B12status is complicated by adaptive changes to maternal and placental physiology that markedly affect concentrations of circulating micronutrients and their functional biomarkers. Validation of new assessment methods by comparison with gold standards is often prevented by ethical considerations. Antenatal screening in the UK is predominantly concerned with the detection of anaemia, although estimation of maternal Fe stores by serum ferritin at the start of antenatal care may be a more effective preventive strategy. Functional assessment of maternal anaemia is highly problematic, so instead reference data are used for its definition. The effect of mild-to-moderate anaemia on pregnancy outcome is unclear because of the crude nature of its assessment and the influence of confounding factors. Fe-deficient erythropoiesis may be detected by assessment of erythrocyte Zn protoporphyrin and reticulocyte Hb, although such measures may be unavailable in many clinical laboratories. Serum soluble transferrin receptor is highly responsive to tissue Fe deficiency and is less affected by inflammation than most other indicators. Direct inter-assay comparison of serum and erythrocyte folate values is inadvisable since recovery rates differ greatly between methods. Serum total homocysteine is a useful functional biomarker of both folate and vitamin B12status but during pregnancy is influenced by other factors that reduce its sensitivity. Isotope-dilution liquid chromatography–tandem MS and serum holo-transcobalamin provide new opportunities to gain detailed data of folate species and vitamin B12fractions in large samples.

Micronutrient Status among Pregnant Women in Zinder, Niger and Risk Factors Associated with Deficiency

“…Change in MN status during pregnancy is a well-established phenomenon, likely due to progressively depleted MN stores, inadequate dietary intake to meet needs for maternal and fetal tissue accumulation, and prioritization of fetal development over maternal status. However, the impact of increased plasma volume in pregnancy and increased erythropoiesis independent of MN deficiency on biomarkers of MN status is unclear, and must be considered in the interpretation of these results [7,39]. …”

The Association between Malaria and Iron Status or Supplementation in Pregnancy: A Systematic Review and Meta-Analysis

“…Despite the evidence that serum ferritin increases as a result of pregnancy per se, infection or inflammation, it remains the international standard for defining iron deficiency [79]. This creates an inherent challenge to measuring iron deficiency using cutoffs of serum ferritin in pregnant populations living in malaria endemic settings (see also Figure S3.1 in File S1).…”

“…Other iron biomarkers have been proposed to replace serum ferritin including sTfR. While it has been suggested sTfR is unaffected by pregnancy or inflammation [84], evidence of how pregnancy affects concentrations of sTfR is lacking [79]. The extent to which sTfR is affected by pregnancy will determine the appropriateness of using sTfR as a biomarker for detecting iron deficiency in pregnancy, especially in malaria endemic settings.…”

The iron regulatory hormone hepcidin is decreased in pregnancy: a prospective longitudinal study

“…Early pregnancy is characterized by a sudden drop in vascular resistance, leading to decreased blood pressure, renal sodium retention, plasma volume expansion and consequently to a decrease in hemoglobin concentration [ 1 ]. In response, erythropoiesis is steadily increased to maintain hemoglobin levels, but at cost of exhausting maternal iron reserves [ 2 ].…”