Prevalence of anemia and associations between neonatal iron status, hepcidin and maternal iron status among neonates born to pregnant adolescents

Whether the association between teenage pregnancy and adverse birth outcomes could be explained by deleterious social environment, inadequate prenatal care, or biological immaturity remains controversial. The objective of this study was to determine whether teenage pregnancy is associated with increased adverse birth outcomes independent of known confounding factors. We carried out a retrospective cohort study of 3,886,364 nulliparous pregnant women <25 years of age with a live singleton birth during 1995 and 2000 in the United States. All teenage groups were associated with increased risks for pre-term delivery, low birth weight and neonatal mortality. Infants born to teenage mothers aged 17 or younger had a higher risk for low Apgar score at 5 min. Further adjustment for weight gain during pregnancy did not change the observed association. Restricting the analysis to white married mothers with age-appropriate education level, adequate prenatal care, without smoking and alcohol use during pregnancy yielded similar results. Teenage pregnancy increases the risk of adverse birth outcomes that is independent of important known confounders. This finding challenges the accepted opinion that adverse birth outcome associated with teenage pregnancy is attributable to low socioeconomic status, inadequate prenatal care and inadequate weight gain during pregnancy.

Hepcidin, a peptide hormone made in the liver, is the principal regulator of systemic iron homeostasis. Hepcidin controls plasma iron concentration and tissue distribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores. Hepcidin acts by inhibiting cellular iron efflux through binding to and inducing the degradation of ferroportin, the sole known cellular iron exporter. Synthesis of hepcidin is homeostatically increased by iron loading and decreased by anemia and hypoxia. Hepcidin is also elevated during infections and inflammation, causing a decrease in serum iron levels and contributing to the development of anemia of inflammation, probably as a host defense mechanism to limit the availability of iron to invading microorganisms. At the opposite side of the spectrum, hepcidin deficiency appears to be the ultimate cause of most forms of hemochromatosis, either due to mutations in the hepcidin gene itself or due to mutations in the regulators of hepcidin synthesis. The emergence of hepcidin as the pathogenic factor in most systemic iron disorders should provide important opportunities for improving their diagnosis and treatment.

Our purpose was to evaluate the association between fetal iron status and mental and psychomotor development at 5 years of age. We evaluated the association of fetal iron status (umbilical cord serum ferritin concentrations) with test scores of mental and psychomotor development of 278 children. Six tests were given, including full-scale intelligence quotient (FSIQ), language ability, fine- and gross-motor skills, attention, and tractability. Compared with children with cord ferritin in the 2 median quartiles, those in the lowest quartile scored lower on every test and had significantly worse language ability, fine-motor skills, and tractability. They were also 4.8-fold more likely to score poorly in fine-motor skills and 2.7-fold more likely to have poor tractability than children in the median quartiles. FSIQ in the highest quartile was slightly, but not significantly, lower than the median quartiles, but the odds ratio for having a FSIQ score of less than 70 for children in the highest quartile was 3.3 (95% CI 1.2-9.1). Poor iron status (low ferritin) in utero appears to be associated with diminished performance in certain mental and psychomotor tests. The reason for the association between high ferritin concentrations and low FSIQ scores is unknown.