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Abnormal iron distribution in infants of diabetic mothers: spectrum and maternal antecedents
M K Georgieff1, M B Landon, M M Mills
1Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis.
Insights
Infants of diabetic mothers often have altered iron distribution due to in utero hypoxemia and polycythemia, leading to lower iron stores. This impacts fetal development and requires further investigation into maternal diabetes effects.
Area of Science:
- Neonatal Medicine
- Pediatric Hematology
- Endocrinology
Background:
- Maternal diabetes mellitus can lead to fetal hypoxemia and polycythemia.
- Chronic hypoxemia in fetuses causes iron redistribution from serum/storage to red blood cells.
Purpose of the Study:
- To investigate iron distribution in term infants born to diabetic mothers.
- To correlate iron profiles with infant size, maternal glycemic control, and fetal factors.
Main Methods:
- Studied iron distribution in 43 term infants of diabetic mothers (appropriate and large for gestational age).
- Assessed serum iron profiles, ferritin, total iron-binding capacity, and free erythrocyte protoporphyrin.
- Correlated iron parameters with glycosylated fetal hemoglobin, macrosomia, hemoglobin, erythropoietin, and erythrocyte/storage iron ratios.
Main Results:
- 65% of infants had abnormal serum iron profiles at birth.
- Hypoglycemic, large-for-gestational-age infants showed higher prevalence of abnormal iron profiles.
- Abnormal iron profiles correlated with higher HbA1c, macrosomia, hemoglobin, erythropoietin, and erythrocyte/storage iron ratios.
- Erythropoietin was inversely correlated with serum iron (r = -0.54, p = 0.003).
- Combined erythrocyte and storage iron pools were lower in infants with abnormal iron values, especially with maternal diabetic vasculopathy.
Conclusions:
- Infants of diabetic mothers exhibit altered iron distribution, characterized by reduced iron pools.
- Findings suggest increased fetal iron utilization for hemoglobin synthesis and potentially reduced iron transfer due to diabetic complications.
- These iron dysregulations may be linked to chronic hypoxemia and polycythemia in infants of diabetic mothers.
Abstract:
Because chronic hypoxemia causes a redistribution of iron from serum and storage pools into an expanding erythrocyte mass, and because infants of diabetic mothers are often hypoxemic in utero and have a high prevalence of polycythemia at birth, we studied iron distribution in 43 term infants of diabetic mothers. Twenty-four infants were at an appropriate size for gestational age; 19 were large for gestational age. At birth, 28 infants (65%) had abnormal serum iron profiles; eight had decreased ferritin concentrations only (stage 1), nine had decreased ferritin and increased total iron-binding capacity values (stage 2), and 11 had these serum findings plus elevated free erythrocyte protoporphyrin concentrations (stage 3). The hypoglycemic infants who were large for gestational age (n = 14) had a higher prevalence of abnormal iron profiles than euglycemic infants who were appropriate in size for gestational age (n = 20; 93% vs 50%; p = 0.009). Progressively abnormal iron profiles were associated with higher glycosylated fetal hemoglobin values, greater degrees of macrosomia, increased hemoglobin and erythropoietin concentrations, and increased erythrocyte/storage iron ratios. Erythropoietin concentrations were inversely linearly correlated with serum iron values (n = 32, r = -0.54; p = 0.003). The combined erythrocyte and storage iron pools were significantly lower in infants with abnormal iron values whose mothers were diabetic, particularly in infants of women with confirmed diabetic vasculopathy. We speculate that these findings are likely due to (1) increased fetal iron utilization during compensatory hemoglobin synthesis in response to chronic hypoxemia and (2) reduced iron transfer during late gestation complicated by diabetes.