Abstract
Iron deficiency in infants and children is often accompanied by anorexia, irritability, inattentiveness, and poor school performance. Chronic iron deficiency in rats results in decreased monoamine oxidase (MAO) activity both in vitro and in vivo. Since MAO is an important enzyme in inactivation of catecholamines, evidence for defective catecholamine degradation secondary to MAO inhibition was looked for in 11 children with iron deficiency anemia. Urinary excretion of Dopamine (DA), Norepinephrine (NE), Epinephrine (E), Metanephrine-normetanephrine (MN-NMN) and 3-methoxy-4-hydroxy mandelic acid (VMA) was measured in 24-hour samples before and after treatment with intramuscular iron. Pretreatment NE excretion was abnormally high. NE excretion decreased significantly (p < .001) and returned to normal within one week of therapy, well before hemoglobin levels had increased substantially. VMA excretion was also higher pre than post-treatment (p < .05). There was no difference between pre and post-treatment levels of DA, E, and MN-NMN. These variations in catecholamine pathways may be responsible for the behavioral changes observed in iron deficiency and provide the first biochemical link between iron deficiency and its multiple symptoms.
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Voorhess, M., Stuart, M., Stockman, J. et al. IRON DEFICIENCY ANEMIA AND ABNORMAL URINARY CATECHOLAMINE EXCRETION. Pediatr Res 8, 439 (1974). https://doi.org/10.1203/00006450-197404000-00593
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DOI: https://doi.org/10.1203/00006450-197404000-00593