SourceClinical Chemistry and Laboratory Medicine, 51, 7, (2013), pp. 1395-401
Article / Letter to editor
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Laboratory of Genetic, Endocrine and Metabolic Diseases
Laboratory of Clinical Chemistry
Clinical Chemistry and Laboratory Medicine
SubjectIGMD 7: Iron metabolism; IGMD 7: Iron metabolism N4i 1: Pathogenesis and modulation of inflammation; IGMD 7: Iron metabolism N4i 3: Poverty-related infectious diseases
Abstract Background: Iron deficiency is a commonly encountered problem in pregnancy and a frequently observed cause of pregnancy-associated anemia. We longitudinally assessed the iron regulatory hormone hepcidin during gestation and postpartum and related hepcidin to conventional indicators of iron status and inflammation. Methods: Thirty-one healthy pregnant women were included and 81 blood samples from the three trimesters, directly and 6 weeks postpartum were analyzed for hemoglobin, the iron parameters: iron, total iron binding capacity, transferrin saturation, ferritin, soluble transferrin receptor and hepcidin, and CRP and leucocytes as markers of inflammation. Results: Hepcidin concentration decreased gradually from the first to the second and third trimester to undetectable levels (</=0.5 nmol/L) which was paralleled by decreasing hemoglobin levels and changes in iron parameters indicative for iron deficiency. During gestation hepcidin levels correlated with iron parameters, but not with inflammatory markers. Postpartum, hepcidin increased immediately to levels similar as assessed at early pregnancy. Conclusions: We conclude that hepcidin levels were suppressed during the second and third trimester of pregnancy, which was likely determined by the occurrence of iron deficiency. These data give insight in iron homeostasis during normal pregnancy.
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