Nonglycosylated Ferritin Predominates in the Circulation of Women with Preeclampsia But Not Intrauterine Growth Restriction (Technical Briefs‪)‬

Three to five percent of pregnancies are complicated by preeclampsia, a multisystemic disorder characterized by hypertension and proteinuria that occurs after 20 weeks of gestation. Although widespread inflammation and endothelial dysfunction appear to be central maternal abnormalities in preeclampsia, the pathogenesis of the syndrome remains poorly understood (1). The intracellular iron storage protein ferritin can hold up to 4000 iron atoms. Low concentrations of ferritin are found in normal serum because of active secretion from reticuloendothelial or parencymal cells (2, 3). During normal pregnancy, serum ferritin concentrations decrease with advancing gestation to reach a nadir at the third trimester (4). The metabolism of the serum iron and iron-binding proteins, ferritin and transferrin, is abnormal in women with preeclampsia (5-8). Median serum ferritin concentrations are approximately fivefold higher during preeclampsia than in normal pregnancy (6, 8, 9). The lowest quartile of ferritin concentrations at 28-30 weeks of gestation is associated with decreased risk of preeclampsia, premature rupture of membranes, and infant admission to the neonatal unit (4). The reasons for the increased serum ferritin with preeclampsia remain unclear. Serum ferritin is a reliable indicator of total body iron status in nondiseased individuals, with low concentrations diagnostic of iron deficiency. However, a high ferritin does not always signify iron excess.