The role of hepcidin in iron homeostasis in preeclamptic pregnant women is unclear. To test the hypothesis that increased serum iron in women diagnosed with preeclampsia results from decreased production of hepcidin, we performed an observational case-control study in which serum hepcidin concentration, dietary iron intake, hematological indices, iron status, liver function, and inflammatory markers in 18 preeclamptic women and 18 healthy normotensive pregnant women of similar age range were evaluated. Iron intake was established via a food frequency questionnaire, whereas hematological indices, iron status, liver function, and inflammatory markers were assessed using standard protocols. Hematocrit was significantly higher (P = .031) in the preeclamptic group compared with the control, whereas erythropoietin level was significantly lower (P = .003). The pronounced inflammatory status of preeclamptic women was confirmed by significantly higher concentrations of interleukin-6 (P = .001), tumor necrosis factor-α (P < .001), and ferritin (P < .001). Nonetheless, the preeclamptic group exhibited significantly higher serum iron (P = .012) and transferrin saturation (P = .006), and these alterations were accompanied by lower hepcidin levels (P = .047). No significant correlations between hepcidin concentration and iron status parameters were observed in either group. However, a positive and significant correlation between hepcidin concentration and C-reactive protein was observed in the preeclamptic group (r = 0.474; P = .047). We conclude that high serum iron in preeclamptic women is likely caused by low production of hepcidin, thus supporting the hypothesis originally stated.
Keywords: Case-control study; Hypertension; Inflammation; Iron overload; Pregnancy.
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