| Literature DB >> 29523273 |
Simona Cardaropoli1, Tullia Todros2, Anna Maria Nuzzo3, Alessandro Rolfo4.
Abstract
Preeclampsia (PE) is a multifactorial pregnancy-induced syndrome and infection could have a role in its etiopathogenesis. Hepcidin, central regulator of iron homeostasis, is an antimicrobial peptide induced by inflammatory/infective stimuli. Therefore, hepcidin could be a good nonspecific marker of infection in PE. In a cross-sectional study, we assessed maternal serum levels (ELISA) and placental expression (Real-Time PCR and ELISA) of hepcidin in PE and normal pregnancies. In a prospective study, hepcidin maternal serum levels were assessed in early pregnancy before PE onset and in age matched controls. Hepcidin protein and gene expressions were significantly decreased in PE placentae with normal fetal growth compared to controls and PE with Fetal Growth Restriction (FGR), respectively. In contrast, we did not find significant differences in maternal serum hepcidin levels in PE vs gestational age-matched controls. Hepcidin serum levels in the first half of pregnancy were found significantly higher in women who subsequently developed PE compared to mothers having a physiological pregnancy until term. Altered hepcidin expression in PE placentae could be explained by direct infective/inflammatory stimuli. Furthermore, high hepcidin levels in maternal serum could be an early marker of PE, further emphasizing the role of inflammatory status before symptoms onset in PE.Entities:
Keywords: Fetal growth restriction; Hepcidin; Placenta; Preeclampsia
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Year: 2018 PMID: 29523273 DOI: 10.1016/j.preghy.2017.12.008
Source DB: PubMed Journal: Pregnancy Hypertens ISSN: 2210-7789 Impact factor: 2.899