Hepcidin in newly diagnosed inflammatory bowel disease in children

Aim Hepcidin is a central regulator of iron homeostasis. Its production is also influenced by systemic inflammation. The aims of this study were to compare hepcidin levels in paediatric patients newly diagnosed with Crohn's disease (CD) and ulcerative colitis (UC) and to determine the associati...

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Published inJournal of paediatrics and child health Vol. 54; no. 12; pp. 1362 - 1367
Main Authors Karaskova, Eva, Volejnikova, Jana, Holub, Dusan, Velganova‐Veghova, Maria, Sulovska, Lucie, Mihal, Vladimír, Horvathova, Monika, Pospisilova, Dagmar
Format Journal Article
LanguageEnglish
Published Australia John Wiley & Sons Australia, Ltd 01.12.2018
Blackwell Publishing Ltd
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Summary:Aim Hepcidin is a central regulator of iron homeostasis. Its production is also influenced by systemic inflammation. The aims of this study were to compare hepcidin levels in paediatric patients newly diagnosed with Crohn's disease (CD) and ulcerative colitis (UC) and to determine the association of hepcidin levels with laboratory and clinical parameters of inflammatory bowel disease (IBD) activity. Methods Children with newly diagnosed IBD between January 2012 and September 2016 were enrolled in this comparative cross‐sectional study. We analysed levels of serum hepcidin, C‐reactive protein, iron, ferritin, soluble transferrin receptors, blood count and faecal calprotectin in all subjects. Serum hepcidin levels were measured by reverse‐phase liquid chromatography. The Paediatric Crohn's Disease Activity Index was used to evaluate CD in children, and Paediatric Ulcerative Colitis Activity Index was used for the assessment of UC disease activity. Results Subjects with CD (n = 53) had significantly higher serum hepcidin levels compared with subjects with UC (n = 23) – 22.6 ng/mL (range 8.5–65.0) versus 6.5 ng/mL (range 2.4–25.8) (P < 0.05). Hepcidin was independently associated with ferritin levels in all IBD patients (P < 0.05). Moreover, there was a significant positive correlation between hepcidin and platelet count (P < 0.05) in children with CD and a negative correlation between hepcidin and faecal calprotectin (P < 0.05) in children with UC. Conclusion Different hepcidin levels between children with newly diagnosed CD and UC suggest the distinct contribution of iron deficiency and/or systemic inflammation to anaemia and may help clinicians choose the best anti‐anaemic treatment.
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ISSN:1034-4810
1440-1754
DOI:10.1111/jpc.14093