P0463 Distinct hepcidin dynamics in crohn’s disease and ulcerative colitis: links to iron homeostasis and inflammatory activity

Background: Hepcidin, the master regulator of systemic iron metabolism, is influenced by iron availability and inflammation.1 In inflammatory bowel disease (IBD), iron deficiency and anaemia are common, yet how hepcidin is regulated in relation to disease phenotype, iron status and inflammatory burden remains incompletely understood.2 We aimed to characterise hepcidin regulation in ulcerative colitis (UC) and Crohn’s disease (CD) according to iron status and inflammatory markers. Methods: In this cross-sectional multicentre study, 589 individuals were enrolled (178 healthy controls, 130 UC, 281CD). Patients were stratified by iron status and activity. Serum hepcidin, iron parameters, and inflammatory and clinical data were collected. Iron deficiency was defined using the ECCO criteria2 , which focuses on ferritin, and a combined ferritin and transferrin saturation definition. Group comparisons, correlations, and multivariable linear regressions were performed. Results: Hepcidin correlated positively with C-reactive protein (CRP) in CD (r=0.125; p=0.038) and negatively with faecal calprotectin (FCAL) in UC (r=-0.311; p.

URI

http://hdl.handle.net/10400.1/28348

Editora

Oxford University Press

DOI

10.1093/ecco-jcc/jjaf231.644

Coleções

FCB2-Artigos (em revistas ou actas indexadas)
ABC2-Artigos (em revistas ou actas indexadas)
ULS_10.1-MED-Artigos

Licença CC

cclicense-by

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