BACKGROUND: Hepcidin is a major regulator of iron homeostasis and a mediator of innate immunity. To date, the role of hepcidin in inflammatory bowel disease (IBD) children is not clearly established. We aimed to assess serum hepcidin concentration in IBD children and correlate hepcidin with iron status parameters and inflammatory markers. METHODS: The study group included 46 pediatric patients with ulcerative colitis and 29 with Crohn's disease. In control group, there were 21 children with functional gastrointestinal disorders. The complete blood count, high-sensitivity C-reactive protein, erythrocyte sedimentation rate, iron, ferritin, transferrin, hepcidin, soluble transferrin receptor, transferrin saturation, and interleukin-6 were measured. The study was approved by the local bioethical committee (KE-0254/22/2013). RESULTS: Mean serum hepcidin concentration was significantly decreased in IBD children (5.98 ng/mL) compared with controls (10 ng/mL) (P = 0.03). Hepcidin did not differ significantly between patients with Crohn's disease (6.9 ± 4.5 ng/mL) and ulcerative colitis (5.4 ± 5.3 ng/mL) (P = 0.07). Hepcidin was significantly decreased in IBD children with iron deficiency (4.9 ± 3.2 ng/mL) compared with healthy controls (10.5 ± 10 ng/mL) (P = 0.02). In anemic children with IBD, serum hepcidin (5.3 ± 4.4 ng/mL) was significantly reduced compared with healthy controls (10.5 ± 10 ng/mL) (P = 0.04), but comparable to nonanemic IBD children (6.6 ± 5.6 ng/mL) (P = 0.62). In IBD, children hepcidin was correlated solely with ferritin (P = 0.007; R = 0.3). CONCLUSIONS: In our study, serum hepcidin concentration was significantly decreased in IBD children compared with controls. Hepcidin correlated positively with ferritin, but not with any of inflammatory markers. It may suggest that in our cohort, hepcidin was regulated predominantly by iron storage level.
BACKGROUND:Hepcidin is a major regulator of iron homeostasis and a mediator of innate immunity. To date, the role of hepcidin in inflammatory bowel disease (IBD) children is not clearly established. We aimed to assess serum hepcidin concentration in IBD children and correlate hepcidin with iron status parameters and inflammatory markers. METHODS: The study group included 46 pediatric patients with ulcerative colitis and 29 with Crohn's disease. In control group, there were 21 children with functional gastrointestinal disorders. The complete blood count, high-sensitivity C-reactive protein, erythrocyte sedimentation rate, iron, ferritin, transferrin, hepcidin, soluble transferrin receptor, transferrin saturation, and interleukin-6 were measured. The study was approved by the local bioethical committee (KE-0254/22/2013). RESULTS: Mean serum hepcidin concentration was significantly decreased in IBD children (5.98 ng/mL) compared with controls (10 ng/mL) (P = 0.03). Hepcidin did not differ significantly between patients with Crohn's disease (6.9 ± 4.5 ng/mL) and ulcerative colitis (5.4 ± 5.3 ng/mL) (P = 0.07). Hepcidin was significantly decreased in IBD children with iron deficiency (4.9 ± 3.2 ng/mL) compared with healthy controls (10.5 ± 10 ng/mL) (P = 0.02). In anemicchildren with IBD, serum hepcidin (5.3 ± 4.4 ng/mL) was significantly reduced compared with healthy controls (10.5 ± 10 ng/mL) (P = 0.04), but comparable to nonanemic IBD children (6.6 ± 5.6 ng/mL) (P = 0.62). In IBD, childrenhepcidin was correlated solely with ferritin (P = 0.007; R = 0.3). CONCLUSIONS: In our study, serum hepcidin concentration was significantly decreased in IBD children compared with controls. Hepcidin correlated positively with ferritin, but not with any of inflammatory markers. It may suggest that in our cohort, hepcidin was regulated predominantly by iron storage level.