Ingo Mecklenburg1, Diana Reznik1, Elizaveta Fasler-Kan2, Jürgen Drewe1, Christoph Beglinger1, Petr Hruz3. 1. Department of Gastroenterology and Hepatology, University Hospital Basel, Basel, Switzerland. 2. Department of Gastroenterology and Hepatology, University Hospital Basel, Basel, Switzerland; University of Applied Sciences Northwestern Switzerland (FHNW), Institute of Chemistry and Bioanalytics, Muttenz, Switzerland. 3. Department of Gastroenterology and Hepatology, University Hospital Basel, Basel, Switzerland. Electronic address: petr.hruz@usb.ch.
Abstract
BACKGROUND AND AIMS: Anemia is a frequent complication of inflammatory bowel disease (IBD). Hepcidin, a key mediator in this anemia, is up-regulated by high iron levels and inflammation, and serum levels are elevated in IBD. However, the extent of inflammatory activity and iron deficiency for the regulation of hepcidin is not known. This study aimed to evaluate serum hepcidin levels in anemic and non-anemic IBD patients, with iron or non-iron deficiency, and active or inactive disease. METHODS: This retrospective, observational study analyzed serum hepcidin levels from 247 patients with IBD (130 Crohn's patients and 117 with ulcerative colitis) recruited at Swiss Inflammatory Bowel Disease Cohort Study centers. Patients were divided into 5 different groups using criteria of active and inactive diseases (C-reactive protein, and CDAI/MTWAI=disease activity-index), anemia (hemoglobin) and iron deficiency (ferritin) and compared to healthy controls with no signs of anemia and normal ferritin levels. Hepcidin was measured using enzyme-linked immunosorbent assay. RESULTS: Independent of inflammatory activity, all patients with decreased ferritin (<30μg/L) had significantly lower hepcidin levels when compared to patients and healthy controls having normal ferritin (>30μg/L). A significant correlation between serum ferritin levels and serum hepcidin was found (Spearman's Rho=0.491; p<0.001). A backward multi-linear stepwise regression analysis showed that only ferritin, and none of the inflammatory markers or age and sex correlated significantly (p=0.005) with hepcidin. CONCLUSION: This retrospective analysis suggests that iron deficiency is the key trigger for hepcidin regulation in IBD patients with anemia.
BACKGROUND AND AIMS: Anemia is a frequent complication of inflammatory bowel disease (IBD). Hepcidin, a key mediator in this anemia, is up-regulated by high iron levels and inflammation, and serum levels are elevated in IBD. However, the extent of inflammatory activity and iron deficiency for the regulation of hepcidin is not known. This study aimed to evaluate serum hepcidin levels in anemic and non-anemic IBDpatients, with iron or non-iron deficiency, and active or inactive disease. METHODS: This retrospective, observational study analyzed serum hepcidin levels from 247 patients with IBD (130 Crohn's patients and 117 with ulcerative colitis) recruited at Swiss Inflammatory Bowel Disease Cohort Study centers. Patients were divided into 5 different groups using criteria of active and inactive diseases (C-reactive protein, and CDAI/MTWAI=disease activity-index), anemia (hemoglobin) and iron deficiency (ferritin) and compared to healthy controls with no signs of anemia and normal ferritin levels. Hepcidin was measured using enzyme-linked immunosorbent assay. RESULTS: Independent of inflammatory activity, all patients with decreased ferritin (<30μg/L) had significantly lower hepcidin levels when compared to patients and healthy controls having normal ferritin (>30μg/L). A significant correlation between serum ferritin levels and serum hepcidin was found (Spearman's Rho=0.491; p<0.001). A backward multi-linear stepwise regression analysis showed that only ferritin, and none of the inflammatory markers or age and sex correlated significantly (p=0.005) with hepcidin. CONCLUSION: This retrospective analysis suggests that iron deficiency is the key trigger for hepcidin regulation in IBDpatients with anemia.
Authors: Meredith A Atkinson; Mary B Leonard; Rita Herskovitz; Robert N Baldassano; Michelle R Denburg Journal: J Pediatr Gastroenterol Nutr Date: 2018-01 Impact factor: 2.839