P0397Soluble Transferrin Receptor as a Reliable Inflammation-Independent Marker of Iron Deficiency in Crohn’s Disease and Ulcerative Colitis

Background Iron deficiency is a common complication in inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD).1 However, standard iron markers are influenced by inflammation, complicating the diagnosis of true iron deficiency.1,2 Soluble transferrin receptor (sTfR) has been proposed as a more reliable, inflammation-independent marker of iron demand.3 This study aimed to assess the utility of sTfR in identifying iron deficiency without anaemia (IDWA). Methods The ID_IBD study was a multicentre, cross-sectional study. Iron status was classified using two approaches: the ECCO consensus definition, focusing on ferritin thresholds adjusted for inflammatory markers (C-reactive protein [CRP] and faecal calprotectin [FCAL]), and a stricter definition that adds transferrin saturation to the ECCO criteria. sTfR levels were compared across groups, and ROC curve analysis was used to identify optimal diagnostic cut-offs. Results This analysis included 411 IBD patients (130 UC, 281 CD) and 178 controls. sTfR showed no correlation with CRP or FCAL. In UC, patients with IDWA had significantly higher sTfR levels (median 1.20 mg/L, IQR 1.02-1.42) compared to non-IDWA patients (median 1.05 mg/L, IQR 0.92-1.22; p = 0.013). Anaemic UC patients also showed elevated sTfR levels (median 1.27 mg/L, IQR 1.14-1.59) compared to non-IDWA individuals (p < 0.001). In CD, sTfR did not significantly differ between IDWA and non-IDWA patients but was significantly higher in anaemic patients (p = 0.003). Conclusion sTfR appears to be an inflammation-independent marker of iron status in IBD. It showed potential for identifying IDWA in UC, while in CD it mainly reflected increased iron demand in anaemia. Further longitudinal studies are warranted to validate its role and assess its clinical utility in IBD. References: 1. Bou-Fakhredin R, Halawi R, Roumi J, Taher A. Insights into the diagnosis and management of iron deficiency in inflammatory bowel disease. Expert Rev Hematol. Sep 2017;10(9):801-808. doi:10.1080/17474086.2017.1355233 2. Oldenburg B, Koningsberger JC, Van Berge Henegouwen GP, Van Asbeck BS, Marx JJM. Review article: iron and in¯ammatory bowel disease. Aliment Pharmacol Ther. 2001;4(15):429-438. doi:10.1046/j.1365-2036.2001.00930.x 3. Krawiec P, Pac-Kozuchowska E. Biomarkers and Hematological Indices in the Diagnosis of Iron Deficiency in Children with Inflammatory Bowel Disease. Nutrients. May 9 2020;12(5)doi:10.3390/nu12051358 Conflict of interest: Portela, Francisco: consulting fees and support from the following companies: Abbvie, Falk, Ferring, Janssen, Lilly, Pfizer, Pharmakern, Takeda and Tillots. Ministro dos Santos, Maria Paula: received fees from AbbVie, Ferring, Janssen, Pfizer, Takeda, and Tillots. Tavares de Sousa, Helena: Personal Fees: Takeda, AbbVie, Janssen, Pfizer, Ferring, Biogen, Lilly - for presenting or advisory board Non-financial Support: Abbvie, Takeda, Janssen, Ferring, Faez Pharma, Tillots, Falk Pharma Roseira, Joana Selas: received a speaking fee from AbbVie and Janssen Fernandes, Samuel Raimundo: None to declare Crespo, Ricardo: No conflict of interest Domingues, Beatriz: No conflict of interest Santiago, Mafalda: No conflict of interest Miranda, Rita: I declare that I have no conflicts of interest. Dias, Sandra: No conflict of interest Dias, Cláudia Camila: No conflict of interest Prof. Dr. Magro, Fernando: served as speaker and received honoraria from Abbvie, Arena, Biogen, Bristol-Myers Squibb, Falk, Ferring, Hospira, Janssen, Laboratórios Vitoria, Pfizer, Lilly, Merck Sharp & Dohme, Sandoz, Takeda, UCB, Vifor