P399 Detection of iron restricted erythropoiesis in patients with IBD: How can we disentangle effects of inflammation?
Aksan, A.(1,2,3)*;Mangold, C.(4);Stötzel, J.(1,3);Tessmer, L.(3,5);Schröder, O.(3,5);Stein, J.M.(3,5,6);
(1)Justus-Liebig University Giessen, Institute of Nutritional Science, Giessen, Germany;(2)Immundiagnostik AG, Medical Affairs, Bensheim, Germany;(3)Interdisciplinary Crohn-Colitis Centre Rhein-Main, Clinical Research, Frankfurt am Main, Germany;(4)Goethe University Frankfurt, Faculty of Medicine, Frankfurt am Main, Germany;(5)DGD Clinics Sachsenhausen, Gastroenterology/Oncology, Frankfurt am Main, Germany;(6)Goethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt am Main, Germany;
Background
Iron deficiency and anaemia are among the most common complications of IBD. While the distinction between functional and absolute iron deficiency (AID) is vital for therapeutic decision-making, inflammation is a frequent confounder in their diagnosis: An indirect indicator of body iron stores, serum ferritin is the most specific biomarker of AID. However, it is also an acute-phase reactant and can thus be obscured by IBD-related inflammation. Patients with active IBD often have anaemia of inflammation (AOI), i.e., reduced availability of iron for erythropoiesis (iron-restricted erythropoiesis, IRE) despite adequate stores. ECCO guidelines suggest adding biomarkers to distinguish functional from absolute ID in AOI. Here, we compared the utility of red cell indices and biochemical markers to detect IRE in IBD and define a decision threshold for the selection of biomarkers to discriminate AID and iron sequestration.
Methods
In an observational cross-sectional study, routine blood samples of patients with IBD were collected. CBC, iron status (serum ferritin, SF; transferrin saturation, TSAT; serum iron % of hypochromic red cells, %HYPO; reticulocyte haemoglobin content, CHr; soluble transferrin receptor, sTfR) and high sensitivity CRP (hsCRP) as inflammatory marker were determined by standard methods. sTfR-F index was calculated (sTfR (mg/L)/log10 SF(μg/L)). Patients with SF<30μg/L were assigned as AID-consistent controls to define decision thresholds for iron markers in patients with SF≥30μg/L which were then used to evaluate IRE in patients with SF≥30μg/L. The accuracy of the markers in the presence/absence of inflammation were assessed and contextual diagnostic thresholds determined.
Results
Samples were collected from 312 patients with IBD (159f/153m;163CD/149UC;42.7±14.5y), of whom 122(39.1%) had inflammation. 43 patients with SF<30μg/L were selected as AID-control group. Results in this group were: TSAT (cut-off 20%; AUCROC 0.730; sens.65%, spe.34%), %HYPO (3.5%; 0.733; 42%, 93%), CHr (32pg; 0.713; 51%, 86%), sTfR (2.70mg/L; 0.775; 81%, 63%), sTfR-F (2.01; 0.914; 88%, 88%). sTfR-F was used as reference for IRE in patients with SF ≥30μg/L. Accuracy of the markers as detectors of IRE is shown in Table 1.
Conclusion
sTfR was the most accurate sole marker of IRE in patients both with and without inflammation, its cut-off being higher in the presence of inflammation. In patients without inflammation, SF was a valuable additional parameter. Relative cost-effectiveness of the markers alone or in combination is under investigation.