Introduction Iron deficiency is a common extra-intestinal complication of IBD and, as large doses of intestinal iron are poorly tolerated by patients with IBD [1] intravenous iron supplementation is often recommended [2]. It is also often stated that, in patients with chronic systemic inflammation, iron is poorly absorbed from the gut. This has been sparsely investigated although we have previously shown that patients with elevated CRP tend to absorb ferrous sulphate less well [3]. The hepatic peptide hepcidin is the master iron regulator. It is not known if hepcidin prevents iron uptake from the gut in practice in anaemic IBD patients.

Method We measured serum hepcidin (using MALDI TOF mass spectrometry) in serum samples stored from a previously published phase III trial using ferric maltol to treat IBD patients with anaemia [4]. We then analysed data from this study retrospectively to assess whether baseline hepcidin or CRP would predict response to oral iron supplementation.

Results The table below gives the baseline characteristics of the study cohort:

There was no correlation at baseline between CRP and hepcidin. Baseline hepcidin was not associated with response to iron replacement either at the primary endpoint (week 12) or at one year follow up. Neither CRP nor hepcidin was associated with haemoglobin response. However week 12 ferritin was inversely correlated to baseline CRP (p=0.004), and there was a trend for an association between TSAT at week 12 and baseline CRP which achieved statistical significance at 12 months (p=0.02).

Conclusion In this study of factors predicting response to oral iron supplementation in IBD patients, the master iron regulator hepcidin did not seem to be a useful marker. However, there was a clear signal that CRP, as an indicator of chronic inflammation, did predict responsiveness of the body’s iron stores to replenishment with orally administered iron. The association between ferritin and CRP at week 12 and also between CRP and TSAT at 12 months but lack of association between CRP and haemoglobin suggests that, in the presence of elevated CRP, iron supplementation may need to be given for longer to replace iron stores. We suggest that the commonly available acute phase protein CRP should be measured in IBD patients with iron deficiency to help clinicians decide on the most appropriate route of iron supplementation

References

1. . Lugg S et al. JCC 2014;8:876–880.

2. . Dignass A et al. JCC 2015;9:211–222.

3. . Iqbal T et al. Dig Dis Sci 2015;60:1375–1381.

4. . Gasche C et al. IBD 2015;21:579–588.

Disclosure of Interest N. Quraishi: None Declared, S Smith: None Declared, D Ward: None Declared, N Sharma: None Declared, M Sampson Conflict with: Shield Therapeutics, C Tselepis: None Declared, T Iqbal Conflict with: speaker fee from Shield