Abstract

Inflammation, but Not the Underlying Disease or Its Location, Predicts Oral Iron Absorption Capacity in Patients With Inflammatory Bowel Disease

Crohns Colitis. 2020 Mar 13;14(3):316-322. doi: 10.1093/ecco-jcc/jjz149.

Aysegül Aksan 1 2, M Wohlrath 1, Tariq H Iqbal 3, A Dignass 4, J Stein 1 5

 
     

Author information

1Interdisciplinary Crohn-Colitis Centre Rhein-Main, Frankfurt am Main, Germany.

2Institute of Pharmaceutical Chemistry, Goethe University Frankfurt am Main, Germany.

3Institute for Cancer Studies, University of Birmingham Cancer Research, Birmingham, UK.

4Department of Gastroenterology, Apaglesion Markus Krankenhaus, Frankfurt am Main, Germany.

5Department of Gastroenterology and Clinical Nutrition, DGD Clinics Sachsenhausen, Frankfurt am Main, Germany.

Abstract

Background and aims: Anaemia is common in patients with inflammatory bowel disease [IBD], its two main aetiologies being iron deficiency anaemia [IDA] and anaemia of chronic inflammation [ACI]. Impaired intestinal iron absorption due to inflammatory cytokines is thought to play a role in ACI. We undertook for the first time a controlled prospective study investigating effects of differing underlying diseases, disease locations, and types of iron deficiency or anaemia on oral iron absorption in adult IBD patients with and without inflammation.

Methods: This study was a comparative, single-centred open clinical trial in adults with IBD [n = 73] and healthy controls [n = 22]. Baseline parameters included blood count, iron status [ferritin, transferrin, transferrin saturation, soluble transferrin receptor, hepcidin, serum iron], high-sensitivity C-reactive protein [hsCRP] and interleukin-6. Iron absorption was tested using one oral, enteric-coated capsule containing 567.7 mg iron[II]-glycine-sulphate complex. Serum iron was determined 60/90/120/180/240 min after ingestion.

Results: Iron absorption capacity was shown to be influenced by inflammation and anaemia or iron deficiency [ID] type but not by underlying disease type or localisation. The ACI group showed a significantly lower iron absorption capacity than all others. Whereas hsCRP levels [-0.387, p < 0.001], IL-6 [-0.331, p = 0.006], ferritin [-0.531, p < 0.001], and serum hepcidin [-0.353, p = 0.003] correlated negatively with serum iron change at 2 h, transferrin showed a positive correlation at the same time point [0.379, p < 0.001].

Conclusions: Underlying disease type and localisation appear to have little effect on iron absorption capacity, whereas lack of response to oral iron correlates well with serum markers of inflammation. Iron absorption capacity is thus significantly reduced in the presence of inflammation.

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