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P170. Impaired intestional iron absorption in patients with inflammatory bowel disease correlates with disease activity

S.M. Loitsch1,2, D. Diehl3, F. Hartmann4,2, A. Dignass5,2, J. Stein3,2

1University of Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany; 2Crohn Colitis Centre Rhein Main, Frankfurt, Germany; 3St. Elisabethen-Hospital, Frankfurt, Germany; 4St. Marienhospital, Frankfurt, Germany; 5Markuskrankenhaus, Frankfurt, Germany

Aim: Anemia is the most prevalent extraintestinal complication of IBD. Although the causes of anemia in IBD are multifactorial, iron deficiency anemia and anemia of inflammation (ACI) are the most common. Although the exact pathogenesis of ACI is unknown, one hypothesis suggests that-caused by the effects of inflammatory cytokines-ACI arises in part as a result of an impaired intestinal iron absorption. Recently it has been shown, that the acute phase protein hepcidin impairs intestinal iron uptake. We therefore hypothesized that iron absorption is impaired in patients with active IBD at least in part through increased hepcidin release by the liver.

Methods: 64 adult subjects were recruited for the study until September 2010. These were 17 healthy controls and with 47 patients with IBD (17 UC, 30 CD). After an overnight fast, serum iron and hemoglobin levels, serum markers of inflammation [IL-6 and C-reactive protein (CRP)] were measured. Serum and urine samples for hepcidin assay were obtained at 8 a.m. and measured by LC-MS. Ferrous sulfate (100 mg) was administered orally, followed by determination of serum iron concentrations hourly for 4 hours. An area under the curve for iron absorption was calculated for each patient data set.

Results: Table 1 demonstrate the mean iron absorption in controls and CD and UC patients. Intestinal iron absorption is significantly decreased in subjects with active CD and UC. There was a strong inverse correlation between the area under the curve of serum iron after oral iron administration and IL-6 as well as CRP. Serum hepcidin correlates with CRP levels and inversely correlates with iron absorption (AUC of serum iron) in CD patients. Serum hepcidin correlates with ferritin levels in CD and UC patients.

Conclusion: Intestinal iron absorption is markedly impaired in IBD patients with active disease compared to healthy controls or patients with inactive disease. There is a significant correlation of iron absorption with disease activity and markers of inflammation.

Table 1: Mean iron absorption in controls, CD and UC patients
 Δ Fe vs. Baseline
 1 h1.5 h2 h3 h4 h
Controls (n = 17)40.56±10.0372.56±14.7996.75±15.30110.00±14.04129.88±12.89
CD Inactive (n = 10)12.56±8.7746.48±10.8357.33±12.3350.32±22.8172.75±32.77
CD Active (n = 20)6.83±6.6429.17±11.3540.20±13.9050.37±15.5927.54±19.52
CU Inactive (n = 6)1.75±8.6631.50±11.7984.75±38.37120.50±48.22126.50±42.50
CU Active (n = 11)14.34±12.7043.37±26.0643.17±26.2058.93±30.969.33±9.46