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P085. Serum hepcidin and prohepcidin concentrations in inflammatory bowel disease

P. Oustamanolakis1, I.E. Koutroubakis1, I. Messaritakis2, N. Malliaraki2, A. Sfiridaki3, E.A. Kouroumalis1

1Department of Gastroenterology, University Hospital, Heraklion, Crete, Greece; 2Laboratory of Biochemistry, University Hospital, Heraklion, Crete, Greece; 3Regional Blood Bank Center, Venizelion Hospital, Heraklion, Crete, Greece

Background-Aim: Hepcidin is produced mainly in the liver, through a precursor protein, prohepcidin. Hepcidin has been found to reduce the amount of circulating iron by preventing its exit from the cells, through binding to ferroportin. Iron upregulates hepcidin in vivo while iron deficiency and hypoxia reduces its production. The aim of this study was to evaluate serum hepcidin and prohepcidin levels in IBD patients and healthy controls and to correlate them with established parameters of anemia assessment, and the inflammation status of each patient.

Materials and methods: 100 consecutive IBD patients were included in the study (CD: 51, males: 58, median age: 49 years, active disease: 20, smokers: 30) and compared with 102 healthy controls (HC). All the full blood counts were processed using the COULTER® LH780 Hematology Analyzer (Beckman Coulter, Inc., CA, USA). Serum concentrations of hepcidin-25 and prohepcidin were measured with commercially available ELISA kits (DRG® International, Inc., NJ, USA) in a blinded fashion.

Results: Table 1 shows the measured laboratory parameters of IBD patients compared with healthy controls.

Table 1
Parameter Median (range)UCCDHCp
Hemoglobin (g/dl)13.3 (9.5–16.6)12.8 (8.6–15.7)15.2 (12.1–18.0)<0.0001
Ferritin (μg/L)42.1 (3.6–381.3)33.4 (2.2–514.0)71.0 (10.0–259.5)0.003
Tsat (%)19.4 (2.2–47.8)14.1 (2.6–52.2)28.9 (8.0–91.8)<0.0001
sTfR (mg/L)1.3 (0.7–6.8)1.5 (0.8–4.4)1.1 (0.5–1.7)<0.0001
CRP (mg/dl)0.37 (0.32–5.3)0.39 (0.32–10.7)0.29 (0.29–1.5)<0.0001
ESR (mm/h)17 (1–80)28 (3–84)5.5 (1–36)<0.0001
Hepcidin (ng/ml)76.3 (16.5–736)70.9 (16.7–306.9)47.0 (8.6–340.2)<0.0001
Prohepcidin (ng/ml)89.1 (13.8–158.3)97.2 (20.1–162.8)121.4 (9.1–265.5)0.03

IBD patients with active disease had higher hepcidin levels compared with patients with inactive disease (p = 0.003). The latter had higher hepcidin levels compared with HC (p < 0.0001). IBD patients with iron deficiency had lower hepcidin levels compared with those without iron deficiency, although the difference was not statistical significant (p = 0.09). Median prohepcidin levels were significantly lower in IBD patients compared with healthy controls (p = 0.03) but when patients with active disease were excluded, the difference was not statistically significant (p = 0.06). IBD patients with iron deficiency had lower prohepcidin levels compared with those without iron deficiency although the difference was not statistical significant (p = 0.17). The correlations between hepcidin or prohepcidin and hemoglobin, ferritin and CRP are shown in Table 2.

Table 2
Parameterrp
Hepcidin-Hgb−0.360.0003
Prohepcidin-Hgb0.65<0.0001
Hepcidin-Prohepcidin−0.330.0009
Hepcidin-Ferritin0.340.0007
Prohepcidin-Ferritin−0.210.04
Hepcidin-CRP0.290.004

Conclusion: Hepcidin and prohepcidin offer a major contribution in the development of anemia in IBD and their regulatory mechanisms may do really share some common steps. There might be a possible increased prohepcidin transformation to its mature form during inflammation process. A common biochemical pathway may takes place – at least to a degree – responsible for the balance between prohepcidin transformation and hepcidin production in the liver.