Serum prohepcidin levels in chronic inflammatory bowel diseases

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Abstract

Background and Aims: One of the major symptoms of chronic inflammatory bowel diseases is anemia. The two most common diseases are Crohn's disease and ulcerative colitis. Anemia may develop due to intestinal bleeding, iron absorption disturbances, or high levels of inflammatory cytokines. It is not clear whether or not hepcidin, the only known hormone regulating cellular iron uptake in mammals is involved. The transcription of hepcidin is controlled by the iron status of the body, hypoxia, and/or inflammation. This study was meant to find relationship between serum prohepcidin levels and clinical parameters of iron homeostasis or inflammatory state in patients suffering from Crohn's disease or ulcerative colitis. Methods: Serum prohepcidin levels were measured with ELISA in 72 patients diagnosed with ulcerative colitis and 30 patients suffering from Crohn's disease. Results: In both groups serum iron levels were lower, while levels of C-reactive protein were higher than in the healthy controls. Serum prohepcidin levels showed no significant differences compared to those in the control group. In the affected patients only weak correlations were observed between prohepcidin levels and diagnostic parameters: in Crohn's disease prohepcidin levels correlated positively with transferrin levels, total iron-binding capacity, transferrin saturation, activity index, and serum albumin levels, while in ulcerative coltitis prohepcidin levels were related to transferrin levels and transferrin saturation. Conclusion: It seems obvious that serum prohepcidin level determination in itself is not a satisfactory diagnostic or prognostic measure in anemia of chronic inflammatory bowel diseases. © 2010 European Crohn's and Colitis Organisation.

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APA

Nagy, J., Lakner, L., Poór Viktor S., V. S., Pandur, E., Mózsik, G., Miseta, A., & Sipos, K. (2010). Serum prohepcidin levels in chronic inflammatory bowel diseases. Journal of Crohn’s and Colitis, 4(6), 649–653. https://doi.org/10.1016/j.crohns.2010.07.010

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