Iqbal T, Diab A, Ward DG, Brookes MJ, Tselepis C, Murray J, Elias E. Is iron overload in alcohol-related cirrhosis mediated by hepcidin? World J Gastroenterol 2009; 15(46): 5864-5866 [PMID: 19998511 DOI: 10.3748/wjg.15.5864]
Corresponding Author of This Article
Dr. Tariq Iqbal, Department of Gastroenterology, University Hospital Birmingham, Vincent Drive, Birmingham B15 2TH, United Kingdom. t.h.iqbal@bham.ac.uk
Article-Type of This Article
Case Report
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World J Gastroenterol. Dec 14, 2009; 15(46): 5864-5866 Published online Dec 14, 2009. doi: 10.3748/wjg.15.5864
Is iron overload in alcohol-related cirrhosis mediated by hepcidin?
Tariq Iqbal, Azzam Diab, Douglas G Ward, Matthew J Brookes, Chris Tselepis, Jim Murray, Elwyn Elias
Tariq Iqbal, Azzam Diab, Elwyn Elias, Department of Gastroenterology, University Hospital Birmingham, Vincent Drive, Birmingham B15 2TH, United Kingdom
Douglas G Ward, Matthew J Brookes, Chris Tselepis, Department of Cancer Studies, University of Birmingham, Vincent Drive, Birmingham B15 2TT, United Kingdom
Jim Murray, Department of Hematology, University Hospital Birmingham, Vincent Drive, Birmingham B15 2TH, United Kingdom
Author contributions: Iqbal T and Tselepis C designed the study and wrote the paper; Diab A collected the patient samples; Ward DG performed the analysis and analyzed the results; Murray J and Elias E provided expertise in hematology and hepatology in the preparation of the manuscript.
Supported by University Hospital Birmingham NHS Foundation Trust
Correspondence to: Dr. Tariq Iqbal, Department of Gastroenterology, University Hospital Birmingham, Vincent Drive, Birmingham B15 2TH, United Kingdom. t.h.iqbal@bham.ac.uk
Telephone: +44-121-4721311
Received: October 12, 2009 Revised: November 2, 2009 Accepted: November 9, 2009 Published online: December 14, 2009
Abstract
In this case report we describe the relationship between ferritin levels and hepcidin in a patient with alcohol-related spur cell anemia who underwent liver transplantation. We demonstrate a reciprocal relationship between serum or urinary hepcidin and serum ferritin, which indicates that inadequate hepcidin production by the diseased liver is associated with elevated serum ferritin. The ferritin level falls with increasing hepcidin production after transplantation. Neither inflammatory indices (IL6) nor erythropoietin appear to be related to hepcidin expression in this case. We suggest that inappropriately low hepcidin production by the cirrhotic liver may contribute substantially to elevated tissue iron stores in cirrhosis and speculate that hepcidin replacement in these patients may be of therapeutic benefit in the future.
