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| Iron overload and HFE gene mutations in Polish patients with liver cirrhosis |
| Katarzyna Sikorska, Tomasz Romanowski, Piotr Stalke, Ewa Izycka-Swieszewska and Krzysztof Piotr Bielawski |
Gdansk, Poland
Author Affiliations: Department of Infectious Diseases, Medical University of Gdansk, ul. Smoluchowskiego 18, 80-218 Gdansk, Poland (Sikorska K, Stalke P); Department of Biotechnology, Intercollegiate Faculty of Biotechnology, University of Gdansk and Medical University of Gdansk, ul. K?adki 24, 80-822 Gdańsk, Poland (Romanowski T and Bielawski KP); Department of Pathology, Medical University of Gdansk, ul. D?binki 7, 80-952 Gdansk, Poland (Izycka-Swieszewska E)
Corresponding Author: Katarzyna Sikorska, MD, PhD, Department of Infectious Diseases, Medical University of Gdansk, ul. Smoluchowskiego 18, 80-218 Gdansk, Poland (Tel: 48-58-3412887; Fax: 48-58-3412887; Email: ksikorska@gumed.edu.pl) |
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Abstract BACKGROUND: Increased liver iron stores may contribute to the progression of liver injury and fibrosis, and are associated with a higher risk of hepatocellular carcinoma development. Pre-transplant symptoms of iron overload in patients with liver cirrhosis are associated with higher risk of infectious and malignant complications in liver transplant recipients. HFE gene mutations may be involved in the pathogenesis of liver iron overload and influence the progression of chronic liver diseases of different origins. This study was designed to determine the prevalence of iron overload in relation to HFE gene mutations among Polish patients with liver cirrhosis.
METHODS: Sixty-one patients with liver cirrhosis included in the study were compared with a control group of 42 consecutive patients subjected to liver biopsy because of chronic liver diseases. Liver function tests and serum iron markers were assessed in both groups. All patients were screened for HFE mutations (C282Y, H63D, S65C). Thirty-six of 61 patients from the study group and all controls had liver biopsy performed with semiquantitative assessment of iron deposits in hepatocytes.
RESULTS: The biochemical markers of iron overload and iron deposits in the liver were detected with a higher frequency (70% and 47% respectively) in patients with liver cirrhosis. There were no differences in the prevalence of all HFE mutations in both groups. In patients with a diagnosis of hepatocellular carcinoma, no significant associations with iron disorders and HFE gene mutations were found.
CONCLUSIONS: Iron disorders were detected in patients with liver cirrhosis frequently but without significant association with HFE gene mutations. Only the homozygous C282Y mutation seems to occur more frequently in the selected population of patients with liver cirrhosis. As elevated biochemical iron indices accompanied liver iron deposits more frequently in liver cirrhosis compared to controls with chronic liver disease, there is a need for more extensive studies searching for the possible influence of non-HFE iron homeostasis regulators and their modulation on the course of chronic liver disease and liver cirrhosis.
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2011, Vol. 10 
