Natural history of chronic hepatitis C development and progression as a consequence of iron and HFE or TfR1 mutations

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Abstract

Introduction and aims

Heavy iron overload is toxic to virtually all cells and tissues. There is growing evidence that only modest amounts of iron in the liver may serve as a comorbid factor to increase the severity and/or rate of progression of liver disease. The aim of this work is to explore the role of iron, hemochromatosis (HFE) mutations, and polymorphisms of the type-1 transferrin receptor (TfR1) gene in the progression of chronic hepatitis C infection and possible therapeutic implications of iron overload on interferon therapy of patients with chronic hepatitis C.

Patients and methods

This study was conducted from 3 October 2012 to 6 January 2016. The researchers studied 300 consecutive patients with chronic hepatitis C and correlated their clinical, laboratory, histopathological, and genetic data. Frequencies of genetic variations were compared with healthy controls.

Results

HFE mutations were more common in patients than in controls (25 vs. 11.7%, P=0.00006), and the C282Y mutation was more common in patients than in controls (48.0 vs. 38.0%, P=0.02). Patients who carried C282Y had higher mean hepatic iron concentrations (P=0.02). Hepatic fibrosis correlated with hepatic iron concentration (P=0.03). HFE and TfR1 polymorphisms had a detectable relation to disease severity and interferon therapy response.

Conclusion

Hepatic iron and HFE and TfR1 mutations were comorbid factors that increased progression of chronic hepatitis C and decreased the response to interferon therapy.

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