Hepatitis C, iron status, and disease severity: Relationship with HFE mutations

Hemochromatosis Gene Mutations: Prevalence and Effects on Pegylated-Interferon and Ribavirin Therapy Response in Chronic Hepatitis C in Sardinia

“…12À14 HFE gene mutations may play a role in the development of significant iron overload in patients with CHC and could represent a clinically relevant comorbid factor in patients with chronic hepatitis C. [15][16][17] There are several host characteristics known to affect outcome of interferon treatment, including age, gender, immune surveillance system, nutritional state and iron status. 18 The aim of our study was to evaluate the impact of HFE gene mutations on disease severity and response to interferon therapy in a cohort of Sardinian patients with Chronic Hepatitis C.…”

Iron Inactivates the RNA Polymerase NS5B and Suppresses Subgenomic Replication of Hepatitis C Virus

“…The most prevalent form of hereditary hemochromatosis is linked to mutations in the HFE gene, encoding an atypical major histocompatibility complex class I type molecule that appears to control dietary iron absorption and body iron reutilization (20). Clinical studies suggest that HFE mutations exacerbate hepatic fibrogenesis in chronic hepatitis C (5), mostly at early stages (8). A failure to find such a correlation in some reports may be related to the lack of control for confounding variables (5).…”

Relationship Between Hemochromatosis Gene Mutations and Degree of Fibrosis in Liver Disease Associated with Chronic Hepatitis B and C

“…30 Moreover, as pointed out by Tung et al, the association between HFE mutations and the severity of both iron accumulation and fibrosis is more evident in patients with compensated disease after controlling for the duration of infection, and disappears in patients with end-stage liver disease. 31 Although most of the patients included in the present study have compensated CVH, we failed to see a contribution of HFE mutations in causing disease progression in patients with CHB or CHC. This might be ascribed to the predominance of the HFE H63D heterozygous variant among our patients, which affects iron homeostasis in CVH to a lower extent than the C282Y variant.…”