| Conclusion | patients with HuLDi00024 have an increased tendency to accumulate iron in the liver, and mutations in the HFE gene play a minor role in hepatic accumulation of iron in these patients.;The presence of HFE mutations is independently associated with iron loading and advanced fibrosis in patients with compensated liver disease from HuLDi00025, especially after controlling for duration of disease.;C282Y or H63D heterozygosity is an independent risk factor for liver fibrosis and cirrhosis in HCV infected individuals.;The presence of the relatively high frequency of A1AT S and HFE H63D allele carriers in Egyptian cases of HCV liver Cirrhosis suggest the necessity to implement routine molecular analysis of these genes for detection of risk genotypes among affected families.;Although HFE mutations (especially the most frequent H63D mutation) are associated with increased iron loading, they are also associated with increased sustained virologic responses in US patients with advanced HuLDi00025.Conclusion1 |
