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    • The current research also analyzed

    2021-12-01

    The current research also analyzed the association of this polymorphism with HCV genotype 1-related hepatic steatosis by gender. Even though the allele and genotypes of this polymorphism an increased the risk of HCV-related hepatic steatosis, neither allele nor genotype frequency of this polymorphism was related to gender in HCV genotype 1-related hepatic steatosis (P = .26 OR = 1.75; P = .49 OR = 1.53 in males, P = .65 OR = 1.20; P = .29 OR = 1.71 in females). There is no any study which evaluating association between gender and this polymorphism, to compare with the current study in the HCV-related steatosis. However, in studies which are different from HCV studies, the authors reported that there was no significant difference between gender and MTP genotypes (García-García et al., 2005; Bernard et al., 2000). These results are similar to result presented in the current study. The present study also investigated relation to MTP polymorphism with lipid parameters, but not significant associations were found. Moreover, Zampino et al. (2008) reported that neither Adenosine-5'-diphosphate synthesis nor genotypes of this polymorphism were associated with lipid parameters in the HCV genotype 3 and HCV genotype non-3. The results of this study were consistent with the results presented in current study. Contrarily, Mirandola et al. (2009) reported that the patients carrying TT genotype had higher HDL cholesterol levels than the G allele carriers, but others of lipid parameters were not significant by MTP polymorphism. Additionally, in studies which are different from HCV studies, while the T allele carriers had lower levels of triglyceride and VLDL cholesterol (García-García et al., 2005), whereas total cholesterol, LDL cholesterol, HDL cholesterol were not association with this polymorphism (García-García et al., 2005; Bernard et al., 2000; Namikawa et al., 2004). Moreover, Ledmyr et al. (2002) reported that individuals with TT genotype had lower the levels of LDL and total cholesterols in the healthy men. The results of all these studies are controversial. Recently, HCV-related hepatic steatosis has been associated with the MTP gene −493G/T polymorphism for HCV genotype-3, but not related to HCV genotype 1. While the T allele of −493G/T polymorphism was determined to have increased the MTP transcription in vitro in healthy persons (Karpe et al., 1998), but hepatic MTP mRNA expression and MTP activity didn't differ according to genotypes of this polymorphism in CHC infection (Mirandola et al., 2009). On the contrary, Nakamuta et al. (2009) reported that the MTP expression level was higher in the total HCV cohort who was composed of genotype 1 and 2 compared to controls. In all these studies, the reasons for having different results which regarding steatosis and lipid levels relation to this polymorphism are not clear. Different populations, different diseases, gene-gene interactions and gene-environment interactions can cause changes in lipid metabolism. In conclusion, the results of current study demonstrate for the first time that MTP gene −493G/T polymorphism has not a major effect on the risk of HCV-related hepatic steatosis in the HCV genotype 1 infection in Turkish population. Considering only one study in HCV genotype 1 infection, further studies are imperative to clarify the association of this polymorphism with HCV genotype 1 infection in HCV-related hepatic steatosis.
    Competing interests
    Authors' contributions
    Acknowledgement The authors thank all the patients who participated in this study. This research was funded by Çukurova University Research Fund TF2011BAP14.
    Introduction Hemochromatosis due to HFE p.C282Y homozygosity in North America occurs predominantly in non-Hispanic whites of European descent [1]. Among persons in North America with hemochromatosis phenotypes, ∼90% have HFE p.C282Y homozygosity [3]. In a screening study of 99,711 adults in North America, the estimated prevalence of p.C282Y homozygosity in non-Hispanic whites was 0.44% (∼1 in 227) [1]. The prevalence of p.C282Y homozygosity is highest in Ireland (∼1.0%), Denmark, United Kingdom, Iceland, and Norway [4], [5]. p.C282Y homozygosity is also common in Australia, New Zealand, and South Africa due to migration of Europeans to these areas [6]. In large countries of Central and South America, patients with hemochromatosis phenotypes are uncommon and the proportions of them who also have p.C282Y homozygosity are low [7], [8], [9]. Among rural-dwelling southern Africans with a high probability of having the putative African iron overload gene, none had p.C282Y [10]. In Asia, hemochromatosis is rare. Novel cases are due to deleterious mutations in genes that encode hemojuvelin (HJV), hepcidin (HAMP), and ferroportin (SLC40A1), but not HFE (HFE) [11]. HFE p.C282Y/H63D compound heterozygosity occurs in 2.0% of non-Hispanic whites in North America [1] but is infrequently associated with morbidity due to iron overload [12], [13].