Table 1.
Demographic, clinical, and genetic features of 216 Italian patients with NAFLD with available re-evaluation of histological siderosis and of 271 healthy controls with normal iron parameters, liver function tests, and metabolic parameters.
Table 2.
Clinical features of 216 Italian patients with NAFLD subdivided according to the p.Ala736Val TMPRSS6 status.
Figure 1.
Effect of TMPRSS6 p.A736V genotype on hepcidin levels (hepcidin <3 nM, median value, panel A) and the hepcidin/ferritin ratio (panel B) in 55 patients with NAFLD (25.5% of the whole series).
Figure 2.
Combined effect of the HFE and TMPRSS6 genotypes on iron status in 216 Italian patients with NAFLD.
A) Prevalence of detectable hepatic iron deposition B) Prevalence of increased ferritin levels (>320/240 ng/ml in M/F). p values are for trend across TMPRSS6 genotypes in patients carrying HFE genotypes at risk or not. * p<0.05 vs. HFE genotypes at risk.
Figure 3.
Frequency distribution of genetic factors influencing iron metabolism in patients with and without hepatic iron accumulation.
Patients positive for the beta-thalassemia trait were classified as “Beta-trait”, next if negative for “Beta-trait” and positive for HFE genotypes at risk as “HFE at risk”, and among the remaining patients those homozygous for the 736V/V TMPSS6 as “736VV”, and the rest as “none”.
Table 3.
Relationship between clinical and genetic variables considered in the study with hepatic iron accumulation in 216 patients with NAFLD (univariate analysis).
Table 4.
Independent determinants of hepatic iron accumulation in 216 patients with NAFLD at multivariate logistic regression analysis.