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industrial fructose included any amount of fructose derived from food sources containing high fructose corn syrup (beverages like soft drink and fruit juices, processed foods like fast-food especially when enriched by industrial sauce), while fruit fructose entailed only whole fruit sources.
In conclusion, we showed that industrial, not fruit fructose intake is associated with the severity of liver fibrosis in a cohort of patients with G1 CHC. These data provide a new target for the management of patients with chronic liver disease in the course of HCV infection.
…...industrial fructose intake (OR 1.147, 95% CI 1.047–1.257, p=0.003) were independently linked to severe fibrosis. No association was found between fructose intake and liver necroinflammatory activity, steatosis, and the features of NASH.
The association of industrial fructose intake with severe liver fibrosis was confirmed at multivariate analysis also in the subgroup of non-diabetic G1 CHC patients (OR 1.153, 95% CI 1.049–1.267, p=0.003), together with older age (OR 1.054, 95% CI 1.008–1.103, p=0.02) and severe necroinflammatory activity (OR 2.713, 95% CI 1.033–7.125, p=0.04), as well as in the subgroup of non-diabetic normal-weight patients, even if this last association was not confirmed at multivariate analysis (OR 1.480, 95% CI 0.946–2.316, p=0.08).
Fibrosis
Older age, high WC, high ALT levels, severe necroinflammatory activity, moderate-severe steatosis, histological features of NASH, and both total and industrial fructose intake (not fruit fructose) were linked to severe fibrosis at univariate analysis (p<0.10). By multivariate logistic regression analysis, only older age (OR 1.048, 95% CI 1.004–1.094, p=0.03), severe necroinflammatory grading (OR 3.325, 95% CI 1.347–8.209, p=0.009), moderate-severe steatosis (OR 2.421, 95% CI 1.017–6.415, p=0.04), and industrial fructose intake (OR 1.147, 95% CI 1.047–1.257, p=0.003) remained associated with severe fibrosis (Table 3). Similarly, when industrial fructose as continuous variable was replaced in the model by industrial fructose as categorical variable, at the cut-off of 8g/day, 14/25 pts with industrial fructose intake 8g/day had F3-F4 fibrosis vs. 18/89 in the group with lower intake (p=0.01); again, fructose remained independently associated with severe fibrosis (OR 4.453, 95% CI 1.618–12.256, p=0.004). Similar data were obtained when total fructose intake was entered in the model instead of industrial fructose intake; the association with severe fibrosis remained statistically significant (OR 1.053, 95% CI 1.002–1.106, p=0.04). The association between industrial fructose intake and severe liver fibrosis did not change when the presence of hypercaloric diet was forced into the model as independent variable (OR 1.158, 95%CI 1.045–1.283, p=0.005). Fig. 2 shows total (A), industrial (B), and fruit (C) fructose intake according to presence/absence of severe fibrosis.
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