Industrial, not fruit fructose intake is associated with the severity of liver fibrosis in genotype 1 chronic hepatitis C patients

Background & Aims: Unhealthy food intake, specifically fructose, has been associated with metabolic alterations and with the severity of liver fibrosis in patients with non-alcoholic fatty liver disease. In a cohort of patients with genotype 1 chronic hepatitis C (G1 CHC), we tested the association of fructose intake with the severity of liver histology. Methods: Anthropometric and metabolic factors, including waist circumference (WC), waist-to-hip ratio (WHR), dorso-cervical lipohypertrophy and HOMA were assessed in 147 consecutive biopsy-proven G1 CHC patients. Food intake, namely industrial and fruit fructose, was investigated by a three-day structured interview and a computed database. All biopsies were scored by an experienced pathologist for staging and grading (Scheuer classification), and graded for steatosis, which was considered moderate-severe if >= 20%. Features of non-alcoholic steatohepatitis (NASH) in CHC were also assessed (Bedossa classification). Results: Mean daily intake of total, industrial and fruit fructose was 18.0 +/- 8.7 g, 6.0 +/- 4.7 g, and 11.9 +/- 7.2 g, respectively. Intake of industrial, not fruit fructose, was independently associated with higher WHR (p = 0.02) and hypercaloric diet (p <0.001). CHC patients with severe liver fibrosis (>= F3) reported a significantly higher intake of total (20.8 +/- 10.2 vs. 17.2 +/- 8.1 g/day; p = 0.04) and industrial fructose (7.8 +/- 6.0 vs. 5.5 +/- 4.2; p = 0.01), not fruit fructose (12.9 +/- 8.0 vs. 11.6 +/- 7.0; p = 0.34). Multivariate logistic regression analysis showed that older age (OR 1.048, 95% CI 1.004-1.094, p = 0.03), severe necroinflammatory activity (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) were independently linked to severe fibrosis. No association was found between fructose intake and liver necroinflammatory activity, steatosis, and the features of NASH. Conclusions: The daily intake of industrial, not fruit fructose is a risk factor for metabolic alterations and the severity of liver fibrosis in patients with G1 CHC.