August 17, 2013

Industrial, not Fruit Fructose Intake is Associated with the Severity of Liver Fibrosis in Genotype 1 Chronic Hepatitis C Patients

Journal of Hepatology

PII: S0168-8278(13)00553-9

doi:10.1016/j.jhep.2013.07.037

© 2013 Published by Elsevier Inc.

Article in Press

Salvatore Petta, Giulio Marchesini, Linda Caracausi, Fabio Salvatore Macaluso,  Calogero Cammà,  Stefania Ciminnisi, Daniela Cabibi, Rossana Porcasi, Antonio Craxì, Vito Di Marco,

Received 6 February 2013; received in revised form 8 July 2013; accepted 15 July 2013. published online 07 August 2013.
Accepted Manuscript

Abstract

Background and Aims

Unhealthy food intake, specifically fructose, has been associated to metabolic alterations and to the severity of liver fibrosis in patients with non-alcoholic fatty liver disease. In a cohort of patients with genotype 1 chronic hepatitis C(G1CHC), 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 G1CHC 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 > or equal to 20%. Features of nonalcoholic 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(>or equal to 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 G1CHC.

Abbreviations: HCV, hepatitis C virus, G1, genotype 1, CHC, chronic hepatitis C, WC, waist circumference, DCL, dorsocervical lipohypertrophy, WHR, waist-to-hip ratio

Keywords: Fructose, Chronic Hepatitis C, Liver Fibrosis

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1 comment:

  1. Actually an OR of 1.147 is a tiny increased risk. Only ORs above 1.5 are considered suggestive of causation, and it's better if they approach 2.
    However the study was not designed to separate the effects of very high fructose intakes from very low; quintiles would have provided this information.
    in this paper,
    "The Impact of Diet on Liver Fibrosis and on Response to Interferon Therapy in Patients With HCV-Related Chronic Hepatitis"
    a high intake of PUFA is associated with steatosis at OR 2.7 (this will be omega-6 linoleic acid from vege oil - if they had ignored omega-3, the OR would be higher). High intakes of total carbohydrate are associated with fibrosis, OR 2.9
    Monounsaturated fat (MUFA) is protective, saturated fat is neutral (it should be protective too, but is more likely to be associated with dietary cholesterol, a risk factor, whereas MUFA is associated with antioxidants).

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