The Impact of Diet on Liver Fibrosis and on Response to Interferon Therapy in Patients With HCV-Related Chronic Hepatitis

Carmela Loguercio, MD; Alessandro Federico, MD; Mario Masarone, MD; Roberto Torella, MD; Marcello Persico, MD


Am J Gastroenterol. 2008;103(12):3159-3166. 

In This Article


Table 1 shows the baseline demographic and metabolic data of the HCV-positive patients and controls. The BMI did not differ between the two groups. The prevalence of alterations in plasma lipid profiles (hypercholesterolemia and/or hypertriglyceridemia) ranged between 15% and 40%, and there were no differences between the two groups or between men and women (data not shown).

Table 2 and Table 3 , respectively, show the intake of micronutrients and macronutrients in patients and controls together with the daily amounts recommended in Italy. We found no differences in nutrient intake between the HCV-positive patients and the control group. However, within each group there were some differences, albeit not significant, related to gender. In both groups, total calorie intake was inversely correlated with age P < 0.01). The intake of animal proteins, carbohydrates, and lipids was directly related to plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (P < 0.01); BMI was related with gamma-glutamyltranspeptidase (γGT) and blood glucose (P < 0.01) (data not shown).

Alcohol was constantly consumed by 60% of liver patients and controls ( Table 4 ). There was no difference in the daily intake of alcohol between HCV patients and controls (median: 46 g and 50 g, respectively, range 10-100 g). Moreover, 48% of men affected by HCV continued to consume >40 g alcohol/day (see Table 4 ). We next divided patients according to the presence/absence of liver cirrhosis, and found no difference between the groups or between men and women (data not shown).

Liver Histology

At liver histology, 58% of patients were affected by steatosis, which was mild in 15%, moderate in 33%, and severe in 10% of cases. The results of the univariate analysis of the association of histology with demographic, dietary, and biochemical parameters in our HCV patients is shown in Table 5 (significant associations are reported in boldface). Alcohol intake was significantly correlated with fibrosis (P < 0.001) and histological steatosis (P < 0.05). Moreover, the variables significantly associated with fibrosis or steatosis were predictive of more severe grading, staging, and steatosis, except for alcohol that was inversely associated with grading. We next included the variables significantly associated with histological parameters in a multivariate analysis. The results showed that the only factors predictive of liver damage, calculated by using the histological scores as continuous variables, were age, BMI, and fasting blood glucose levels. The OR were: age >50 yr versus steatosis: OR 2.7 (0.8-3.4); versus inflammation: OR 4.3 (2.5-11.7); versus fibrosis: OR 7.5 (3.5-18.0). BMI > 25 versus steatosis: OR 1.5 (0.8-2.3); versus inflammation: OR 0.4 (0.2-0.9); versus fibrosis: OR 3.6 (2.1-10.8). Blood glucose versus steatosis: OR 1.3 (0.2-2.7); versus inflammation: OR 0.4 (0.1-0.9); versus fibrosis: OR 1.9 (0.9-2.7).

Lastly, we carried out a logistic regression analysis with the components of diet as continuous variables and with all the variables that were significantly related to staging, grading, or steatosis. We adjusted for the confounding effects of age (≤50 yr vs >50) and BMI (<25 vs≥25), and found that alcohol was the independent factor most closely related to liver damage (OR 4.6; 95% CI 2.7-10.8) ( Table 6 ).

RESPONSE TO IFN. The univariate analysis of epidemiological, nutritional, and histological factors in relation to the response to antiviral treatment is shown in Table 7 . Besides the association between gender, age, genotype, and fibrosis, also obesity, some nutrients, and alcohol consumption were significant. At multivariate analysis, age, BMI, steatosis, fibrosis, and HCV genotypes were independent predictors of the outcome to therapy in our HCV-infected patients ( Table 8 ).


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