293; group C versus group D, P = 0.165) were not significant, although the comparison of group A versus group B was close to statistical significance (P = 0.053). Accordingly, among the components of the chi-squared test (final value, 23.7), when comparing the SVR rates among the four groups, the major contribution was provided

by group A (chi-squared, 15.9; P < 0.01). this website In patients with easy-to-treat HCV genotypes, no association was detected between the combined assessment of the IL-28B rs12979860 C/T polymorphism and the serum vitamin D level and the rate of SVR achievement: group A, 17/22 (77.3%); group B, 19/22 (86.4%); group C, 29/32 (90.6%); and group D, 22/25 (88.0%) (P = 0.251) (Fig. 1). Because SVR rates were significantly influenced by the interaction between IL-28B genotypes and vitamin D serum levels only in difficult-to-treat HCV genotypes (Fig. 1), further analysis was performed only in this subgroup

of patients. Stepwise logistic regression analysis was performed to verify whether the combined assessment of the IL-28B genotype and the serum vitamin Cisplatin manufacturer D level could be an independent predictor of SVR achievement. The variables included were those listed in Table 3 (except for liver histology due to insufficient data) and pretreatment serum vitamin D level, either alone or in combination with the IL-28B genotype, as in groups A-D. The only independent predictors of SVR selected by the analysis were the combined assessment of the IL-28B genotype and the serum vitamin D level and Phospholipase D1 baseline HCV RNA level, with an area under the ROC curve of 0.854 (Table 7). In the analysis of both pretreatment and in-treatment variables, RVR was the strongest predictor of SVR (OR 22.5, 95% CI 5.16-98.5; P < 0.001). Recently, it has been recognized that vitamin D deficiency is common among patients with chronic liver disease. This trend occurs not only in patients with chronic cholestatic liver disease or advanced fibrosis/cirrhosis, where it can be

expected, but also in mild chronic hepatitis C.21 In chronic cholestasis, decreased intestinal absorption of vitamin D is a plausible mechanism for vitamin D deficiency, whereas in end stage liver disease, an impaired liver synthesis of 25-OH vitamin D may occur.22 The reasons why vitamin D deficiency occurs in patients with chronic hepatitis C are far less clear. An explanation of this finding likely requires taking into account the multiple interconnections between vitamin D, the immune response, and inflammatory status.23, 24 In agreement with the above reports, in the present study that included only patients with chronic hepatitis C, the occurrence of vitamin D deficiency (≤20 ng/mL) was observed in approximately one-half of the patients and severe vitamin D deficiency (≤10 ng/mL) in approximately 16% of them.