FIB 4 values inversely correlated with TGF-beta1 (Rho correlation coefficient −0.38; p=0.0155). as well as with liver stiffness values (Rho
correlation coefficient −0.31; p=0.0498. CD14 (soluble and surface) levels were significantly different between HIV+ vs the healthy controls, HIV+HCV+ vs the healthy controls, HCV+ vs HIV+ HCV+ (p< 0.0001, Kruskal-Wallis test). IL17 was significantly different between HCV+ vs the others 3 groups. Bacterial DNA Crizotinib datasheet was significantly different in HIV+ vs the others 3 groups Conclusions: Foxp3+ levels are higher in patients with HIV, but they do not influence liver fibrosis staging. TGF-b1 levels inversely correlate with fibrosis suggesting a protective effect. Our data show that the group of HIV- HCV+ has increased levels of bacterial DNA, CD14 (soluble and surface) and IL17 expression of a major translocation as compared with the others groups. The existent correlation between the translocation index and FIB4 suggest that fibrosis stage JAK inhibitor may depend on immunoactivation caused by bacterial translocation Disclosures: The followinq
people have nothinq to disclose: Paolo Sacchi, Raffaele Bruno, Serena M. Cima, Marta Corbella, Giuditta Comolli, Antonella Chiesa, Fausto Baldanti, Catherine Klersy, Stefano Novati, Mara Mariconti, Claudio Baldi Background/Aims: Biological and epidemiological data suggest that vitamin D levels may influence cancer development. Several single nucleotide polymorphisms have been described in the vitamin D receptor (VDR) gene in association with cancer risk. We aimed to investigate the association of VDR polymorphisms with hepatocellular carcinoma MCE公司 (HCC) development in chronic hepatitis C patients. Methods: In a cross-sectional, hospital-based setting, 340 patients (201 chronic hepatitis, 47 cirrhosis and 92 HCC) and 100 healthy controls receiving VDR genotyping (bat-haplotype: Bsml rs1544410 C, Apal rs7975232 A and Taql rs731236 A) and interleukin (IL)−28B genotyping
were enrolled. Results: Patients with HCC had a higher frequency of Apal CC genotype (P=0.018) and bAt[CCA]-hapiotype (P=0.019) as compared to control subjects. There were no differences in Bsml, Taql and IL28B polymorphisms between two groups. In patients with chronic hepatitis C, HCC subjects had a higher frequency of Apal CC genotype and bAt[CCA]-haplotype than those with chronic hepatitis (P=0.001 and 0.002, respectively) and cirrhosis (P=0.019 and 0.026, respectively). After adjusting age and sex, logistic regression analysis showed that Apal CC genotype (odds ratio: 3.02, 95% confident interval: 1.65-5.51) was independently associated with HCC development. Conclusion: VDR Apal polymorphism may play a role in the development of HCC among chronic hepatitis C patients. Further explorations of this finding and its implications are required.