4 kPa) compared to rapid fibrosers (median 8.9, 10.9, 11.8, and 13.0 kPa). The 12-month staging was significantly correlated with TE values at month 6 (rho = 0.48, P = 0.006), at month

9 (rho = 0.78, P < 0.0001), and at month 12 (rho = 0.83, P < 0.0001). Rapid fibrosers had significantly higher aspartate aminotransferase serum levels at 3, 6, 9, 12 months, γ-glutamyl transferase serum levels at 6 and 12 months, bilirubin at 6 months, and TE values at 6, 9, and 12 months compared to slow fibrosers. Moreover, rapid selleckchem fibrosers were more often recipients of aged grafts compared to slow fibrosers, further confirming the prognostic relevance of donor age in this setting of patients. In results from a longitudinal mixed model for repeated measurements,

the slope of TE variations was significantly greater in rapid fibrosers (0.40 kPa/month) than in slow fibrosers (−0.05 kPa/month) (P < 0.0001; Fig. 1), further confirming the results of the study by Carrion et al. (0.42 and 0.05 kPa/month in rapid and slow fibrosers, respectively).2 The rates of patients with TE > 7.9 kPa, the optimal TE cut-off for S ≥ 3 diagnosis previously identified by us,3 at 3, 6, 9, and 12 months were 29%, 26%, 31%, and 28% in slow fibrosers and 60%, 67%, 100%, and 95% in rapid fibrosers (P = 0.22, P = 0.06, P = 0.001, and P = 0.001, respectively). By logistic regression analysis, TE > 7.9 kPa at month 6 was the only independent predictor of significant fibrosis at month 12 (P = 0.02, odds ratio = 6.0, 95% confidence interval = 1.2-28.8). By applying MK-2206 nmr in our cohort the bilirubin plus TE model constructed by Carrion et al.2 for identifying rapid fibrosers at month 6, we could correctly classify 67% of our rapid fibrosers, compared to 70% of rapid IKBKE fibrosers identified by Carrion et al. Interestingly, the 7.9 kPa TE cut-off at month 6 could identify the same proportion (67%) of rapid fibrosers in our cohort. In conclusion,

in an external validation group of liver graft recipients with recurrent hepatitis C, repeated TE examinations early after OLT helped to identify patients at risk of progressive graft disease, with a potential benefit for clinical management. Cristina Rigamonti*, Maria Francesca Donato*, Massimo Colombo*, * First Division of Gastroenterology, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy. “
“Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois College of Medicine at Chicago, Chicago, IL, USA Activation of hepatic stellate cells and development of chronic inflammation are two key features in the progression of hepatic fibrosis. We have shown that in vitro activated stellate cells increase their expression of CXCL12 as well as the receptor CXCR4 and that receptor engagement promotes a profibrogenic phenotype.