4 to 4.4-fold in the former and 1.2 to 1.6-fold in the latter group, selleck bio P = 0.019). Altogether these findings confirm our original observation and other more recent reports on the major influence of the biochemical profile on LS in the setting of both acute and chronic liver damage[8-10]. Finally, we found that prolonged biochemical remissions were associated with progressive reductions of FS values. LS declined yearly at about 0.2-fold in treated patients followed-up prospectively for 48 mo, and a proportion of patients who maintained evidence of cirrhosis at US achieved values of FS < 11.8 kPa. This was responsible for the worse diagnostic performance of FS in treated patients in whom the sensitivity for detecting cirrhosis fell from 86.5% to 54.2% in untreated vs treated patients with fibrosis �� S5 (Table (Table6).

6). Altogether, these data suggest a non-linear correlation between the overall kinetics of LS and histological staging during antiviral treatment. Future studies should be addressed to understand the relations among the reductions of LS, necrosis, inflammation and fibrosis in the separate settings of different fibrosis stages (i.e. �� S3/< S3 and presence/absence of cirrhosis) and liver disease etiology (i.e. HBV and HCV). In fact, much of the LS changes depend on the different elastic relations among fine blocks of the liver structure. Thus, the interplay between the extent and structure of the collagen septa within the fine liver block, and the different type and extent of liver inflammatory infiltrate within them, might account for both the different FS cut-offs between CHB and CHC patients and for the different kinetics of FS and fibrosis decline during antiviral therapy.

In conclusion, our study suggests that the LS provides a useful non-invasive tool to monitor liver disease in the chronic HBV carrier. In the inactive carrier, it helps to identify non-HBV-related causes of liver damage and transient reactivation of HBV liver disease. In the CHB patient, provided that the pattern of biochemical activity is taken into account, LS values < 7.5 exclude Cilengitide the presence of significant fibrosis (�� S3) with a high NPV (97.3%) and low negative likelihood ratio (0.07). FS values �� 11.8 kPa are highly specific (96.3%) for cirrhosis and show good PPV (86.5%) and positive likelihood ratio (23.18). In the HBV carrier with LS values ranging from 7.5 to 11.8 kPa, which are indicative of significant liver disease, liver biopsy remains the gold standard for an accurate grading and staging of liver disease. Finally, in CHB patients the monitoring of LS appears useful to highlight major changes in intrahepatic liver disease and warrants a more appropriate timing for control liver biopsies.