7 vs. 14.6 kPa, P>0.05). All these results might have caused some overlapping values www.selleckchem.com/products/17-AAG(Geldanamycin).html between patients with F3 and F4. The prediction of LRE development using LSM was imperfect. Although patients with baseline LSM values >19 kPa were at a significantly greater risk of LRE development (HR, 7.176) than were those with baseline LSM values ��19 kPa, 55.6% of patients with LSM values >19 kPa developed no LRE and 6.9% of those with LSM values ��19 kPa did. In the sub-group analysis, we found no significant predictor of discordant results regarding LRE development. Because this finding might be related to statistical error due to the short-term follow-up period and the low number of LREs, large-scale studies with long-term follow-up are needed to elucidate a novel serological predictor of LRE development.

When we increased the sensitivity of cutoff LSM value up to 89.5%, 9.1 kPa was selected. Using this cutoff value, we can clinically identify the sub-group of patients at low risk of LRE development (1.6%), such that these patients can be reassured. LSM has been known to predict fibrosis regression in response to long-term antiviral treatment [46]. Thus, we further analyzed the role of LSM as a dynamic indicator of LRE development using cutoff LSM values of 19 kPa or relative change in LSM values from baseline, but the results were negative. However, small sample size of some groups (n=11 and 12, respectively) might be related to type II error. Furthermore, because the study by Jung et al.

[14] revealed that LSM change, similar to baseline LSM value, can influence HCC development, large cohorts with sufficient events will likely be required to investigate the usefulness of serial LSM value follow-up in patients with chronic viral hepatitis. We included only patients with histologically advanced liver fibrosis (��F3). However, because histologic evaluation grades liver fibrosis categorically, it cannot exactly represent the continuous spectrum of liver fibrosis, especially between adjacent fibrosis grades. Furthermore, because histologic evaluation of liver fibrosis can be influenced by intra- and interobserver variability, the over- or underestimation of liver fibrosis inevitably occurs. Considering these limitations of histologic evaluation, some patients who were excluded due to F0�CF2 liver fibrosis may represent underestimations of F3 or F4 fibrosis, which might have resulted in selection bias, a major limitation of this study.

Thus, further validation of LSM cutoff values for predicting advanced liver fibrosis regardless of histologic data should be performed. Furthermore, the significantly higher proportion of patients with F4 fibrosis may be another bias of this study. Batimastat In conclusion, our data suggest that LSM can be a useful predictor of LRE development in CHB patients showing histologically advanced liver fibrosis.