# Ultrasound-Based Liver Stiffness Surveillance in Patients Treated for Chronic Hepatitis B or C
## 3 Chb
\begin{table}
\begin{tabular}{c c c c c c} \hline \hline
**Study/Year** & **Size** & **Follow-Up Timeframes** & **Baseline Pathology** & **Multiple Biopsies** & **LS-Decline Correlates** \\ \hline [PERSON] 2011 [52] & 45 & Baseline–yearly-\(\gamma\)5/\(\gamma\)3–\(\gamma\)5 & Yes & No & NA \\ \hline \multirow{3}{*}{[PERSON] 2011 [51]} & \multirow{3}{*}{426} & \multirow{3}{*}{Baseline-\(\gamma\)3} & \multirow{3}{*}{No} & \multirow{3}{*}{No} & Subsequent ALT \\  & & & & & normalization in the \\  & & & & & treated/persistently normal \\ \hline [PERSON] 2014 [53] & 83 & 411.5 \(\pm\) 149.5 days & No & No & NA \\ \hline [PERSON] 2017 [7] & 534 & Baseline–wk24–wk102 & Yes & Yes & * Higher changes of [PERSON] stage \\ \hline \multirow{3}{*}{[PERSON] 2017 [54]} & \multirow{3}{*}{334} & \multirow{3}{*}{24 wk} & \multirow{3}{*}{No} & Higher baseline AST/lower \\  & & & & & ALT/higher \\  & & & & & \(\alpha\)-stepforegni/higher \\  & & & & LS/longer course of \\  & & & & & antiviral therapy \\ \hline \multirow{3}{*}{[PERSON] 2017 [50]} & \multirow{3}{*}{120} & Baseline–yearly-\(\gamma\)5 & Yes & No & Lower baseline LS values \\  & & & & & (<12.0 kPa) \\ \hline [PERSON] 2017 [8] & 71 & Baseline–wk26–wk35–wk204 & Yes & Yes & Higher baseline LS \\ \hline [PERSON] 2018 [55] & 189 & Baseline–wk24 & No & No & Higher baseline LS \\ \hline [PERSON] 2018 [56] & 104 & Baseline-\(\gamma\)3 & Yes & No & NA \\ \hline \hline \end{tabular} \(\;\)LS, liver stiffness; wk, week; y, year; LS decline, defined as the value equal to the baseline minus the follow-up; NA, not available; \({}^{\text{a}}\) for the group with paired liver biopsies.  
\end{table} 
Table 2: Published studies on liver stiffness surveillance in patients with chronic hepatitis B. Therefore, biochemical response, followed by fibrosis reversal and time elapsed, but not the virologic response, aided in understanding of the liver stiffness kinetics in the CHB cohort under surveillance. In conclusion, liver stiffness could be a promising and significant biomarker in evaluating CHC or CHB across on- and off-treatment timeframes [44; 57]. Elastography-based liver-stiffness surveillance alone conveys chronological and informative patient information. In addition, it facilitates the characterization of patient cohorts undergoing antiviral treatment worldwide by collaboratively delineating the time elapsed, virologic response, biochemical response, and fibrosis reversal. In groups with uniform virologic responses to DAAs for CHC and nucleoside and nucleotide analogs for CHB, declines in liver stiffness can be explained by the early concurrent biochemical response over time (from 24 weeks to 3 years), followed by fibrosis reversal and time elapsed. Future studies should quantify the concurrent true liver collagen content and define the fibrosis stage to help specify the kinetics and validate the cutoff values of liver stiffness when dichotomizing fibrosis stages over time. This review was supported in part by a grant (MOST 104-2314-B-039-014) from the Ministry of Science and Technology, Taiwan. This manuscript was edited by Wallace Academic Editing. [PERSON] and [PERSON] performed the reviews; [PERSON] and [PERSON] wrote the paper. The authors declare no conflicts of interest.