# Ultrasound-Based Liver Stiffness Surveillance in Patients Treated for Chronic Hepatitis B or C
## 2 Chc  
Among liver fibrosis surveillance reports of patients with CHC, comparisons were made in terms of the therapy (including the untreated group), kinetics of liver stiffness, time elapsed, virologic response, and biochemical response (Table 1). A study [29] reported the kinetics and correlates of liver stiffness over an elapsed time on 126 patients with CHC who received pegIFN-based therapy. At the EOT, 48 weeks after the EOT, and 96 weeks after the EOT, liver stiffness declined significantly from the baseline in the group with sustained virologic response (SVR; \(n=57\); \(-16.2\%\), \(-32.2\%\), and \(-43.5\%\) change, respectively) compared with the non-SVR group (\(n=69\); \(-7.2\%\), \(-2.1\%\), and \(+17.3\%\) change, respectively; \(p=0.0127\), \(p<0.0001\), and \(p<0.0001\), respectively). After further stratification by biochemical responses, at the EOT, 48 weeks after the EOT, and 96 weeks after the EOT, liver stiffness still declined significantly in patients with a biochemical response (\(n=16\); \(-17.9\%\), \(-30.0\%\), and \(-27.1\%\), respectively) compared with the group without a biochemical response (\(n=53\); \(-4.1\%\), \(+6.4\%\), and \(+30.6\%\), respectively; \(p=0.0270\), \(p<0.0001\), and \(p<0.0001\), respectively) among patients without SVR. Therefore, both virologic response and biochemical response influenced the decline in liver stiffness. In another study including 180 patients [30], liver stiffness declined significantly from the baseline in the SVR (\(n=93\)) and relapse (\(n=28\)) groups, but not in the nonresponder (\(n=24\)) or untreated (\(n=35\)) group. Correlation among the declines in liver stiffness were further estimated through univariate and multiple regressions in the group with relatively high pretreatment liver stiffness values (deduced as METAVIR F3 or F4 stages, \(n=67\)). This indicated that the beneficial effects of pegIFN-based therapy on the decline in liver stiffness were independently associated with milder fibrosis stage (also indicated by a lower hyaluronic acid level), more severe inflammatory activity (indicated by a higher alanine aminotransferase (ALT) level) at the baseline, virologic response, and a longer pegIFN therapy course. The reason for this result is that liver stiffness typically reflects the degrees of both fibrosis and necroinflammation and that pretreatment fibrosis is inversely correlated with treatment response. SVR is approximately equivalent to the cessation of viral replication, necroinflammation, and fibrosis progression [31]. Patients with long-term virus-eradicated status after SVR develop fewer adverse outcomes, such as cirrhosis, decompensation, and hepatocellular carcinoma, than those without SVR do. In general, post-treatment SVR status outweighed baseline hepatitis C virus (HCV) RNA in the studies to correlate with significant declines in liver stiffness. Apart from studies in which the cohorts were not stratified [32; 33; 34; 35; 36], non-SVR generally accounted for nonsignificant declines in liver stiffness. However, those who experienced a relapse in the non-SVR group still could exhibit significant declines in liver stiffness [30; 37; 38]. In the untreated groups recruited in various studies [29; 30; 37], nonsignificant declines in liver stiffness were observed throughout the timeframes. However, SVR does not necessarily terminate the progression of disease course, particularly in patients with advanced cirrhosis at the baseline [4]. In a cohort of patients (\(n=226\)) with HCV-related cirrhosis and clinically significant portal hypertension (CSPH) receiving DAA therapy, hepatic vein pressure gradient decreased by 10% in 62% of patients but CSPH persisted in 78% of patients despite achieving SVR. One third of patients with a reduction in liver stiffness measurement to below 13.6 kPa (cutoff for ruling out CSPH at the baseline) after SVR still had CSPH, indicating the suboptimal discriminative capacity of liver stiffness measurement for patients with CSPH after an SVR [22].