# Ultrasound-Based Liver Stiffness Surveillance in Patients Treated for Chronic Hepatitis B or C
## 1 Introduction  
Chronic hepatitis (CH) B and C treatment is a major global healthcare challenge. Antiviral treatment can alter natural history and reduce risks of cirrhosis, hepatic decompensation, and hepatocellular carcinoma [1; 2]. Antiviral therapy in patients with CHB with decompensated cirrhosis improves hepatic reserve and reduces mortality [2; 3]. With the advent of direct-acting antivirals (DAAs) for CHC, recent studies have demonstrated that DAA therapy can improve hepatic reserve and delay progression in patients with CHC with decompensated cirrhosis [4]. Furthermore, most patients with CHB or CHC--even those without a treatment response--benefit from antiviral treatment, evidenced by a marked early resolution in hepatic necorinflammation [5; 6] and a fibrosis reversal over time [7; 8].  
However, a virologic response to CHB or CHC treatment does not ensure zero risk of liver-related adverse endpoints after virologic response [9; 10; 11]. Therefore, both on-treatment and off-treatment parameters over time should be investigated to further gain insight into the natural history and treatment-modified disease course of chronic viral hepatitis [10; 11; 12].  
Elastography noninvasively quantifies tissue elasticity and stiffness. By using external or internal impulses, elastographic techniques determine tissue stiffness by calculating tissue strains or shearwave velocities [13]. Currently, in noninvasive liver fibrosis evaluation in either a clinical or research setting [14], baseline liver stiffness is a well-established and promising noninvasive biomarker for assessing pretreatment fibrosis in patients with chronic liver diseases [15] and for predicting liver-related events [16]. The evolving modes of ultrasound-based elastography possess promising and comparable validity and reliability for evaluating fibrosis [17; 18], despite the limitations, ranging from poor acoustic windows to the motion effects related to measurement variability [19].  
Recent studies have further revealed that liver stiffness measurement is a promising solution to modeling liver disease progression and regression on a continuous noncategorical scale as changes in liver stiffness per year or liver stiffness progression or regression rate to refine liver stiffness measurement-based prognostics [7; 20; 21; 22; 23]. Regarding the heterogeneous surveillance intervals in reports using liver stiffness measurements, the durations were significantly shorter either during treatment or between the end of treatment (EOT) and follow-up in patients with CHB and CHC than those reported in histological studies with follow-up periods of up to 10 years [24; 25]. Studies applying paired liver biopsies (pre- and post-antiviral treatment) have reported rates of cirrhosis reversal of up to 74% of patients with CHB and 18-64% of patients with CHC with cirrhosis over long-term intervals of up to 5 and 10 years, respectively [9; 24; 25; 26]. Nonetheless, the paradigms of liver stiffness measurements have shifted focus from the outdated cross-sectional liver fibrosis staging alone to comprehensive liver-relevant risk estimation [27]. However, diverse ranges of cohort characteristics, disease types, surveillance protocols and timeframes, and necroinflammatory resolution or biochemical responses, factors explaining the magnitude or kinetics in liver stiffness change, virologic responses, fibrosis reversals, and noninvasive surveillance results have rarely been reviewed collectively [28].  
In this study, we searched and reviewed representative reports on liver stiffness surveillance with no less than two surveillance visits in PubMed, Medline, and Cochrane Library databases for papers published between January 2010 and January 2018. Articles not written in English were excluded.