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Noninvasive Risk Stratification After HCV Eradication in Patients With Advanced Chronic Liver Disease
Georg Semmler1,2, Teresa Binter1, Karin Kozbial1
1Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Insights
Noninvasive markers like liver stiffness measurement and VITRO ratio effectively predict liver decompensation after hepatitis C cure. This aids in stratifying patients with advanced chronic liver disease for personalized management.
Area of Science:
- Hepatology
- Viral Hepatitis Research
- Noninvasive Liver Disease Assessment
Background:
- Hepatitis C virus (HCV) cure is achieved, but risk stratification for complications like hepatic decompensation and hepatocellular carcinoma in patients with advanced chronic liver disease (ACLD) remains challenging.
- Noninvasive markers of portal hypertension, including liver stiffness measurement (LSM) and the von Willebrand factor/platelet count ratio (VITRO), are investigated for their predictive capabilities post-HCV cure.
Purpose of the Study:
- To evaluate the predictive value of noninvasive surrogates of portal hypertension for hepatic decompensation and hepatocellular carcinoma development.
- To assess the utility of LSM and VITRO in risk stratification for patients with ACLD after achieving HCV cure.
Main Methods:
- A cohort of 276 patients with pretreatment ACLD and posttreatment follow-up data on LSM and VITRO were analyzed.
- Liver stiffness measurement (LSM) by transient elastography and the von Willebrand factor/platelet count ratio (VITRO) were measured posttreatment.
- Patients were followed for a median of 36.6 months to assess the development of hepatic decompensation and hepatocellular carcinoma.
Main Results:
- Posttreatment LSM and VITRO demonstrated excellent predictive performance for hepatic decompensation (AUROC 0.875 and 0.925, respectively).
- A combined algorithm using FU-LSM and FU-VITRO successfully stratified patients into low-risk (no decompensation), high-risk (17.4% decompensation at 3 years), and gray-zone groups.
- The algorithm's prognostic value was validated in internal and external cohorts, confirming its reliability in risk assessment.
Conclusions:
- Posttreatment LSM and VITRO are strong, independent predictors of hepatic decompensation in HCV-induced ACLD.
- A combined algorithm utilizing these noninvasive markers effectively rules in/out clinically significant portal hypertension and stratifies patients by risk.
- These accessible markers facilitate personalized management and risk stratification after sustained virological response to HCV therapy.
Background And Aims:
Risk stratification after cure from hepatitis C virus (HCV) infection remains a clinical challenge. We investigated the predictive value of noninvasive surrogates of portal hypertension (liver stiffness measurement [LSM] by vibration-controlled transient elastography and von Willebrand factor/platelet count ratio [VITRO]) for development of hepatic decompensation and hepatocellular carcinoma in patients with pretreatment advanced chronic liver disease (ACLD) who achieved HCV cure.
Approach And Results:
A total of 276 patients with pretreatment ACLD and information on pretreatment and posttreatment follow-up (FU)-LSM and FU-VITRO were followed for a median of 36.6 months after the end of interferon-free therapy. FU-LSM (area under the receiver operating characteristic curve [AUROC]: 0.875 [95% confidence interval [CI]: 0.796-0.954]) and FU-VITRO (AUROC: 0.925 [95% CI: 0.874-0.977]) showed an excellent predictive performance for hepatic decompensation. Both parameters provided incremental information and were significantly associated with hepatic decompensation in adjusted models. A previously proposed combined approach (FU-LSM < 12.4 kPa and/or FU-VITRO < 0.95) to rule out clinically significant portal hypertension (CSPH, hepatic venous pressure gradient ≥10 mm Hg) at FU assigned most (57.3%) of the patients to the low-risk group; none of these patients developed hepatic decompensation. In contrast, in patients in whom FU-CSPH was ruled in (FU-LSM > 25.3 kPa and/or FU-VITRO > 3.3; 25.0% of patients), the risk of hepatic decompensation at 3 years following treatment was high (17.4%). Patients within the diagnostic gray-zone for FU-CSPH (17.8% of patients) had a very low risk of hepatic decompensation during FU (2.6%). The prognostic value of this algorithm was validated in an internal (n = 86) and external (n = 162) cohort.
Conclusion:
FU-LSM/FU-VITRO are strongly and independently predictive of posttreatment hepatic decompensation in HCV-induced ACLD. An algorithm combining these noninvasive markers not only rules in or rules out FU-CSPH, but also identifies populations at negligible versus high risk for hepatic decompensation. FU-LSM/FU-VITRO are readily accessible and enable risk stratification after sustained virological response, and thus facilitate personalized management.
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