Author information

¹Division of Gastroenterology and Hepatology, Miami VA Medical System, Miami, Florida; Division of Digestive Health and Liver Diseases, University of Miami Miller School of Medicine, Miami, Florida. Electronic address: binu.john@miami.edu.

²Department of Health Behavior and Policy, Virginia Commonwealth University, Richmond, Virginia.

³Division of Gastroenterology and Hepatology, University of Pennsylvania and Philadelphia VA Medical Center, Philadelphia, Pennsylvania.

⁴Division of Gastroenterology and Hepatology, Portland VA Medical Center and Oregon Health University, Portland, Oregon.

⁵Section of Digestive Diseases, Yale School of Medicine and VA Connecticut Healthcare System, West Haven, Connecticut.

⁶Department of Surgery, Miami VA Medical System, University of Miami Miller School of Medicine, Miami, Florida.

⁷Division of Digestive Health and Liver Diseases, University of Miami Miller School of Medicine, Miami, Florida.

⁸Department of Radiation Oncology, Central Virginia Health System and Virginia Commonwealth University, Richmond, Virginia.

Abstract

Background & aims: Patients with cirrhosis secondary to chronic hepatitis C virus (HCV) are at risk for hepatocellular carcinoma (HCC) despite a sustained virological response (SVR). We examined whether post-SVR liver stiffness measurement (LSM) could be used to stratify HCC risk.

Methods: This was a retrospective cohort study of 1850 participants identified from the Veterans Health Administration, with HCV cirrhosis and SVR, followed up over 5099 person-years, from the time of post-SVR elastography until death, HCC, or the end of the study.

Results: The risk of HCC increased by 3% with every 1-kPa increase in LSM (adjusted hazard ratio [aHR], 1.03, 95% confidence interval [CI], 1.01-1.04; P < .001) and decreased with the number of years from SVR (aHR, 0.79; 95% CI, 0.70-0.90; P = .0003). The adjusted annual risk of HCC was 2.03% among participants with post-SVR LSM <10 kPa, 2.48% in LSM 10-14.9 kPa (aHR, 1.71; 95% CI, 1.01-2.88; P = .046), 3.22% for LSM 15-19.9 kPa (aHR, 1.59; 95% CI, 0.78-3.20; P = .20), 5.07% among LSM 20-24.9 kPa (aHR, 2.55; 95% CI, 1.30-5.01; P = .01), and 5.44% in LSM ≥25 kPa (aHR, 3.03; 95% CI, 1.74-5.26; P < .0001). The adjusted annual risk of HCC was < 0.4% in participants with LSM <5 kPa and without diabetes mellitus.

Conclusions: LSM predicts rates of HCC in patients with HCV cirrhosis after SVR at multiple cutoff levels and offers a single test to predict portal hypertension-related complications and HCC. Patients with LSM <5 kPa in the absence of diabetes mellitus had a low risk of HCC in which surveillance could be discontinued.