Age-male-albumin-bilirubin-platelet score stratifies hepatocellular carcinoma risk after sustained virological response in hepatitis C-related compensated advanced chronic liver disease

Abstract

BACKGROUND

Hepatocellular carcinoma (HCC) remains an important long-term complication after sustained virological response (SVR) in patients with hepatitis C virus (HCV)-related compensated advanced chronic liver disease (cACLD). Current guidelines generally recommend lifelong semiannual surveillance for patients with advanced fibrosis or cirrhosis; however, the residual risk of HCC after viral eradication is heterogeneous. We hypothesized that simple noninvasive scores could identify a very-low-risk subgroup suitable for individualized surveillance intensity.

AIM

To compare the performance of noninvasive scores for predicting HCC after SVR and to identify a very-low-risk subgroup.

METHODS

This single-center retrospective cohort study included 571 adults with HCV-related cACLD who achieved SVR at 12 weeks after treatment completion following interferon-free sofosbuvir-based direct-acting antiviral therapy between 2013 and 2023. The fibrosis-4 index, aspartate aminotransferase-to-platelet ratio index, albumin-bilirubin score, and age-male-albumin-bilirubin-platelet (aMAP) score were calculated. HCC risk was evaluated using Kaplan-Meier analysis, Cox proportional hazards regression, and time-dependent receiver operating characteristic curves at 1 year, 3 years, 5 years, and 8 years.

RESULTS

During a median follow-up of 4.59 years, 78 patients (13.7%) developed de novo HCC [annual incidence rate: 3.12%; 95% confidence interval (CI): 2.50-3.80]. Compared with those who did not develop HCC, patients who developed HCC had higher baseline liver stiffness, higher prevalence of diabetes mellitus and esophageal varices, lower platelet counts and albumin levels, and higher bilirubin levels. Among the evaluated scores, the aMAP score showed the highest discriminatory performance, with an 8-year area under the receiver operating characteristic curve of 0.74 (95%CI: 0.67-0.80). An exploratory aMAP threshold of < 55 identified 18.6% of patients with no observed HCC events, whereas patients with an aMAP score ≥ 60 had the highest annual HCC incidence of 6.42% per year.

CONCLUSION

The aMAP score effectively stratifies the risk of HCC after SVR and may support individualized surveillance intensity in patients with HCV-related cACLD. However, the exploratory aMAP threshold requires external validation.

Keywords: Hepatitis C virus; Compensated advanced chronic liver disease; Direct-acting antiviral therapy; Sustained virological response; Hepatocellular carcinoma; Age-male-albumin-bilirubin-platelet score; Risk stratification; Surveillance de-escalation

Core Tip: This retrospective cohort study evaluated the age-male-albumin-bilirubin-platelet (aMAP) score for predicting hepatocellular carcinoma (HCC) risk after sustained virological response in patients with hepatitis C virus-related compensated advanced chronic liver disease. Among 571 patients followed for a median of 4.59 years, 78 developed HCC. The aMAP score outperformed other noninvasive scoring systems, and an exploratory threshold of < 55 identified 18.6% of patients with no observed HCC events. These findings suggest that the aMAP score may support individualized surveillance intensity; however, the threshold requires external validation before routine clinical implementation.