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<p>Mac-2-binding protein glycosylation isomer (M2BPGi), a promising biomarker for predicting hepatocellular carcinoma (HCC), was evaluated in predicting HCC occurrence after hepatitis C virus (HCV) cure with direct-acting antivirals (DAAs). 704 eligible patients underwent biannual surveillance, including alpha-fetoprotein (AFP) and liver imaging studies, to detect HCC occurrence. Serum M2BPGi levels were measured at both pretreatment and sustained virologic response (SVR<sub>12</sub>). The cumulative HCC incidence was estimated by Kaplan-Meier analysis, and risk factors by Cox proportional hazards models. During a median follow-up of 4.5 years, 50 patients (7.1%) developed HCC, with cumulative incidence rates of 7.8% and 12.8% at 5 and 10 years. HCC incidence was higher in patients with pretreatment M2BPGi ≥ 4.0 and SVR12 ≥ 2.0 (<i>p</i> &lt; 0.001). Multivariable analysis identified that M2BPGi levels ≥ 4.0 COI at pretreatment (adjusted hazard ratio [aHR]: 3.33; 95% confidence interval [CI]: 1.54–7.23, <i>p</i> = 0.002) and ≥ 2.0 COI at SVR<sub>12</sub> (aHR: 2.60; 95% CI: 1.16–5.79, <i>p</i> = 0.020) were significantly associated with HCC occurrence in addition to age, sex, liver stiffness measurement (LSM), alanine transaminase (ALT) quotient, and AFP. In conclusion, serum M2BPGi may serve as a valuable biomarker for HCC risk after HCV cure with DAAs.</p>

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Serum Mac-2 binding protein glycosylation isomer in predicting hepatocellular carcinoma occurrence among patients with direct-acting antiviral-induced HCV cure

  • 期刊论文

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  • 发表日期：

    2026年1月19日

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  • Yu-Ping Chang,
  • Yun-Chu Chen,
  • Tung-Hung Su,
  • Shang-Chin Huang,
  • Tai-Chung Tseng,
  • Pei-Jer Chen,
  • Chun-Jen Liu,
  • Jia-Horng Kao,
  • Chen-Hua Liu

摘要

Mac-2-binding protein glycosylation isomer (M2BPGi), a promising biomarker for predicting hepatocellular carcinoma (HCC), was evaluated in predicting HCC occurrence after hepatitis C virus (HCV) cure with direct-acting antivirals (DAAs). 704 eligible patients underwent biannual surveillance, including alpha-fetoprotein (AFP) and liver imaging studies, to detect HCC occurrence. Serum M2BPGi levels were measured at both pretreatment and sustained virologic response (SVR12). The cumulative HCC incidence was estimated by Kaplan-Meier analysis, and risk factors by Cox proportional hazards models. During a median follow-up of 4.5 years, 50 patients (7.1%) developed HCC, with cumulative incidence rates of 7.8% and 12.8% at 5 and 10 years. HCC incidence was higher in patients with pretreatment M2BPGi ≥ 4.0 and SVR12 ≥ 2.0 (p < 0.001). Multivariable analysis identified that M2BPGi levels ≥ 4.0 COI at pretreatment (adjusted hazard ratio [aHR]: 3.33; 95% confidence interval [CI]: 1.54–7.23, p = 0.002) and ≥ 2.0 COI at SVR12 (aHR: 2.60; 95% CI: 1.16–5.79, p = 0.020) were significantly associated with HCC occurrence in addition to age, sex, liver stiffness measurement (LSM), alanine transaminase (ALT) quotient, and AFP. In conclusion, serum M2BPGi may serve as a valuable biomarker for HCC risk after HCV cure with DAAs.