External validation of models to predict hepatocellular carcinoma in Hepatitis C Virus cured F3‐F4 patients

• Published in: United European gastroenterology journal Vol. 12; no. 7; pp. 901 - 910
• Main Authors: Carvalho‐Gomes, Ângela, Valcheva Valcheva, Tsveta Vladi, Sahuco, Iván, Vidal, Enrique, Martínez‐Arenas, Laura, Vinaixa, Carmen, Aguilera, Victoria, García García, Sónia, Berenguer, Marina
• Format: Journal Article
• Language: English
• Published: England John Wiley and Sons Inc 01.09.2024
• Subjects: HCC‐models; Hepatitis C Virus; Hepatobiliary; hepatocellular carcinoma; Original; patient monitoring; sustained viral response; sustained viral response; HCC‐models; patient monitoring; hepatocellular carcinoma; Hepatitis C Virus
• ISSN: 2050-6406; 2050-6414; 2050-6414
• DOI: 10.1002/ueg2.12571

Background & Aims Several hepatocellular carcinoma (HCC) risk‐models have been developed to individualise patient surveillance following sustained viral response (SVR) in Hepatitis C Virus patients. Validation of these models in different cohorts is an important step to incorporate a more personalised risk assessment in clinical practice. We aimed at applying these models to stratify the risk in our patients and potentially determine cost‐saving associated with individualised HCC risk‐stratification screening strategy. Methods Patients with baseline F3‐4 fibrosis treated with new oral direct‐acting antivirals who had reached a SVR were regularly followed as part of the HCC surveillance strategy. Six models were applied: Pons, aMAP, Ioannou, HCC risk, Alonso and Semmler. Validation of the models was performed based on sensitivity and the proportion of patients labelled as “high risk”. Results After excluding 557 with less than 3 fibrosis, 12 without SVR, 18 with a follow up (FU) <1 year, 17 transplant recipients, 16 lost to FU and 31 with HCC at time of antiviral therapy, our cohort consisted of 349 F3‐4 SVR patients. Twenty‐three patients (6.6%) developed HCC after a median FU of 5.12 years. The sensitivity of the different models varied between 0.17 (Semmler7noalcohol) and 1 (Alonso A and aMAP). The lowest proportion of high‐risk patients corresponded to the Semmler‐noalcohol model (5%). Sixty‐three and 90% of the Alonso A and aMAP patients, respectively were labelled as high risk. The most reliable HCC risk‐model applied to our cohort to predict HCC development is the Alonso model (based on fibrosis stage assessed by liver stiffness measurements or Fibrosis‐4 index (FIB‐4) at baseline and after 1 year, and albumin levels at 1 year) with a‐100% sensitivity in detecting HCC among those at high risk and 63% labelled as high risk. The application of the model would have saved the cost of 1290 ultrasound no longer being performed in the 37% low‐risk group. Conclusion In our cohort, the Alonso A model allows the most reliable reduction in HCC screening resulting in safely stopping life‐long monitoring in about a third of F3‐F4 patients achieving SVR with DAAs.