Incidence, Predictors, and Course of Hepatocellular Carcinoma Following Direct-Acting Antivirals Therapy in a Prospective Genotype-3 Predominant HCV Elimination Compensated Cirrhosis Cohort.

Premkumar M, Sharma P, Gupta P, +17 more, Reddy KR.

Journal ArticleAbstract only — full text under license

AI summary — for doctors, generated from the abstract only

In a large Indian hepatitis C elimination program cohort dominated by genotype 3, direct-acting antiviral therapy achieved over 95% cure rates regardless of HCC status, but de novo HCC still developed in about 3.2% of cirrhotic patients after cure (incidence 985 per 100,000 person-years), supporting continued HCC surveillance after HCV cure.

What was studied

A prospective cohort study within India's National Viral Hepatitis Control Programme, evaluating direct-acting antiviral (DAA) treatment outcomes, sustained virologic response (SVR-12) rates, and incidence/predictors of hepatocellular carcinoma (HCC) in patients with predominantly genotype-3 HCV-related compensated cirrhosis, comparing those with HCC at presentation versus those developing de novo HCC after cure, from October 2018 to December 2024.

Key findings

Among 51,865 HCV patients, 4646 had compensated cirrhosis and 652 had HCC; SVR-12 was achieved in 97.8% (360/368) of HCV-cirrhosis patients with HCC at presentation and 96.9% (3874/3994) of those without HCC at presentation (P=0.366), showing DAAs worked similarly well regardless of HCC status.
De novo HCC occurred post-cure in 3.2% (128/3994) of patients over a median 4-year follow-up, an incidence of 985 per 100,000 person-years; 60.2% of these cases were caught at early BCLC stage A.
Liver stiffness at SVR-48 (adjusted hazard ratio 1.01, 95% CI 1.001-1.030) and ALBI score at SVR-12 (adjusted hazard ratio 1.31, 95% CI 1.1-1.4) independently predicted de novo HCC; recurrence rate was lower in de novo HCC than in HCC-at-presentation patients (2.2 vs 17.6 per 100 person-years), and of de novo HCC patients, 21.1% died and 3.1% underwent transplantation.

Clinical relevance

The findings suggest that while DAA therapy achieves excellent cure rates in genotype-3-predominant HCV cirrhosis regardless of HCC status, patients remain at meaningful ongoing risk of developing new HCC after cure, particularly those with higher post-treatment liver stiffness or ALBI scores, supporting the authors' call for mandatory HCC surveillance even after successful HCV cure.

Who should care

HepatologyMedical Gastroenterology

Limitations

Important limitations may not be assessable from the abstract alone.

DAA therapy cured over 95% of HCV-cirrhosis patients in this large Indian cohort, but nearly 1% per year developed new HCC after cure, reinforcing the need for continued HCC surveillance post-cure.

This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.

Abstract

Background

Genotype-3 HCV cirrhosis is a major risk for hepatocellular carcinoma (HCC). We assessed DAA treatment-related SVR rates, and HCC characteristics and outcomes in a prospective, predominantly genotype-3 compensated cirrhosis cohort participating in the National Viral Hepatitis Control Programme (NVHCP) for HCV elimination in India.

Methods

Viremic HCV-related HCC diagnosed at presentation and within 6 months (pre-DAAs), and those with post-SVR-12 HCC (post-DAAs) between 15 October 2018 and 31 December 2024, were evaluated.

Results

Among 51,865 HCV patients, 4646 had compensated cirrhosis, 652 had HCC, of whom 399 were treated at the hub. 368/399 (92.2%) at presentation had viremic HCV-cirrhosis related HCC (aged 61.5 ± 10.5 years, 65.2% men, 77.8% genotype-3, median ALBI -2.0, with presentation in BCLC stages A (26.1%), B (25.3%), C (12.8%), and D (35.9%), 16% had portal vein thrombosis while 31 (7.8%) did not have cirrhosis. Ultimate SVR-12 after one or more DAAs courses was in 360/368 (97.8%) in HCV-cirrhosis with HCC(at presentation) and in 3874/3994 (96.9%; P = 0.366) with HCV-cirrhosis without HCC. De novo HCC post SVR-12 was in 128/3994 (3.2%), median follow-up of 4 years, an incidence of 985 per 100,000 person-years; aged 57.6 ± 8.6 years, 77.3% men, 71.6% genotype-3, BCLC stages were A (60.2%), B (28.9%), and C (10.9%). Liver stiffness at SVR-48 (aHR 1.01, 95% CI: 1.001-1.030, P = 0.021) and ALBI score at SVR-12 (aHR 1.31, 95% CI: 1.1-1.4, P = 0.034) independently predicted de novo HCC. The recurrence rate was lower in patients with de novo HCC than in those with HCC at presentation (2.2 vs 17.6 per 100 person-years). 27 (21.1%) died, 4 (3.1%) underwent transplantation.

Conclusion

DAAs achieved an SVR-12 rate exceeding 95% in genotype-3 predominant HCV-compensated cirrhosis, with and without HCC. Incidence of de novo HCC post SVR-12 was 985 per 100,000 person-years, and 60% had BCLC Stage A. Post-SVR LSM and ALBI score predicted risk of HCC. Our data argue for mandatory HCC surveillance under the NVHCP for all patients with HCV-cirrhosis in India.

DOI

10.1016/j.jceh.2026.103609

PMID

42614665

Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.

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