Metabolic factors drive early increase in hepatic steatosis despite improvement in non-invasive fibrosis markers after hepatitis C eradication with direct-acting antivirals - 19/06/25
Highlights |
• | Hepatic steatosis increases after eradication of hepatitis C virus (HCV) by direct acting-antivirals despite significant fibrosis reduction by non-invasive tests. |
• | New-onset steatosis occurred in over one-third of patients without baseline hepatic steatosis. |
• | Controlled attenuation parameter and lipid profiles worsened post-sustained virological response (SVR), especially in patients without pre-therapy hepatic steatosis. |
• | Metabolic dysfunction-associated steatotic liver disease remains the predominant steatotic phenotype both before and after HCV clearance. |
• | Higher BMI post-SVR independently predicts persistent or incident hepatic steatosis. |
Abstract |
Background |
While direct-acting antivirals (DAAs) achieve high sustained virologic response (SVR) rates in people with hepatitis C virus (HCV), their impact on hepatic steatosis (HS) remains unclear.
Methods |
We conducted a retrospective cohort study of 108 HCV patients from McGill University and the University of Milan who achieved SVR following DAAs. Controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were used to assess HS and liver fibrosis at baseline and 24 weeks post-SVR. HS was defined as CAP ≥248 dB/m, significant liver fibrosis as LSM ≥8 kPa, and metabolic dysfunction-associated steatotic liver disease (MASLD) as HS plus ≥1 cardiometabolic risk factors. Changes were evaluated using Wilcoxon signed-rank test and standardized mean difference (SMD). Multivariable logistic regression identified predictors of post-SVR HS.
Results |
HS prevalence increased from 47 % to 61 % post-SVR (p = 0.0007, SMD = 0.30). Among patients with baseline HS, 88 % had persistent steatosis. New-onset steatosis developed in 37 % of patients without baseline HS, with a significant CAP increase (p < 0.0004, SMD=0.48). In patients without baseline HS, total cholesterol and triglycerides increased (p = 0.0084, SDM = 0.43 and p < 0.0001, SDM = 0.71, respectively), whereas in those with baseline HS, only total cholesterol rose (p = 0.0296, SDM = 0.50). MASLD remained the leading etiology at both time points (94 % at baseline, 92 % post-SVR). Significant fibrosis declined markedly from 49 % to 17 % (p < 0.0001, SMD = –0.80). Higher BMI at 24 weeks was independently associated with HS (adjusted odds ratio 1.92, 95 %CI 1.22–3.03).
Conclusions |
Despite improvement in liver fibrosis markers, HS often persists or emerges following DAAs therapy, particularly alongside metabolic dysfunctions marked by elevated cholesterol and triglycerides.
Le texte complet de cet article est disponible en PDF.Graphical abstract |
Keywords : Metabolic dysfunction-associated steatotic liver disease, Body mass index, Liver stiffness measurement, Controlled attenuation parameter, Sustained virological response
Plan
Vol 49 - N° 7
Article 102639- juillet 2025 Retour au numéro
Article précédent
- Circulating tumor DNA in peripheral blood may predict the efficacy of immune-targeted therapy in patients with hepatocellular carcinoma
- Su-Su Zheng, Dai Zhang, Jing-Fang Wu, Hong Chen, Zhen-Zhen Zhang, Guo-Bin Chen, Xiao-Ying Xie, Bo-Heng Zhang
- Liver fibrosis evaluation in patients with psychiatric diseases
- Paul Carrier, Morgane Chalange, Murielle Girard, Aurélie Prémaud, Mireille Okassa, Aurélie Lacroix, Marilyne Debette-Gratien, Brigitte Plansont, Alexandre Buisson, Benjamin Calvet, Céline Rigaud, Jérôme Boursier, Philippe Nubukpo, Véronique Loustaud-Ratti
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?