The impact of metabolic dysfunction-associated steatotic liver disease on the efficacy of pegylated interferon-based therapy in patients with chronic hepatitis B

代谢功能障碍相关脂肪肝对慢性乙型肝炎患者聚乙二醇干扰素治疗疗效的影响

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Abstract

INTRODUCTION: The impact of metabolic dysfunction-associated steatotic liver disease (MASLD) on the efficacy and prognosis of pegylated interferon (Peg-IFN)-based therapy for chronic hepatitis B (CHB) remains controversial and requires further investigation. METHODS: A total of 620 CHB patients receiving Peg-IFN-based therapy were enrolled and categorized into MASLD-CHB (n = 247) and CHB (n = 373) groups. Propensity score matching (PSM) was employed to balance baseline differences. Kaplan-Meier survival analysis and LASSO-Cox regression were applied to identify independent predictors of complete virological response (CVR) and hepatitis B surface antigen (HBsAg) seroclearance. RESULTS: After PSM, 247 patients were included in each group. Compared with the MASLD-CHB group, the CHB group exhibited significantly higher cumulative CVR rates at month 3 (36.84% vs. 24.54%, p = 0.041), month 12 (77.19% vs. 62.72%, p = 0.013), end of treatment (EOT) (78.94% vs. 65.45%, p = 0.019), and end of follow-up (EOF) (80.70% vs. 68.18%, p = 0.026). The median time to the first CVR was shorter in the CHB group (4.4 vs. 5.5 months, p = 0.030). LASSO-Cox regression revealed HBV DNA (HR: 0.486, 95% CI: 0.297-0.793, p = 0.004), MASLD (HR: 0.736, 95% CI: 0.550-0.986, p = 0.040), HBsAg (HR: 0.808, 95% CI: 0.706-0.926, p = 0.002), HBeAg positivity (HR: 0.611, 95% CI: 0.433-0.862, p = 0.005), and triglycerides (HR: 0.793, 95% CI: 0.661-0.951, p = 0.012) as independent suppressors of CVR. Multiple factors were associated with HBsAg seroclearance (p < 0.05). At the EOF, the MASLD-CHB group had higher liver stiffness measurement values (8.10 [6.40, 9.60] vs. 6.20 [5.00, 7.50]) and a greater proportion of moderate-to-severe fibrosis (18.7% vs. 5.9%, p < 0.01). CONCLUSION: In CHB patients receiving Peg-IFN-based therapy, concurrent MASLD may impede the reduction of HBV DNA levels, delay the time of first CVR, and potentially accelerate liver fibrosis progression.

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