干扰素α可能会诱导肝脏肥胖症,通过增加甘油三水平来促进HBsAg损失
Lili Wu1,2, Zhihui Li1,2, Na Gao1,2
1Department of Infectious Diseases, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Heliyon
|July 8, 2024
概括
代谢综合征的组成部分,如糖尿病,可能会阻碍乙型肝炎的表面抗原的损失,在基化干扰素α治疗期间. 然而,干扰素α可以诱导肝脏肥胖症,通过增加甘油三来促进抗原损失.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 病毒学 病毒学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 代谢综合征 (MetS) 和乙型肝炎表面抗原 (HBsAg) 损失之间的关系尚未完全理解,特别是在接受基化干扰素-α (PEG-IFN) 治疗的患者中.
- 研究影响HBsAg损失的MetS因素对于优化慢性乙型肝炎 (CHB) 患者的治疗策略至关重要.
研究的目的:
- 探索 PEG-IFN.N. 治疗的CHB患者中代谢综合征和HBsAg损失之间的相关性.
- 确定与成功的HBsAg损失相关的因素,并了解IFN-α在这个过程中的作用.
主要方法:
- 对412名低HBsAg量化的CHB患者进行了回顾性分析,这些患者之前接受了核胺类同类药物 (NUC) 并转换为或增加PEG-IFN治疗.
- 收集了与MetS相关的人口和生化数据,包括禁食血糖 (FBG),糖化白蛋白,血脂和尿酸.
- 使用HepG2.2.15细胞系进行体外实验,以评估干扰素-α (IFN-α) 的疗效.
主要成果:
- 没有达到HBsAg损失的患者患糖尿病和高血压的比例更高.
- 在未治愈的组中观察到高血糖和糖化白蛋白,而治愈组的血脂和尿酸水平较高.
- 在所有患者中,PEG-IFN治疗增加了甘油三水平和肝硬化;基线尿酸升高和肝硬化与HBsAg损失有关.
结论:
- 干扰素-α (IFN-α) 可能通过诱导肝硬化和通过ACSL1.1升高调节增加甘油三水平来促进HBsAg损失.
- 伴随性糖尿病似乎是CHB患者在PEG-IFN治疗中实现HBsAg损失的负面预测因素.
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