在核类类似物时代,抑制慢性乙型肝炎的肝癌发生
Hiroki Nishikawa1,2, Soo Ki Kim3, Akira Asai4
1Second Department of Internal Medicine, Osaka Medical and Pharmaceutical University, Takatsuki, Japan; hiroki.nishikawa@ompu.ac.jp.
In vivo (Athens, Greece)
|December 26, 2023
概括
核酸相似物 (NA) 抑制乙型肝炎病毒 (HBV) 复制,但实现功能治愈 (HBsAg损失) 仍然具有挑战性. 本综述检查了NA疗法.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 病毒学 病毒学
- 在瘤学瘤学.
背景情况:
- 肝细胞癌 (HCC) 与乙型肝炎病毒 (HBV) 携带者密切相关,占日本病毒性肝炎相关癌症的很大一部分.
- 核类型 (NA) 是慢性乙型肝炎的标准抗病毒疗法,抑制HBV复制并改善肝酶水平.
- 虽然在抑制HBVDNA方面有效,但NAs的HBsAg损失 (功能治愈) 率很低,HCC仍然可以在治疗期间或治疗后发展.
研究的目的:
- 审查核胺类同类 (NA) 治疗在预防乙型肝炎病毒 (HBV) 衍生的肝细胞癌 (HCC) 的疗效.
- 评估NA疗法的当前局限性,以实现慢性乙型肝炎患者的功能治愈 (HBsAg损失).
- 探索在接受或完成NA治疗的患者中HCC的发病率.
主要方法:
- 关于治疗慢性乙型肝炎的核化物模拟 (NA) 疗法的文献综述.
- 在NA治疗期间分析HBV DNA抑制,HBsAg损失率和HCC发病率的数据.
- 检查NAs影响HBV复制和致癌的机制.
主要成果:
- 核胺类类似物 (NA) 在抑制HBVDNA和改善氨酸转移酶水平方面表现出高效.
- 通过NA治疗实现HBsAg损失 (功能治愈) 的速度很低,表明病毒清除不完全.
- 在治疗中或治疗后的患者中报告了肝细胞癌 (HCC) 病例,突出了残留风险.
结论:
- 虽然核类相似物 (NA) 有效控制乙型肝炎病毒 (HBV) 复制,但它们并不总是导致功能治愈.
- 在NA治疗期间或之后,肝细胞癌 (HCC) 发展的持续风险需要持续监测和潜在的新治疗策略.
- 需要进一步的研究来优化NA治疗,并开发新的方法来实现持续的病毒抑制和预防HBV衍生的致癌症.
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