在克罗恩病治疗因弗力西马布失效的机制
S Nikolaus1, A Raedler, T Kühbacker
1Christian-Albrechts-University, First Department of Medicine, Kiel, Germany.
在大多数患者中,Infliximab最初改善了克罗恩病的症状,但在症状复发之前,许多人因为免疫标记物如瘤缩因子-α (TNF-alpha) 和核因子kappa B (NFkappaB) 被重新激活而复发.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 克罗恩氏病与瘤死亡因子-α (TNF-α) 的升高有关.
- 核因子卡帕B (NFkappaB) 调节炎症基因转录.
- 抗TNF抗体Infliximab在4周内在30-50%的耐火克罗恩病患者中实现了缓解.
研究的目的:
- 调查治疗失败背后的临床和免疫机制在克罗恩病患者接受infliximab.
- 评估因弗利西马布的疗效持续时间,并确定复发的预测因素.
主要方法:
- 24名患有活跃的,耐固醇克罗恩病的患者接受了一次infliximab输液.
- 使用克罗恩病活动指数 (CDAI) 监测临床反应16周.
- 在粘膜活检中测量了TNF-α分泌和NFkappaB p65水平.
主要成果:
- 88%的患者在1周后实现了缓解,但在16周内缓解率显著下降.
- 到第16周,90%的患者出现复发.
- 提升的TNF-α分泌和NFkappaB p65在不响应者中先发生临床复发.
结论:
- 在克罗恩病中,infliximab可快速改善症状,但持续反应有限.
- 免疫系统的重新激活,表明TNF-alpha和NFkappaB的增加,临床复发之前.
- 了解这些免疫变化对于管理克罗恩病至关重要.
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