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炎症性肠病患者对抗肿瘤坏死因子治疗缺乏反应或反应丧失的病因及管理

Etiology and Management of Lack or Loss of Response to Anti-Tumor Necrosis Factor Therapy in Patients With Inflammatory Bowel Disease.

作者信息

Fine Sean, Papamichael Kostantinos, Cheifetz Adam S

机构信息

Dr Fine is director of the Center for Inflammatory Bowel Disease at Brown Medicine at the Warren Alpert Medical School of Brown University in Providence, Rhode Island. Dr Papamichael is a research fellow in the Division of Gastroenterology at Beth-Israel Deaconess Medical Center in Boston, Massachusetts. Dr Cheifetz is director of the Center for Inflammatory Bowel Diseases at Beth-Israel Deaconess Medical Center.

出版信息

Gastroenterol Hepatol (N Y). 2019 Dec;15(12):656-665.

PMID:31892912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6935028/
Abstract

The management of patients with moderate to severe inflammatory bowel disease was transformed with the arrival of anti-tumor necrosis factor (TNF) therapy. Nevertheless, a considerable number of patients do not respond to anti-TNF induction therapy (primary nonresponse) or lose response to treatment over time after initially experiencing clinical improvement (secondary loss of response). Studies suggest that these outcomes are often due to inadequate drug concentrations. Therapeutic drug monitoring (TDM) is a practical tool that can be used to better define the etiologies of and help manage primary nonresponse or secondary loss of response. Proactive TDM, or drug titration to a target trough concentration, can improve the efficacy of anti-TNF treatment and lead to favorable clinical outcomes. However, in patients with adequate anti-TNF drug concentrations and active disease, alternate pathways of inflammation (not driven by TNFa agents) are at play, and therapies with another mechanism of action should be employed.

摘要

随着抗肿瘤坏死因子(TNF)疗法的出现,中重度炎症性肠病患者的管理发生了变革。然而,相当一部分患者对抗TNF诱导疗法无反应(原发性无反应),或在最初出现临床改善后随着时间推移失去对治疗的反应(继发性反应丧失)。研究表明,这些结果通常是由于药物浓度不足所致。治疗药物监测(TDM)是一种实用工具,可用于更好地确定原发性无反应或继发性反应丧失的病因并帮助进行管理。主动TDM,即药物滴定至目标谷浓度,可提高抗TNF治疗的疗效并带来良好的临床结果。然而,在抗TNF药物浓度充足但疾病仍活跃的患者中,存在其他炎症途径(不由TNFα药物驱动),应采用具有另一种作用机制的疗法。

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