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拟议的临床阶段,以改善免疫检查点抑制剂相关肺炎的个体化治疗。

Proposed clinical phases for the improvement of personalized treatment of checkpoint inhibitor-related pneumonitis.

机构信息

State Key Laboratory of Respiratory Disease, National Clinical Research Centre for Respiratory Disease, First Affiliated Hospital, Guangzhou Institute of Respiratory Health, Guangzhou Medical University, Guangzhou, China.

Affiliated Dongguan People's Hospital, Dongguan Institute of Respiratory and Critical Care Medicine, Southern Medical University, Dongguan, China.

出版信息

Front Immunol. 2022 Jul 20;13:935779. doi: 10.3389/fimmu.2022.935779. eCollection 2022.

DOI:10.3389/fimmu.2022.935779
PMID:35967342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9364904/
Abstract

BACKGROUND

Checkpoint inhibitor-related pneumonitis (CIP) is a lethal immune-related adverse event. However, the development process of CIP, which may provide insight into more effective management, has not been extensively examined.

METHODS

We conducted a multicenter retrospective analysis of 56 patients who developed CIP. Clinical characteristics, radiological features, histologic features, and laboratory tests were analyzed. After a comprehensive analysis, we proposed acute, subacute, and chronic phases of CIP and summarized each phase's characteristics.

RESULTS

There were 51 patients in the acute phase, 22 in the subacute phase, and 11 in the chronic phase. The median interval time from the beginning of CIP to the different phases was calculated (acute phase: ≤4.9 weeks; subacute phase: 4.9~13.1 weeks; and chronic phase: ≥13.1 weeks). The symptoms relieved from the acute phase to the chronic phase, and the CIP grade and Performance Status score decreased (<0.05). The main change in radiologic features was the absorption of the lesions, and 3 (3/11) patients in the chronic phase had persistent traction bronchiectasis. For histologic features, most patients had acute fibrinous pneumonitis in the acute phase (5/8), and most had organizing pneumonia in the subacute phase (5/6). Other histologic changes advanced over time, with the lesions entering a state of fibrosis. Moreover, the levels of interleukin-6, interleukin-10 and high-sensitivity C-reactive protein (hsCRP) increased in the acute phase and decreased as CIP progressed (IL-6: 17.9 vs. 9.8 vs. 5.7, P=0.018; IL-10: 4.6 vs 3.0 vs. 2.0, P=0.041; hsCRP: 88.2 vs. 19.4 vs. 14.4, P=0.005).

CONCLUSIONS

The general development process of CIP can be divided into acute, subacute, and chronic phases, upon which a better management strategy might be based devised.

摘要

背景

免疫检查点抑制剂相关肺炎(CIP)是一种致命的免疫相关不良事件。然而,CIP 的发展过程可能为更有效的管理提供线索,但尚未得到广泛研究。

方法

我们对 56 例发生 CIP 的患者进行了多中心回顾性分析。分析了临床特征、影像学特征、组织学特征和实验室检查。经过全面分析,我们提出了 CIP 的急性、亚急性和慢性期,并总结了各期的特点。

结果

急性期有 51 例,亚急性期有 22 例,慢性期有 11 例。计算了从 CIP 开始到不同阶段的中位间隔时间(急性期:≤4.9 周;亚急性期:4.9~13.1 周;慢性期:≥13.1 周)。症状从急性期缓解到慢性期,CIP 分级和体力状态评分下降(<0.05)。影像学特征的主要变化是病变吸收,慢性期 3 例(3/11)患者持续存在牵引性支气管扩张。组织学特征方面,急性期 8 例患者大多为急性纤维蛋白性肺炎(5/8),亚急性期 6 例患者大多为机化性肺炎。其他组织学变化随时间推移而进展,病变进入纤维化状态。此外,白细胞介素-6(IL-6)、白细胞介素-10(IL-10)和高敏 C 反应蛋白(hsCRP)水平在急性期升高,随着 CIP 的进展而降低(IL-6:17.9 比 9.8 比 5.7,P=0.018;IL-10:4.6 比 3.0 比 2.0,P=0.041;hsCRP:88.2 比 19.4 比 14.4,P=0.005)。

结论

CIP 的总体发展过程可分为急性期、亚急性期和慢性期,在此基础上可以制定更好的管理策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/5607f37eef25/fimmu-13-935779-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/e3869dc305dc/fimmu-13-935779-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/658dbd43cbd2/fimmu-13-935779-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/d93827b81f21/fimmu-13-935779-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/74a96c4a8374/fimmu-13-935779-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/028ef34ca54d/fimmu-13-935779-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/5607f37eef25/fimmu-13-935779-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/e3869dc305dc/fimmu-13-935779-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/658dbd43cbd2/fimmu-13-935779-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/d93827b81f21/fimmu-13-935779-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/74a96c4a8374/fimmu-13-935779-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/028ef34ca54d/fimmu-13-935779-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/9364904/5607f37eef25/fimmu-13-935779-g006.jpg

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