Asthma and COVID-19: Unveiling Outcome Disparities and Treatment Impact Based on Distinct Endotypes.

Benjamin Sines, Cameron B Morrison, Jenna M Donaldson, Asiyah Ahmad, Ashok Krishnamurthy, David B Peden, Camille Ehre
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Abstract

Rationale: Epidemiologic studies on patients with asthma and in vitro data suggest a protective role of type 2 (T2) inflammation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Objectives: Using a large, multisite cohort, we studied clinical outcomes after SARS-CoV-2 infection in multiple asthma endotypes and examined the effects of T2-directed biologics in infected patients with asthma. Methods: The National COVID Cohort Collaborative Data Enclave was used to identify and stratify patients with asthma by endotype to include those with non-T2 and T2 asthma, as well as exposure to T2-directed biologic therapy. We evaluated the risk of hospitalization, invasive mechanical ventilation, and 90-day mortality by endotype and exposure to biologics. Results: For this study, 402,376 patients met the inclusion criteria, of whom 138,142 (34%) were characterized as having non-T2 asthma and 264,234 (66%) as having T2 asthma, a group further divided into 104,823 (26%) atopic, 84,440 (21%) eosinophilic, and 74,971 (19%) T2-high asthmatic endotypes. Compared with patients with non-T2 asthma, those with atopic and T2-high asthma experienced decreased odds of hospitalization and 90-day mortality. Conversely, patients with eosinophilic asthma experienced higher odds of hospitalization, intubation, and 90-day mortality. Exposure to T2-directed biologic therapies did not alter outcomes after propensity score matching. In contrast, maximum eosinophil count and recent systemic corticosteroid use were directly correlated with increased odds of all outcomes. Conclusions: Coronavirus disease (COVID-19) outcomes differ depending on asthma endotype, with patients with atopic asthma experiencing lower odds and those with eosinophilic asthma experiencing higher odds of deleterious outcomes. T2-directed biologic treatment did not alter these outcomes, but recent systemic corticosteroid use predisposes all patients with asthma to adverse outcomes.

哮喘与 COVID-19:揭示基于不同内型的结果差异和治疗影响。
理由:对哮喘患者的流行病学研究和体外数据表明,T2 炎症在 SARS-CoV-2 感染中起保护作用:我们利用一个大型、多站点队列研究了多种哮喘内型感染 SARS-CoV-2 后的临床结果,并考察了 T2 定向生物制剂对感染哮喘患者的影响:我们利用国家 COVID 队列协作组织 (N3C) 的数据飞地 (Data Enclave) 来识别哮喘患者并按内型进行分层,包括非 T2 型和 T2 型哮喘患者,以及接受过 T2 型生物制剂治疗的患者。我们按内型和生物制剂暴露情况评估了住院、侵入性机械通气和 90 天死亡率的风险:在这项研究中,402,376 名患者符合纳入标准,其中 138,142 人(34%)为非 T2 哮喘患者,264,234 人(66%)为 T2 哮喘患者,这一群体又分为 104,823 人(26%)特应性、84,440 人(21%)嗜酸性粒细胞和 74,971 人(19%)T2-高哮喘内型。与非 T2 哮喘患者相比,特应性和 T2 高哮喘患者的住院几率和 90 天死亡率都有所下降。相反,嗜酸性粒细胞哮喘患者的住院、插管和 90 天死亡率较高。在进行倾向评分匹配后,接受 T2 定向生物疗法并不会改变预后。相反,嗜酸性粒细胞最高计数和近期使用全身性皮质类固醇与所有结果的几率增加直接相关:COVID-19结果因哮喘内型而异,特应性哮喘患者出现有害结果的几率较低,而嗜酸性粒细胞哮喘患者出现有害结果的几率较高。T2定向生物治疗不会改变这些结果,但近期全身使用皮质类固醇会使所有哮喘患者易出现不良后果。本文根据知识共享署名非商业性无衍生品许可 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/) 条款公开发表。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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