肺纤维化以肺实质破坏为特点，并可增加患者的患病率和死亡率。肺纤维化通常出现在SARS-CoV-2感染住院后。因为有药物可以改变肺纤维化的风险，我们调查了不同药物治疗（阿米奥达鲁、抗癌化疗、皮质类固醇和利妥昔单抗）与COVID-19后肺纤维化发病率是否存在差异。我们使用全国COVID-19合作队(N3C)的数据试验室，该试验室汇总和协调美国境内的COVID-19数据，以评估COVID-19诊断后至少60天内的肺纤维化发病率，病例为2020年1月1日至2022年7月6日期间住院的18岁以上对无已存在的肺纤维化进行筛选。我们使用倾向性得分根据已知影响肺纤维化发病率的协变量将COVID-19前暴露于药物和未暴露于药物的队列进行1:1的匹配，并估计药物暴露与COVID-19后肺纤维化风险的关系。敏感性分析考虑了住院后至少30天或90天以及COVID-19阴性N3C人群的肺纤维化发病率。在5923394名COVID-19患者中，我们分析了452951名住院成年患者，其中肺纤维化发病率为每100人年1.1例。本次研究的主要分析包含了277984名住院成年COVID-19患者，并且所有接受药物治疗的队列均与未接受药物治疗的队列良好匹配（标准化均值差<0.1）。利妥昔单抗的COVID-19后肺纤维化发病率比（IRR）为2.5（95% CI 1.2-5.1，P = 0.01），化疗IRR为1.6（95% CI 1.3-2.0，P < 0.0001），皮质类固醇IRR为1.2（95% CI 1.0-1.3，P = 0.02）。阿米奥达鲁的暴露与COVID-19后肺纤维化发病没有明显的关联（IRR = 0.8，95% CI 0.6-1.1，P = 0.24）。在敏感性分析中，COVID-19前皮质类固醇使用与COVID-19后肺纤维化没有一致的关联。在COVID-19阴性住院人群（n = 1240461）中，总体肺纤维化发病率较低（每100人年0.6例），接受这四种药物治疗的患者肺纤维化发病率也较低。在住院患者中，COVID-19感染前最近使用利妥昔单抗或抗癌化疗与COVID-19后肺纤维化的风险增加有关。本文描述的分析是在NCATS N3C数据试验室（https://covid.cd2h.org）和N3C归因与出版政策v1.2-2020-08-25b支持下，通过访问数据或工具进行的，受到NIHK23HL146942，NIHK08HL150291，NIHK23HL148387，NIHUL1TR002389，NCATSU24 TR002306以及来自University of Chicago的Walder Foundation/Center for Healthcare Delivery Science and Innovation的SECURED资助。WFP获得了Greenwall Foundation的资助。感谢那些在数据中包含信息的患者以及为发展这一社区资源做出贡献的组织和科学家们（https://ncats.nih.gov/n3c/resources/data-contribution/data-transfer-agreement-signatories，https://doi.org/10.1093/jamia/ocaa196）。 Copyright © 2023 The Author(s).

Pulmonary fibrosis is characterized by lung parenchymal destruction and can increase morbidity and mortality. Pulmonary fibrosis commonly occurs following hospitalization for SARS-CoV-2 infection. As there are medications that modify pulmonary fibrosis risk, we investigated whether distinct pharmacotherapies (amiodarone, cancer chemotherapy, corticosteroids, and rituximab) are associated with differences in post-COVID-19 pulmonary fibrosis incidence.We used the National COVID-19 Cohort Collaboration (N3C) Data Enclave, which aggregates and harmonizes COVID-19 data across the United States, to assess pulmonary fibrosis incidence documented at least 60 days after COVID-19 diagnosis among adults hospitalized between January 1st, 2020 and July 6th, 2022 without pre-existing pulmonary fibrosis. We used propensity scores to match pre-COVID-19 drug-exposed and unexposed cohorts (1:1) based on covariates with known influence on pulmonary fibrosis incidence, and estimated the association of drug exposure with risk for post-COVID-19 pulmonary fibrosis. Sensitivity analyses considered pulmonary fibrosis incidence documented at least 30- or 90-days post-hospitalization and pulmonary fibrosis incidence in the COVID-19-negative N3C population.Among 5,923,394 patients with COVID-19, we analyzed 452,951 hospitalized adults, among whom pulmonary fibrosis incidence was 1.1 per 100-person-years. 277,984 hospitalized adults with COVID-19 were included in our primary analysis, among whom all drug exposed cohorts were well-matched to unexposed cohorts (standardized mean differences <0.1). The post-COVID-19 pulmonary fibrosis incidence rate ratio (IRR) was 2.5 (95% CI 1.2-5.1, P = 0.01) for rituximab, 1.6 (95% CI 1.3-2.0, P < 0.0001) for chemotherapy, and 1.2 (95% CI 1.0-1.3, P = 0.02) for corticosteroids. Amiodarone exposure had no significant association with post-COVID-19 pulmonary fibrosis (IRR = 0.8, 95% CI 0.6-1.1, P = 0.24). In sensitivity analyses, pre-COVID-19 corticosteroid use was not consistently associated with post-COVID-19 pulmonary fibrosis. In the COVID-19 negative hospitalized population (n = 1,240,461), pulmonary fibrosis incidence was lower overall (0.6 per 100-person-years) and for patients exposed to all four drugs.Recent rituximab or cancer chemotherapy before COVID-19 infection in hospitalized patients is associated with increased risk for post-COVID-19 pulmonary fibrosis.The analyses described in this publication were conducted with data or tools accessed through the NCATS N3C Data Enclave https://covid.cd2h.org and N3C Attribution & Publication Policy v1.2-2020-08-25b supported by NIHK23HL146942, NIHK08HL150291, NIHK23HL148387, NIHUL1TR002389, NCATSU24 TR002306, and a SECURED grant from the Walder Foundation/Center for Healthcare Delivery Science and Innovation, University of Chicago. WFP received a grant from the Greenwall Foundation. This research was possible because of the patients whose information is included within the data and the organizations (https://ncats.nih.gov/n3c/resources/data-contribution/data-transfer-agreement-signatories) and scientists who have contributed to the on-going development of this community resource (https://doi.org/10.1093/jamia/ocaa196).© 2023 The Author(s).