Language
English
Publication Date
12-1-2022
Journal
Intensive Care Medicine
DOI
10.1007/s00134-022-06877-w
PMID
36074167
PMCID
PMC9453725
PubMedCentral® Posted Date
9-8-2022
PubMedCentral® Full Text Version
Post-print
Abstract
Immunomodulation and immunity from vaccination and natural infection have reduced mortality from coronavirus disease 2019 (COVID-19). However, there are ongoing concerns regarding emerging variants and residual pulmonary sequelae in survivors, given that the lungs are the principal site for the triumvirate of infection, inflammation and injury. The initial waves of acute, severe COVID-19 were profoundly inflammatory, usually manifest as organising pneumonia ± acute respiratory distress syndrome (ARDS). The extent of the fibrogenic potential of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and the modifiability of the pathogenic processes and disease course are unclear. Interestingly patients can develop ‘post-COVID interstitial lung disease’ (PC-ILD) irrespective of having ARDS during the acute phase. Here, we describe our evolving understanding of PC-ILD and the critical need to identify risk factors, including within the critical care setting. We also discuss immunopathomechanisms that may facilitate early intervention to prevent, slow or arrest progression of lung damage e.g. with immunomodulatory and/or anti-fibrotic agents.
Keywords
Humans, COVID-19, Lung Diseases, Interstitial, SARS-CoV-2, Lung, Retrospective Studies
Published Open-Access
yes
Recommended Citation
Puja Mehta, Ivan O Rosas, and Mervyn Singer, "Understanding Post-COVID-19 Interstitial Lung Disease (Ild): A New Fibroinflammatory Disease Entity" (2022). Faculty and Staff Publications. 4746.
https://digitalcommons.library.tmc.edu/baylor_docs/4746
Included in
Critical Care Commons, Health Services Research Commons, Medical Sciences Commons, Pulmonology Commons, Sleep Medicine Commons