Management of chronic pulmonary disease in the time of coronavirus disease 2019

Abstract

Purpose of review: The purpose of this review is to discuss the most recent data describing the impact of coronavirus disease 2019 (COVID-19) on the pediatric population with chronic pulmonary disease. We specifically focus on children with asthma, cystic fibrosis (CF), and lung transplant recipients.

Recent findings: Children with asthma, CF, and lung transplant recipients do not appear to have an increased risk of morbidity or mortality with COVID-19 infection compared to the general pediatric population. Data does not support the change or withdrawal of any asthma or CF maintenance medications; however, does advocate for the cessation of aerosolized medications whenever possible to minimize transmission risk. It may not be necessary to adjust immunosuppressive therapy when managing COVID-19 in pediatric lung transplant patients. Mechanisms of infection in airway epithelial cells in children may differ from adults, resulting in a milder phenotype.

Summary: Current data about pediatric patients with chronic lung disease infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is promising but remains scarce. Additional study is needed to definitively understand the complex interplay of the SARS-CoV-2 virus in the airway of children with chronic lung disease, how it differs from adults, and how best to manage the symptoms of acute infection.

Figure 1:

COVID-19 Associated Hospitalizations by Age. (Source: COVID-NET: COVID-19-Associated Hospitalization Surveillance Network, Centers for Disease Control and Prevention. https://gis.cdc.gov/grasp/COVIDNet/COVID19_5.html. Accessed on [Feb 1, 2021].)

Figure 2:

Ciclesonide interaction with SARS-CoV-2 A space-filling or stick model demonstrating potential binding site interaction between esterified ciclesonide (des-CIC) and active sites (red regions) of SARS-CoV-2 NSP15 endonuclease. (Source: Kimura H, Kurusu H, Sada M, Kurai D, Murakami K, Kamitani W, et al. Molecular pharmacology of ciclesonide against SARS-CoV-2. Journal of allergy and clinical immunology. 2020;146(2):330–1.)

Figure 3:

Immunopathogenesis of COVID-19 and Asthma. Schematic comparing aberrant immune response with SARS-CoV-2 infection with a more trained immune response with allergens and respiratory viruses (RV). (Source: Wang JY, Pawankar R, Tsai HJ, Wu LSH, Kuo WS. COVID‐19 and asthma, the good or the bad? Allergy (Copenhagen). 2020.)

Figure 4:

SARS-CoV-2 and Cystic Fibrosis. Schematic representing interaction of ACE2, TMPRSS2, and SARS-CoV-2 during lung infection. Panel A: Angiotensin-converting enzyme (ACE) cleaves angiotensin I (Ang I) to angiotensin II (Ang II) which is proinflammatory. ACE2 processes proinflammatory Ang II to angiotensin 1–7 which is anti-inflammatory. A decrease in ACE and/or increase in ACE2 will decrease inflammation and lung damage from SARS-CoV-2 infection. Panel B: SARS-CoV-2 S-protein binds to ACE2. It is cleaved by TMPRSS2 and Furin which facilitates viral entry into cell. Serine protease inhibitors, found in CF, inhibit TMPRSS2 thus reducing SARS-CoV-2 entry into airway epithelial cells. (Source: Stanton BA, Hampton TH, Ashare A. SARS-CoV-2 (COVID-19) and cystic fibrosis. American journal of physiology Lung cellular and molecular physiology. 2020;319(3):L408-L15.)