Pulmonary Fibrosis after COVID-19 is Associated with Severity of Illness and Blood Leukocyte Telomere Length

Abstract

The risk factors for development of fibrotic interstitial lung abnormalities (ILA) after severe COVID-19 are incompletely described and the extent to which CT findings correlate with symptoms and physical function after hospitalization remain unclear. At 4 months after hospitalization, fibrotic ILA was more common in those who underwent mechanical ventilation (72%) than in those who did not (20%). We demonstrate that severity of initial illness, duration of mechanical ventilation, lactate dehydrogenase on admission, and leukocyte telomere length are independent risk factors for fibrotic ILA. These fibrotic changes correlate with lung function, cough and measures of frailty, but not with dyspnea.

Liquid biomarkers of macrophage dysregulation and circulating spike protein illustrate the biological heterogeneity in patients with post-acute sequelae of COVID-19

“…This is also in line with the lower levels of CCL2/MCP-1 and IL-8 in individuals with ongoing PASC as compared to individuals without PASC after SARS-CoV-2 infection that was also observed by others [40]. CCL2/MCP-1, IL-8, IL-18 and IL-23 have all been described as pro-fibrotic in lung, liver and/or heart [48][49][50][51] and might indicate ongoing tissue damage in PASC [52,53]. Interestingly, IL-8 was found in all PASC-associated cytokine signatures underscoring its importance for long-lasting sequelae.…”

A MUC5Bgene polymorphism, rs35705950-T, confers protective effects in COVID-19 infection

“…Parenchymal fibrosis is a late complication of respiratory infections with COVID-19 (2)(3)(4). Among chronic lung diseases, idiopathic pulmonary fibrosis (IPF) (5), a disorder characterized by progressive pulmonary scarring which is associated with a median survival of 2-3 years in the absence of lung transplantation (6), shares several risk factors with those for severe COVID-19 disease, including advanced age (7), cardiovascular disease, diabetes, and history of smoking (5).…”

Pulmonary fibrosis and follow-up of COVID-19 survivors: an urgent need for clarification

“…(2) O impacto da atividade inflamatória autoimune desencadeada pela infecção viral e a presença de características genéticas e anormalidades pulmonares intersticiais prévias podem determinar um risco maior de fibrose pulmonar pós-COVID-19; entretanto, essas hipóteses precisam ser esclarecidas. (1,5) Um estudo recente mostrou que o menor comprimento dos telômeros de leucócitos sanguíneos foi identificado como um fator de risco de ocorrência de alterações tomográficas semelhantes à fibrose em pacientes quatro meses após a COVID-19, o que reforça a hipótese de suscetibilidades genéticas para a ocorrência de fibrose pulmonar pós-COVID-19. (5) Além disso, são necessários mais estudos nos quais se avaliem características histológicas em pacientes com fibrose pulmonar pós-COVID-19 para aumentar o conhecimento a respeito dessa entidade.…”

“…(1,5) Um estudo recente mostrou que o menor comprimento dos telômeros de leucócitos sanguíneos foi identificado como um fator de risco de ocorrência de alterações tomográficas semelhantes à fibrose em pacientes quatro meses após a COVID-19, o que reforça a hipótese de suscetibilidades genéticas para a ocorrência de fibrose pulmonar pós-COVID-19. (5) Além disso, são necessários mais estudos nos quais se avaliem características histológicas em pacientes com fibrose pulmonar pós-COVID-19 para aumentar o conhecimento a respeito dessa entidade. Biomarcadores séricos como Krebs von den Lungen-6 são promissores para prever um maior risco de fibrose pulmonar pós-COVID-19, mas precisam ser explorados em estudos futuros.…”