Pulmonary Post-Acute-Covid-19-Illness Sequelae

Abstract

Pulmonary function abnormalities in post-acute-COVID-19-illness survivors could be due to a decrease in both diffusing capacity of the lung for carbon dioxide (DLCO) and transfer coefficient of the lung for carbon monoxide (KCO) [1]. Alveolar-capillary damage, microvascular pathological lesions, or anemia can contribute to reduction of the KCO [1]. Post-acute-COVID-19-illness pulmonary fibrosis and post-acute-MERS-associated pulmonary fibrosis were highly associated with old aging ranging from 60- to 70-years age group (13 out of 30 (43.3 %)), demonstrated by Wong et al and Das et al [2, 3]. Post-acute-COVID-19-illness pulmonary fibrosis was 1.3 times more predominant in males, compared to females, possibly explained by the effect of androgen that promotes the transcription of transmembrane protease serine 2 gene, and was much higher incidence in cigarette smoker (18 of 30 patients (60 %)), compared to non-smoking patients [4, 5]. This gene impairs hose’s antibody response and facilitates the fusion of the virushose cells. Dyspnea, the most common persistent symptom of the pulmonary sequelae ranged from 42 % to 66 % prevalence at 60-100 days of following-up, supported by the result of lower median 6-minutes walking distance comparing to the normal reference values in one-fourth of the patients at 6 months in the post-acute- OVID-19-illlness Chinese study that was similar to the prevalence in SARS and MERS survivors [6-11].