We read with great interest the series of cases reported by MO et al. [1], describing pulmonary function after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in hospitalised patients. The authors describe a significant correlation between diffusing capacity of the lung for carbon monoxide (D LCO) and clinically defined pneumonia severity. Lung involvement of varying extent has been found on computed tomography (CT) in at least 80% of patients with SARS-CoV-2 infection [2, 3]. Extensive injury to alveolar epithelial cells and endothelial cells, with secondary fibroproliferation is a signature of pulmonary SARS-CoV-2 infection [4] and indicates a potential for chronic vascular and alveolar remodelling leading to lung fibrosis and/or pulmonary hypertension. We conducted a retrospective study in patients with SARS-CoV-2 pneumonia to assess the pulmonary functional status 1 month after symptom onset and correlate lung function alteration with the severity of pneumonia. Patients under the age of 85 years with confirmed SARS-CoV-2 infection (positive RT-PCR on nasopharyngeal swab) and respiratory symptoms, discharged from

The clinical expression of idiopathic pulmonary fibrosis (IPF) is directly related to multiple alterations in lung function. These alterations derive from a complex disease process affecting all compartments of the lower respiratory system, from the conducting airways to the lung vasculature. In this article we review the profound alterations in lung mechanics (reduced lung compliance and lung volumes), pulmonary gas exchange (reduced diffusing capacity, increased dead space ventilation, chronic arterial hypoxaemia) and airway physiology (increased cough reflex and increased airway volume), as well as pulmonary haemodynamics related to IPF. The relative contribution of these alterations to exertional limitation and dyspnoea in IPF is discussed.