Home > Pulmonology > ERS 2020 > COVID-19 and the Lung > Secondary pulmonary fibrosis: a possible long-term effect of severe COVID-19

Secondary pulmonary fibrosis: a possible long-term effect of severe COVID-19

Presented by
Prof. Francesco Blasi , University of Milan, Italy
ERS 2020


Some COVID-19 patients may develop fibrotic abnormalities. Patients with severe acute disease are particularly at risk [1].

At present, the long-term pulmonary consequences of COVID-19 remain speculative [2]. “However, we know that the severity of COVID-19 is related to symptoms at discharge,” said Prof. Francesco Blasi (University of Milan, Italy). Particularly patients who suffer from severe COVID-19 disease which requires admission in an intensive care unit seem to be at risk. In the first large series of hospitalised patients with COVID-19 in Wuhan (China), chest computer tomography (CT) showed bilateral ground glass opacities with or without consolidation and with lower lobe predilection in all patients [2,3]. Although the virus is eradicated in patients who have recovered from COVID-19, this does not, in itself, preclude the development of progressive, fibrotic irreversible interstitial lung disease.

Prof. Blasi discussed an early analysis of discharged COVID-19 patients (enrolled between 5 February and 17 March 2020); 47% of patients showed impaired diffusing capacity of the lungs for carbon monoxide (DLCO) and 25% had a reduced total lung capacity (TLC). Impaired diffusion capacity was found in 30.4% of patients with mild disease, 42.4% of patients with pneumonia, and 84.2% of patients that suffered from severe pneumonia. “Not only impaired diffusion, but also CT changes are noticed. In particular in patients with severe disease,” Prof. Blasi said [1,4].

The correlation between severe pneumonia during a COVID-19 infection and secondary fibrosis can be explained by acute or chronic inflammation that leads to damage of the alveolar epithelium. In this state, proinflammatory cytokines such as TGFβ, TNFa, and IL-6 are released. They activate fibroblasts and myofibroblasts, which leads to excessive deposition of collagen and other extracellular matrix components, as well as the destruction of normal lung architecture. The similar cytokine profiles in idiopathic pulmonary fibrosis and COVID-19 suggest an analogous pathomechanism of pulmonary fibrosis in those diseases (see Figure) [5]. Viral infections may act as triggers for the initiation of lung fibrosis or promote exacerbations of existing lung fibrosis. Especially elderly male patients are prone to viral-induced fibrosis due to immunosenescence.

Figure: The pathogenesis of pulmonary fibrosis. Modified from [5]

With regard to therapy of SARS-CoV-2-associated pulmonary fibrosis, anything from traditional Chinese medicine to steroids and antifibrotics has been considered. “Steroids seem to work according to our experience: they improve and reduce pulmonary involvement and also improve exercise tolerance. But I think antifibrotics could be another interesting approach,” concluded Prof. Blasi.

    1. Blasi S. Long-term impact the lung and beyond. COV3651, ERS International Virtual Congress 2020, 7-9 Sept.
    2. Spagnolo P et al. Lancet Respir Med 2020;8:750-72.
    3. Wang D, et al. JAMA 2020;323:1061-1069.
    4. Hu Q, et al. Eur J Radiol 2020; 128:109017.
    5. Lechowicz K, et a.l J. Clin. Med. 2020;9:1917.


Posted on