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

Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9

“…Similarly, Patil et al [ 8 ] associated the impact of 600 patients with lung fibrosis post-COVID-19, evaluated at six weeks post-discharge from the hospital, with the severity of the initial disease and the duration, and comorbidities (diabetes). In the absence of the consistent data/protocol available for diagnostic tests, or a specific anti-fibrotic therapy, clinicians suggest a clinical visit and an imaging test, at 1, 3, 6, and 12 months after discharge for those with moderate/severe pneumonia in the infectious phase of COVID-19 [ 9 ]. However, clinicians propose complementary strategies to reduce the risk to develop pulmonary fibrosis, such as inhibition of viral replication, a long-standing inhibition of the inflammatory response, or the administration of anti-fibrotic therapy [ 10 ].…”

Current Understanding of Post-COVID Pulmonary Fibrosis: Where Are We?

“…Elderly, obese, smokers and diabetics, and patients that required mechanical ventilation and had severe acute respiratory distress syndrome, with high levels of C-reactive protein, D-dimer and interleukin-6 seem to have a greater risk of long-term pulmonary involvement. 7 , 8 , 9 Additionally, the hyperstimulation of the immune system associated with systemic inflammation secondary to COVID-19 can trigger autoimmune responses, with production of cytokines and autoantibodies, which may contribute to the development and progression of pulmonary parenchymal lesions. 7 , 8 Genetic predisposition, such as the identification of shortening of leucocyte telomeres, is also speculated as a potential risk factor for the occurrence of definitive pulmonary fibrosis after COVID-19.…”

“… 10 , 11 Patients with chronic interstitial lung diseases (ILDs) are at increased risk of progression of lung parenchymal lesions after the acute phase of COVID-19. 9 …”

“… 16 However, the role of antifibrotic drugs in post-COVID-19 fibrosis is unclear and may be considered in rare scenarios, such as those with the progressive phenotype over time, although this needs to be confirmed in randomized controlled trials. 5 , 7 , 9 Although corticosteroids may be used in the acute phase of COVID-19, their role in preventing or attenuating chronic ILD is controversial, but may be considered in those with areas suggestive of organizing pneumonia on CT scan. 7 Lung transplantation may be an alternative for patients with irreversible disease undergoing long periods of extracorporeal membrane oxygenation, although the main indications and contraindications remain under discussion.…”

Pseudo-honeycombing in a patient with coronavirus disease 2019 pneumonia

“…Recent studies have documented the development of fibrosis, both histologically and radiologically, during the evolution of Covid-19 pneumonia 1 , 2 . Although pulmonary fibrosis occurs late (after Covid-19) in most cases, some reports show that it can appear in the early stages of the disease 3 .…”