IPF characteristically affects men in their seventh or eighth decade of life,5 commonly with comorbidities such as hypertension, diabetes, and ischaemic heart disease, and with a history of cigarette smoke exposure.IPF is a progressive disease in which lung function inexorably declines, leading to respiratory failure and eventually death with lung transplantation being the only treatment that improves outcomes.7 The incidence of IPF is rising and the disease is estimated to affect 3 million people worldwide.8,9 A large proportion of patients with IPF are treated with one of the two available antifibrotic drugs, pirfenidone and nintedanib, that have been shown to slow the rate of lung function decline.10,11 Given the rapid global spread of the COVID-19 pandemic, and with efforts largely focused on the management of the most acutely unwell patients with COVID-19 pneumonia, the IPF clinical and research communities have had little time to collect sufficient data to thoroughly evaluate the potential risks and benefits of initiating and continuing antifibrotic therapy in this setting. To our knowledge, there are as yet no data reporting the incidence or mortality of SARS-CoV-2 infection in patients with IPF. Given that the risk factors for poor outcomes in SARS-CoV-2 infection are common in this patient group, who are further debilitated by reduced pulmonary reserve, it is possible that the prognosis is even worse for patients with IPF than for the general population. In this Personal View, we address the role of antifibrotic therapy in patients with IPF who contract SARS-CoV-2 infection and the scientific rationale for their use or discontinuation. We also consider the potential novel role of antifibrotic therapy in the management of patients without IPF who develop COVID-19 pneumonia, acute lung injury, and ARDS. Finally, we consider the fibrotic consequences for patients who survive COVID-19-related ARDS. Conclusion
The COVID-19 pandemic is bringing huge economic, social, and health-care challenges. As the wave of viral infection recedes, other problems will emerge that will need to be addressed. In this context, it is important to try and predict and prepare for these challenges. Many of the epidemiological risk factors and biological processes that lead to viral-induced ARDS are shared with IPF. In addition, many of the current and emerging antifibrotic drugs could have therapeutic potential for treating severe COVID-19 and preventing the long-term fibrotic consequences that might follow this pandemic. Ultimately, we hope the observations highlighted in this Personal View will help the respiratory and critical care communities to work together on well designed studies of antifibrotic therapies for severe COVID-19 pneumonia.
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