These diseases are not only independently associated with increased prevalence of COVID-19 but also associated with poor prognosis in patients with the disease.
We propose that patients with AATD are a susceptible population for COVID-19. First, for patients with AATD who do not have enough functional α1-antitrypsin, TMPRSS2 would be activated more easily, allowing SARS-CoV-2 entry into cells. Second, α1-antitrypsin has inhibitory effects on thrombin and plasmin, so AATD could be associated with an increased risk of coagulation disorder. Third, insufficient anti-inflammation, anti-cell death, anti-protease, and anticoagulation effects of α1-antitrypsin could increase the likelihood of severe acute lung injury. Patients with AATD who are infected with SARS-CoV-2 might, therefore, have worse outcomes than do members of the general population (figure). Since patients with AATD might have an increased risk of adverse outcomes from COVID-19, we propose the following call to action for the management of patients with AATD, with or without COVID-19.
