Discussion
So far, there are no specific treatments for COVID-19. There is great concern regarding the duration of hospital treatment required in severe forms, because in the context of a pandemic, prolonged hospitalization means that health services may not be able to meet the demand generated by the disease. Therefore, we consider that one of the main aims for the treatment of severe pneumonia caused by COVID-19 should be to reduce the length of stay. Recent studies have shown that pulmonary inflammation and extensive lung damage in SARS patients can lead to more severe conditions [1, 2]. Furthermore, researchers have shown that SARS-CoV-2 binds to the angiotensin 2-converting enzyme (ECA2) to gain access to cells. This enzyme is fundamental both in the inactivation of angiotensin II (ANGII) and in the inactivation of bradykinin. The accumulation of bradykinin in the lungs is a common effect after the use of ECA2 inhibitors. In animal models, ECA2 inactivation leads to severe pneumonitis, and bradykinin inhibition fully recovers lung function and structure [9].
Several previous clinical trials have already shown the efficacy of both C1 esterase and icatibant, both bradykinin inhibitors, for use in a condition called hereditary angioedema. Considering our hypothesis that the release of bradykinin could be responsible for the hyperinflammatory state of the airway in SARS-CoV-2 infection and that its inhibition could reduce such inflammation, we imagine that the use of such drugs would help reduce the complications caused by COVID-19 pneumonia and consequently reduce the duration of hospitalization. This would mean a great gain for the health system since it would allow greater patient turnover, besides reducing the chance of secondary infections inherent in a long hospitalization.