Reply: COVID-19, A and Hypersensitivity Pneumonitis

Dear Editors:

I appreciate your interest in our study, and would like to share clinical experiences regarding the article titled “COVID-19: A Clinical Syndrome Manifesting as Hypersensitivity Pneumonitis,” in which the use of steroids was demonstrated to not be efficacious, albeit the underlying asthma [1]. COVID-19 can be defined as a hypersensitivity reaction by SARS-CoV-2 infection. Its exact pathophysiology may be unraveled in future through extensive scientific evidence. Its clinical manifestations are greatly diverse, and the immune system (including innate and adaptive immunity) seems to play a major role in clearing the virus. Many cells, such as monocytes, macrophages, eosinophils, neutrophils, and lymphocytes might contribute to the surge of cytokines that induce inflammation and cell death. Excessive inflammation can promote the extracellular spread of the virus and lead to lung destruction. We have suggested in our report that prednisolone (PD) could be important for treatment of this condition; based on the hypothesis that COVID-19 is a hypersensitivity pneumonitis (HP) [2].

Homeostasis of human cells is regulated by the secretion of the stress hormone glucocorticoid, to varying degrees, under different external stimuli. PD has been the most effective and safer drug for HP for a long time. It can strongly suppress several cytokines, such as IL-1, IL-6, TNF-α, and type-2 biomarker [3, 4]. Further, the short course of PD does not lower the overall immunity, and hypersensitivity reactions are less common than methylprednisolone [5]. If oral PD is administered at an earlier stage of infection, fewer side effects will develop, since the inflammatory cascade might be overcome at a lower dose of PD.