Aspects of pharmacotherapy with steroids in SARS-CoV-2 infection (literature review)

Abstract

In recent years, the SARS-CoV-2 pandemic has posed a significant challenge to global public health. Furthermore, infection with SARS-CoV-2 can result in acute respiratory distress syndrome due to excessive systemic inflammation, leading to multiple organ failure and eventual death. Furthermore, the challenge of reducing excessive systemic inflammation, specifically by decreasing the production of pro-inflammatory cytokines in response to SARS-CoV-2, remains unresolved. The use of glucocorticosteroids for SARS-CoV-2 infection remains controversial. Further research is required to support the routine use of steroids in intensive care protocols for SARS-CoV-2, as the current basis is insufficient. This review provides an analysis of literary sources, guidelines, and modern international recommendations on pathogenetic therapy of SARS-CoV-2 to prevent and eliminate hyperproduction of pro-inflammatory cytokines using glucocorticosteroid agents. The aim of this work is to analyse contemporary literary sources on the clinical and pharmacological justification for the use of glucocorticosteroids in clinical practice for SARS-CoV-2 infection. The scientific literature analysis indicates that glucocorticosteroid therapy cannot be recommended for routine use in therapeutic practice for patients with SARS-CoV-2 infection. Thus, with a mild course of SARS-CoV-2 infection, when the patient does not need oxygen support, glucocorticosteroids are contraindicated. Whereas in severe course, in acute respiratory distress syndrome with severe respiratory failure, their use is absolutely necessary, and they are recommended for mandatory use. There is a need for a generalised definition of the optimal glucocorticosteroid agent, including indications, dosage, and duration of use in SARS-CoV-2 infection therapy programs. Keywords: systemic inflammatory reaction, proinflammatory cytokines, hypothalamic-pituitary-adrenal system, glucocorticosteroids.