The Cytokine Status of Covid-19 Patients

Brief Summary

Detailed Description

The causative agent of coronavirus 2019 (COVID-19) disease, which started in Wuhan province of China in December 2019, was severe acute respiratory failure syndrome coronavirus 2 (SARS-CoV-2), which quickly spread all over the world and caused a pandemic. COVID-19 can cause death with symptoms such as fever, cough, muscle pain, shortness of breath, and pneumonia (1). Pulmonary pathology of COVID-19 is diffuse alveolar damage, focal reactive hyperplasia of pneumocytes with patchy inflammatory cells, intravascular thrombosis, monocyte, macrophage and lymphocyte infiltration into pulmonary spaces. Severe infiltration of pulmonary tissue affects alveolar gas exchange. In addition, cardiovascular morbidity, tachyarrhythmia and thromboembolic events are observed in 1/5 of the hospitalized patients with troponin elevation, which is closely related to mortality. In severe COVID-19 infections, after pulmonary inflammation, cardiovascular organ failure, cytokine storm, hemophagocytosis, septic shock, develops due to uncontrolled hypoxia, and isolated organ failure turns into multi-organ failure. It is noteworthy that it causes lymphopenia in patients. In the studies , the blood levels of certain inflammatory cytokines, interleukin-1β,interleukin-6 and TNF-α, were evaluated. In addition, blood values of a limited number of cytokines were investigated in a similar way in a limited number of studies published in our country. We aimed to study IL-1β, IFN-α2, IFN-γ, TNF-α, MCP-1 (CCL2), IL-6, IL-8 (CXCL8), IL-10, IL-12p70, IL-17A, IL-18, IL-23, IL-33 at Covid 19 and healthy volunteers.

Primary Outcomes