Perfil clínico, oxidativo e inflamatório em pacientes com SARS-CoV-2

Abstract

In December 2019, cases of serious illness that caused an outbreak of pneumonia of unknown origin were reported in Wuhan, Hubei Province, China. Soon after, the number of cases skyrocketed dramatically, spreading across China and the world. The causative agent of the disease was called the new coronavirus, “SARS-CoV-2”. The clinical condition caused by the novel coronavirus has been referred to as COVID-19. Among the most common symptoms of COVID19 are fever, cough, fatigue and shortness of breath, while other symptoms include sputum production, headache, diarrhea, dyspnea and lymphopenia. Transmission occurs from person to person, mainly via direct contact or through droplets spread by coughing or sneezing from an infected individual, or through direct contact with infected people. Therefore, this study aimed to verify the clinical and oxidative status of patients with COVID-19 correlating with the severity of the disease, as well as characterizing changes in serum inflammatory mediators in hospitalized patients, correlating with death. The study involved 28 patients with mild COVID-19, who were in isolation at home; 65 patients admitted to the intensive care unit (ICU) of the HUSM, with moderate or severe COVID-19 and 50 participants in the control group. Clinical and social data were obtained through their electronic medical records. Oxidative stress markers were determined by quantifying oxidative damage markers such as thiobarbituric acid reactive substances (TBARS), as well as oxidative stress protectors (protein thiol groups (P-SH), vitamin C, ferric reduction ability of plasma (FRAP), Uric acid (UA), in addition to verifying the activity of enzyme δaminolevulinate dehydratase (δ-ALA-D). Inflammatory mediators were determined by measuring the levels of interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-4 (IL-4), interleukin-17 (IL-17), tumour necrosis factor alfa (TNF-α) and interferon-gamma (IFN-γ). Through the results obtained, we verified that patients with COVID-19 have an increase in oxidative damage markers (TBARS) and a decrease in antioxidant defenses (NP-SH, vitamin C, FRAP, UA), including the activity of the δ-ALA-D enzyme .In addition, the results of laboratory tests were evaluated, comparing the results of recovered patients with those who died. We found that geriatric patients, especially men, with comorbidities such as obesity and/or chronic diseases are more likely to develop the most severe form of COVID-19 than other patient groups. Patients with moderate/severe COVID-19 have higher oxidative stress and have lower δ-ALA-D enzyme activity compared to the control group.Levels of all inflammatory parameters were elevated in the moderate/severe COVID-19 serum compared to the control group. Laboratory parameters (urea, LDH, D-dimer,TAP/INR,AST, ALT) are increased in patients who died compared to recovered patients, with only the lymphocyte level being lower in patients who died compared to recovered patients. In conclusion, oxidative stress and interleukins can be used in clinical practice as a predictor of worsening of the clinical picture.