ABSTRACT
BACKGROUND: The hemostasis system has been extensively investigated in patients in the acute phase of coronavirus disease 2019 (COVID-19). In contrast, the post-COVID syndrome is a poorly known entity, and there is a lack of information on the mechanisms underlying the hemostasis abnormalities in the post-COVID period. AIM: To analyze the potential changes in the parameters of the hemostasis system in the post- COVID period in the plasma of donors with different titers of anti-SARS-CoV-2 IgG. METHODS: The plasma from 160 donors who had recovered from COVID infection was used in the study. Based on the results of the Abbott SARS-CoV-2 IgG serological assay, all donors were divided into several groups: 5 ± 3 (n = 20); 55 ± 5 (n = 20); 65 ± 5 (n = 20); 75 ± 5 (n = 20); 85 ± 5 (n = 20); 95 ± 5 (n = 20); 125 ± 5 (n = 20); 175 ± 5 (n = 20) Index (S/C). A total of 20 healthy individuals without anti-SARS-CoV-2 IgG constituted the control group. Key laboratory parameters, such as fibrinogen concentrations, soluble fibrin monomer complex (SFMCs), and Ddimer, were investigated. In addition, the qualitative composition of the fraction of SFMCs was analyzed. RESULTS: The slight increase in the concentration of fibrinogen, SFMCs, and D-dimers in some donor groups have been found, which could cause the development of hemostasis disorders. In the fraction of SFMCs, the increase in the number of protein fragments with a molecular weight of less than 250 kDa and an increase in the level of proteins with a molecular weight of more than 270 kDa was revealed. CONCLUSION: The obtained results indicated the relationship between the changes in the parameters of the hemostasis system and the titers of anti-SARS-CoV-2 IgG in donors in the post-COVID period. It can be assumed that donors with higher titers of anti-SARS-CoV-2 IgG (>55 ± 5 Index (S/C)) are more prone to hemostasis abnormalities in the post-COVID period since a pronounced imbalance in the levels of SFMCs and D-dimer characterizes them. The appearance of protein fragments of different molecular weights in the fraction of SFMC points to uncontrolled activation of biochemical processes involving molecules of fibrinogenic origin. Additional studies are required to elucidate the role of anti-SARS-CoV-2 IgG in the post-COVID period.
Subject(s)
COVID-19 , Humans , Fibrinogen , SARS-CoV-2 , Antibodies, Viral , Immunoglobulin GABSTRACT
BACKGROUND: Severe acute respiratory syndrome-related Coronavirus 2 (SARS-CoV-2) іnfection induces a pro-inflammatory state of an organism with long-term systemic consequences as a result. Systemic inflammation, characterized by a high circulating level of inflammatory cytokines, is a significant factor influencing articular cartilage metabolism in osteoarthritis (OA). This study aimed to determine the levels of pro-inflammatory and anti-inflammatory cytokines in plasma of patients with OA following SARS-CoV-2 infection and to compare them with those of healthy controls. METHODS: The experiment involved patients of the Orthopedic Specialty Clinic aged 46 to 69 diagnosed with knee OA. Among persons with joint pathology a group of convalescent patients from 6-9 months after COVID-19 was identified. The control group involved relatively healthy donors. The plasma levels of pro-inflammatory (IL-1β, IL-6, IL-8, IL-12β, tumor necrosis factor α [TNF-α], interferon-gamma [IFN-γ]) and anti-inflammatory (IL-4 and IL-10) cytokines were determined by enzyme-linked immunosorbent assay. RESULTS: It was established that in patients with OA, as well as after suffering from SARS-CoV-2 infection, an increase in the plasma levels of IL-1β was observed against the background of a decrease in the levels of IL-4, IL-8, IL-10, IL- 12β, TNF-α and IFN-γ, compared to the healthy controls. COVID-19 more significantly influenced the plasma levels of pro-inflammatory cytokines IL-1β and IL-12β. CONCLUSIONS: The results indicate the imbalance of pro- and anti-inflammatory cytokines in the plasma in patients with OA for a long post- COVID. Сhanges in the levels of inflammatory mediators suggest distinct immunoregulatory mechanisms involved in the pathogenesis of both joint pathology and systemic disorders caused by SARS-CoV-2. [ FROM AUTHOR]