Clinical cases of vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA vasculitis) induced by COVID-19

Abstract

COVID-19 is similar to immunoinflammatory rheumatic diseases in clinical manifestations, immune responses and pathogenetic mechanisms. Specific autoantibodies as markers of autoimmune diseases can be detected in patients with coronavirus infection. Most often, after COVID-19, antinuclear antibodies, antibodies to phospholipids, to cardiolipin, to β2-glycoprotein, to cytoplasmic antigens SS-A and SS/B, and cyclic citrulline-containing peptide are detected. In moderate and severe cases of COVID-19 infection with pulmonary-renal syndrome, cytokine storm, antineutrophil cytoplasmic antibodies, antibodies to myeloperoxidase and to proteinase 3 have become more frequent, which can trigger neutrophil NETosis with the formation of extracellular neutrophil traps — networks and induce the development of autoimmune processes and the appearance of de novo immunoinflammatory rheumatic diseases: arthritis , systemic lupus erythematosus, vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA vasculitis). Our study presents 4 clinical cases of patients with ANCA vasculitis with a history of recent coronavirus infection, chronologically verified. The average time after COVID-19 and the onset of ANCA vasculitis was about 3 months; damage to the upper respiratory tract, lower respiratory tract, skin and renal syndromes were observed. The severity of ANCA vasculitis did not depend on the severity of coronavirus infection: a mild course of COVID-19 infection did not exclude a severe course of ANCA vasculitis. It is recommended that all patients during and after coronavirus infection with post-COVID syndrome in the presence of damage to the ENT organs, kidneys, and skin are screened the presence of antineutrophil cytoplasmic antibodies to exclude the onset of ANCA vasculitis.