Circulating immune complexes in the pathogenesis of post-COVID joint syndrome

Background. A common manifestation of the post-COVID syndrome is damage to the articular apparatus. Considering the role of circulating immune complexes in the occurrence of postinfectious and immune lesions of joints, as well as their participation in the immunopathogenesis of the acute period of infection, it can be assumed that they are involved in the formation of joint syndrome after COVID-infection.
The aim. To assess the involvement of circulating immune complexes in the pathogenesis of various clinical variants of post-COVID joint syndrome.
Materials and methods. Sixty two patients with post-COVID syndrome and complaints of damage to the musculoskeletal system were examined. All patients had suffered coronavirus infection during the previous 12 months. All patients underwent radiographic and ultrasound examination of the joints. In the blood serum the total content of IgM, IgG and IgE was determined. Circulating immune complexes in peripheral blood were determined by precipitation method.
Results. The post-COVID joint syndrome in the examined patients manifested itself in four variants, which differed clinically and had different immunological characteristics. High levels of circulating immune complexes were detected in arthralgia, arthritis, and the onset of arthropathy and were accompanied by elevated titers of IgM and IgG. With the progression of arthropathy, the circulating immune complexes content in the blood of patients often corresponds to the borderline level with low IgM and IgG values. An increased IgE titer was recorded in the blood of patients with arthritis, onset and progression of arthropathy, and there were no manifestations of allergy and the allergic history was negative in the majority of the examined.
Conclusion. Thus, the immunocomplex mechanism of damage plays an important role in the pathogenesis of arthralgia, arthritis and the onset of osteoarthropathy, but not its progression in post-COVID syndrome. IgE is actively involved in the formation of arthritis, the progression of osteoarthropathy, and especially in its onset.

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