Abstract
Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease of unknown etiology, characterized by overproduction of organ-nonspecific autoantibodies to various components of the cell nucleus and cytoplasm and the development of immune-inflammatory damage to internal organs. The debut of SLE is preceded by an asymptomatic period, characterized by impaired immunological tolerance to its own autoantigens, determined by the multifaceted interaction of external, genetic and epigenetic factors, hormonal disorders, microbiome pathology, stress effects, etc. Development of a certain spectrum of clinical symptoms characteristic of SLE along with the detection of a reflects the progression of the immunopathological process in SLE, however, there is no generally accepted term that defines the patient’s condition, which has individual serological and clinical signs characteristic of this disease. In rheumatology, the concept of «incomplete» SLE is currently most often used. The problems of early diagnosis of SLE, clinical and laboratory predictors of the transformation of “incomplete” SLE into “reliable” SLE, difficulties in diagnosing SLE during the COVID-19 pandemic are considered. Particular attention is paid to the comparative characteristics of the immunopathological mechanisms of SLE and COVID-19.
Highlights
The debut of Systemic lupus erythematosus (SLE) is preceded by an asymptomatic period, characterized by impaired immunological tolerance to its own autoantigens, determined by the multifaceted interaction of external, genetic and epigenetic factors, hormonal disorders, microbiome pathology, stress effects, etc
Particular attention is paid to the comparative characteristics of the immunopathological mechanisms of SLE and COVID-19
Поэтому развитие клинических симптомов (лихорадка, усталость, депрессия, выпадение волос, головные боли, когнитивные нарушения, миалгии, артральгии и др.), с одной стороны, наблюдаемых при «длительном» COVID-19, а с другой стороны, входящих в критерии Системная красная волчанка (СКВ) [13, 17], в сочетании с обнаружением антинуклеарному фактору (АНФ), аФЛ и/или других «волчаночных» аутоантител может привести к гипердиагностике СКВ на разных стадиях болезни, в том числе и на «преклинической», а следовательно, к неоправданному назначению противовоспалительной терапии
Summary
Полученные при изучении сывороток кровных родственников пациентов СКВ, свидетельствуют о более выраженном увеличении уровня ИФН-ассоциированных хемокинов, таких как MCP-3 и MIP-1β (macrophage inflammatory protein-1 alpha), а также SCF (stem cell factor), BlyS (B-lymphocyte stimulator) наряду со снижением концентрации TGF-β и ИЛ-10 у тех из них, у которых в дальнейшем развилась СКВ [52]. В преклиническую фазу СКВ нарушения выявляются редко комплемента (характерные биомаркеры активности СКВ) чаще имело место у пациентов с «достоверной», чем c «вероятной» СКВ [37], и при заболеваниях, напоминающих СКВ, в том числе НЗСТ, хотя в других исследованиях подобной ассоциации выявлено не было [54].
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