International Journal of Rheumatic Diseases, Год журнала: 2023, Номер 26(12), С. 2373 - 2376

Опубликована: Дек. 1, 2023

Multiple environmental factors have been implicated in developing systemic lupus erythematosus (SLE). Infections, particularly viral infections, extensively studied as potential triggers for SLE.1 Several viruses, such human endogenous retroviruses, Epstein–Barr virus, parvovirus B19, cytomegalovirus, and immunodeficiency virus (HIV), possible SLE triggers. The emergence of the SARS-CoV-2 which causes COVID-19, has associated with production various autoantibodies including antinuclear antibodies (ANA), anti-Ro/Sjögren's syndrome A antibodies, antiphospholipid antibodies. These observed 11% to 53.6% people acute phase disease, a higher frequency critically ill COVID-19 patients.2-6 Moreover, high ANA titers were found 43.6% patients at 12 months post-COVID-19 symptom onset.7 Additionally, cases de-novo reported during after infection or vaccination.8-10 Distinguishing between new onset so-called "long COVID" can be challenging due shared characteristics two conditions. For instance, arthritis musculoskeletal symptoms are present over 85% 65% persons 2 years contracting SARS-CoV-2.6, 11 Therefore, analyzing temporal association is crucial identifying clinical clues that aid differentiating these Kioi et al12 describe case an older adult who developed persistent pleural effusion lymphopenia following infection. An immunological study revealed presence autoantibodies, leading diagnosis SLE. authors also analyzed 9 similar 90% exhibited 60% had serositis. Based on findings, al suggest prolonged and/or should evaluated autoantibodies.12 Pleural uncommon infection, estimated prevalence only 6.7% recently published meta-analysis 103 studies included 9907 confirmed patients.13 On other hand, pleuritis common lung issue Up 50% noticeable effusion, detected up 93% necropsy studies.14 In contrast, frequent hematological abnormality occurring 35% 83% 75% active disease.15, 16 although would seem less helpful disorders, its persistence resolution episode may raise suspicion autoimmune origin (Figure 1). Other findings help distinguish COVID-19. platelet count below 100 000/μL 5% whereas it occurs 20%–40% patients.17, 18 series reviewed by al,12 thrombocytopenia was 50%. Renal damage severity rates exceeding 20% hospitalized intensive care unit patients.19 SLE, nephritis approximately patients.20 Interestingly, renal involvement new-onset Mok al,21 no relationship Elevated C-reactive protein (CRP) commonly laboratory result while remains unchanged slightly elevated flare.22, 23 critical patients, 25% showed increase procalcitonin levels, most probably bacterial infection.24, 25 D-dimer levels linked flare 89%, 70% severe exhibit increased levels.26, 27 differential when unrelated respiratory disease severity. characteristic supports causal relatively short interval appearance symptoms. al, 8 out within 30 days infection.21 Furthermore, Chang al28 data from extensive global database risk (adjusted hazard ratio [HR] 2.98; 95% CI 2.78–3.20) among 887 455 individuals compared non-COVID-19 6-month follow-up period. However, another Tesch al29 examined cohort 640 701 non-vaccinated polymerase chain reaction-confirmed 2020 incidence rate 1.35 (95% 0.92–1.95) 3 15 emerge shortly suggesting specific pathogenic mechanisms. spectrum manifestations different stages differentiated distribution considered early diagnosis. Acute infections trigger flares pre-existing conducted across multiple centers Italy, 5.9% experienced SARS-CoV-2.30 Contributing exacerbation include inflammatory state induced suspension treatment shortage medications confinement.31 results reaction where innate adaptive immune systems wrongly respond cellular particles contain nucleic acid, continuous type 1 interferon (IFN).11 Various mechanisms cause this process. Cellular caused releases cell-free DNA peptidyl arginine deiminase enzymes (PADs) into extracellular space, creation autoantibodies.32 temporary impairment acquired immunity triggered could loss self-tolerance self-antigens inappropriate reconstitution predisposing conditions.33 addition, components resemble proteins through molecular mimicry.34 Some behave autoantigens development certain peptides SARS-CoV-2.35 hypothesized inflammation prompt system generate against antigens share structural similarities self-antigens. This cross-reactive response both non-self-antigens.28 activate Toll-like receptors (TLRs) produce pro-inflammatory cytokines, IFN. Excessive IFN infections.34 consistent release I changes T cell function, chronic tissues, damage.11 It important acknowledge current evidence falls definitively establishing cause-and-effect autoimmunity. partly limitations inherent designs, primarily observational nature. Syed difference exposed matched controls HR 1.02; 0.51–2.05) 458 147 adults infection.36 Xu bidirectional analysis, support idea genetic predisposition causally contributes COVID-19.37 their influenced not accounted (confounding factors). several factors, consistency studies, relationship, biological plausibility, enhance reliability persuasiveness association. conclusion, ranges organ-specific conditions cutaneous vasculitis thrombocytopenic purpura like idiopathic myopathies.9 Evidence basic research suggests essential recognize lab condition so they promptly diagnosed treated. To gain thorough understanding progression conduct in-depth affected extended Abraham Edgar Gracia-Ramos Miguel Angel Saavedra participated design, conception, writing, review final approval manuscript. None. declare conflict interest. will available ResearchGate https://www.researchgate.net/ embargo date publication allow commercialization findings.

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