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10.3389/fimmu.2020.587517

http://scihub22266oqcxt.onion/10.3389/fimmu.2020.587517
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suck abstract from ncbi


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pmid33123171      Front+Immunol 2020 ; 11 (ä): 587517
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  • Clinical, Serological, and Histopathological Similarities Between Severe COVID-19 and Acute Exacerbation of Connective Tissue Disease-Associated Interstitial Lung Disease (CTD-ILD) #MMPMID33123171
  • Gagiannis D; Steinestel J; Hackenbroch C; Schreiner B; Hannemann M; Bloch W; Umathum VG; Gebauer N; Rother C; Stahl M; Witte HM; Steinestel K
  • Front Immunol 2020[]; 11 (ä): 587517 PMID33123171show ga
  • BACKGROUND AND OBJECTIVES: Understanding the pathophysiology of respiratory failure in coronavirus disease 2019 (COVID-19) is indispensable for development of therapeutic strategies. Since we observed similarities between COVID-19 and interstitial lung disease in connective tissue disease (CTD-ILD), we investigated features of autoimmunity in SARS-CoV-2-associated respiratory failure. METHODS: We prospectively enrolled 22 patients with RT-PCR-confirmed SARS-CoV-2 infection and 10 patients with non-COVID-19-associated pneumonia. Full laboratory testing was performed including autoantibody (AAB; ANA/ENA) screening using indirect immunofluorescence and immunoblot. Fifteen COVID-19 patients underwent high-resolution computed tomography. Transbronchial biopsies/autopsy tissue samples for histopathology and ultrastructural analyses were obtained from 4/3 cases, respectively. RESULTS: Thirteen (59.1%) patients developed acute respiratory distress syndrome (ARDS), and five patients (22.7%) died from the disease. ANA titers >/=1:320 and/or positive ENA immunoblots were detected in 11/13 (84.6%) COVID-19 patients with ARDS, in 1/9 (11.1%) COVID-19 patients without ARDS (p = 0.002) and in 4/10 (40%) patients with non-COVID-19-associated pneumonias (p = 0.039). Detection of AABs was significantly associated with a need for intensive care treatment (83.3 vs. 10%; p = 0.002) and occurrence of severe complications (75 vs. 20%, p = 0.03). Radiological and histopathological findings were highly heterogeneous including patterns reminiscent of exacerbating CTD-ILD, while ultrastructural analyses revealed interstitial thickening, fibroblast activation, and deposition of collagen fibrils. CONCLUSIONS: We are the first to report overlapping clinical, serological, and imaging features between severe COVID-19 and acute exacerbation of CTD-ILD. Our findings indicate that autoimmune mechanisms determine both clinical course and long-term sequelae after SARS-CoV-2 infection, and the presence of autoantibodies might predict adverse clinical course in COVID-19 patients.
  • |Adult[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Autoantibodies/blood[MESH]
  • |Betacoronavirus/immunology[MESH]
  • |COVID-19[MESH]
  • |Connective Tissue Diseases/immunology/*pathology[MESH]
  • |Coronavirus Infections/immunology/*pathology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Lung Diseases, Interstitial/immunology/*pathology[MESH]
  • |Lung/pathology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/immunology/*pathology[MESH]
  • |Prospective Studies[MESH]
  • |SARS-CoV-2[MESH]


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