SARS‐CoV‐2 infection as a trigger of autoimmune response
Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to aut...
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Published in | Clinical and translational science Vol. 14; no. 3; pp. 898 - 907 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
John Wiley & Sons, Inc
01.05.2021
John Wiley and Sons Inc Wiley |
Subjects | |
Online Access | Get full text |
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Abstract | Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy.
Study Highlights
WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC?
☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID‐19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) infection and autoimmune disease onset.
WHAT QUESTION DID THIS STUDY ADDRESS?
☑ In this monocentric study, we demonstrated how SARS‐CoV‐2 infection could be associated with an autoimmune response and development of autoantibodies.
WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE?
☑ Patients with COVID‐19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome.
HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE?
☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. |
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AbstractList | Abstract Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? ☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID‐19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) infection and autoimmune disease onset. WHAT QUESTION DID THIS STUDY ADDRESS? ☑ In this monocentric study, we demonstrated how SARS‐CoV‐2 infection could be associated with an autoimmune response and development of autoantibodies. WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? ☑ Patients with COVID‐19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome. HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID-19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID-19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin-6 concentrations were also increased, supporting the major role of this interleukin during COVID-19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID-19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID-19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS-CoV-2 infection. In addition, we highly recommend checking patients with COVID-19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? ☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID-19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) infection and autoimmune disease onset. WHAT QUESTION DID THIS STUDY ADDRESS? ☑ In this monocentric study, we demonstrated how SARS-CoV-2 infection could be associated with an autoimmune response and development of autoantibodies. WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? ☑ Patients with COVID-19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome. HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS-CoV-2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID-19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID-19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID-19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin-6 concentrations were also increased, supporting the major role of this interleukin during COVID-19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID-19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID-19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS-CoV-2 infection. In addition, we highly recommend checking patients with COVID-19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? ☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID-19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) infection and autoimmune disease onset. WHAT QUESTION DID THIS STUDY ADDRESS? ☑ In this monocentric study, we demonstrated how SARS-CoV-2 infection could be associated with an autoimmune response and development of autoantibodies. WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? ☑ Patients with COVID-19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome. HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS-CoV-2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID-19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance.Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID-19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID-19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin-6 concentrations were also increased, supporting the major role of this interleukin during COVID-19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID-19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID-19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS-CoV-2 infection. In addition, we highly recommend checking patients with COVID-19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? ☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID-19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2) infection and autoimmune disease onset. WHAT QUESTION DID THIS STUDY ADDRESS? ☑ In this monocentric study, we demonstrated how SARS-CoV-2 infection could be associated with an autoimmune response and development of autoantibodies. WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? ☑ Patients with COVID-19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome. HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS-CoV-2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID-19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. Study Highlights WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? ☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID‐19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) infection and autoimmune disease onset. WHAT QUESTION DID THIS STUDY ADDRESS? ☑ In this monocentric study, we demonstrated how SARS‐CoV‐2 infection could be associated with an autoimmune response and development of autoantibodies. WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? ☑ Patients with COVID‐19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome. HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy.Study HighlightsWHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC?☑ Recent data sustain the idea that autoimmune phenomena exist in patients with coronavirus disease 2019 (COVID‐19), but other investigations are necessary to define the possible link between severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) infection and autoimmune disease onset.WHAT QUESTION DID THIS STUDY ADDRESS?☑ In this monocentric study, we demonstrated how SARS‐CoV‐2 infection could be associated with an autoimmune response and development of autoantibodies.WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE?☑ Patients with COVID‐19 having an increased level of inflammatory markers and strong autoantibodies positivity (i.e., antinuclear antibodies and antineutrophil cytoplasmic antibodies) presented the worst clinical outcome.HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE?☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. |
Author | Sacchi, Maria C. Agatea, Lisa Stobbione, Paolo Stecca, Anna Tozzoli, Renato Bonometti, Ramona Lauritano, Ernesto C. Guaschino, Roberto Tamiazzo, Stefania Roveta, Annalisa De Gaspari, Piera |
AuthorAffiliation | 7 Endocrinology Unit S. Giorgio Hospital Pordenone Italy 4 Neuroimmunology Laboratory Pediatric Research Institute Città della Speranza Foundation Padova Italy 5 Emergency Medicine Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy 6 IRFI (Infrastruttura Ricerca Formazione Innovazione) “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy 2 Rheumatology Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy 1 Autoimmunology and Analysis Laboratory Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy 3 Laboratory Department Affiliated to Euroimmun Padova Italy |
AuthorAffiliation_xml | – name: 3 Laboratory Department Affiliated to Euroimmun Padova Italy – name: 7 Endocrinology Unit S. Giorgio Hospital Pordenone Italy – name: 5 Emergency Medicine Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy – name: 1 Autoimmunology and Analysis Laboratory Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy – name: 4 Neuroimmunology Laboratory Pediatric Research Institute Città della Speranza Foundation Padova Italy – name: 6 IRFI (Infrastruttura Ricerca Formazione Innovazione) “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy – name: 2 Rheumatology Unit “SS Antonio e Biagio e Cesare Arrigo” Hospital Alessandria Italy |
Author_xml | – sequence: 1 givenname: Maria C. surname: Sacchi fullname: Sacchi, Maria C. email: csacchi@ospedale.al.it organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 2 givenname: Stefania surname: Tamiazzo fullname: Tamiazzo, Stefania organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 3 givenname: Paolo surname: Stobbione fullname: Stobbione, Paolo organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 4 givenname: Lisa surname: Agatea fullname: Agatea, Lisa organization: Affiliated to Euroimmun – sequence: 5 givenname: Piera surname: De Gaspari fullname: De Gaspari, Piera organization: Città della Speranza Foundation – sequence: 6 givenname: Anna surname: Stecca fullname: Stecca, Anna organization: Affiliated to Euroimmun – sequence: 7 givenname: Ernesto C. surname: Lauritano fullname: Lauritano, Ernesto C. organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 8 givenname: Annalisa surname: Roveta fullname: Roveta, Annalisa organization: IRFI (Infrastruttura Ricerca Formazione Innovazione) “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 9 givenname: Renato surname: Tozzoli fullname: Tozzoli, Renato organization: S. Giorgio Hospital – sequence: 10 givenname: Roberto surname: Guaschino fullname: Guaschino, Roberto organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital – sequence: 11 givenname: Ramona surname: Bonometti fullname: Bonometti, Ramona organization: “SS Antonio e Biagio e Cesare Arrigo” Hospital |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33306235$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1007/s10067-018-4062-x 10.1002/jmv.26232 10.3906/sag-2004-168 10.3389/fimmu.2020.01441 10.1016/S1474-4422(18)30279-5 10.1038/s41392-020-0191-1 10.4158/EP.5.3.109 10.1111/j.1365-2249.2008.03834.x 10.1136/bmj.m1936 10.1016/j.jbi.2008.08.010 10.1186/s40425-018-0343-9 10.1111/cts.12805 10.1016/j.autrev.2020.102591 10.3390/ijms21093330 10.1007/s00281-017-0629-x 10.1111/j.1365-2036.2011.04932.x 10.5114/reum.2018.77976 10.1136/annrheumdis-2020-218009 10.1080/23744235.2019.1690676 10.1056/NEJMc2007575 10.1053/sarh.2002.28303 10.1001/jama.2020.3204 10.1016/j.jbi.2019.103208 |
ContentType | Journal Article |
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References | 2019; 95 2009; 42 2020; 382 2002; 31 2009 2020; 369 2009; 155 2020; 79 2020; 323 2020; 11 2012; 35 1999; 5 2020; 19 2018; 6 1993; 14 13 2018; 17 2020; 5 2020; 52 2017; 39 2020; 50 2020 2020; 24 2020; 22 2020; 21 2018; 56 2018; 37 Tomer Y (e_1_2_9_8_1) 1993; 14 e_1_2_9_11_1 e_1_2_9_10_1 e_1_2_9_13_1 e_1_2_9_12_1 Coomes EA (e_1_2_9_22_1) Bonometti R (e_1_2_9_32_1) 2020; 24 e_1_2_9_15_1 e_1_2_9_14_1 e_1_2_9_17_1 e_1_2_9_16_1 Betterle C (e_1_2_9_6_1) 2009 e_1_2_9_19_1 Sacchi MC (e_1_2_9_31_1) 2020; 24 e_1_2_9_20_1 Pesce G (e_1_2_9_7_1) 2009 e_1_2_9_21_1 e_1_2_9_24_1 e_1_2_9_23_1 e_1_2_9_5_1 e_1_2_9_4_1 e_1_2_9_3_1 e_1_2_9_2_1 Infantino M (e_1_2_9_18_1) 2020; 22 Connell NT (e_1_2_9_30_1) e_1_2_9_9_1 e_1_2_9_26_1 e_1_2_9_25_1 e_1_2_9_28_1 e_1_2_9_27_1 e_1_2_9_29_1 |
References_xml | – volume: 11 start-page: 1441 year: 2020 article-title: Immune response, inflammation, and the clinical spectrum of COVID‐19 publication-title: Front Immunol – volume: 37 start-page: 875 year: 2018 end-page: 884 article-title: Anti‐neutrophil cytoplasmic antibodies and their clinical significance publication-title: Clin Rheumatol – volume: 35 start-page: 292 year: 2012 end-page: 299 article-title: The impact of intestinal resection on serum levels of anti‐Saccharomyces cerevisiae antibodies (ASCA) in patients with Crohn’s disease publication-title: Aliment Pharmacol Ther – volume: 382 year: 2020 article-title: Coagulopathy and antiphospholipid antibodies in patients with Covid‐19 publication-title: N Engl J Med – year: 2020 article-title: The cytokine storm and COVID‐19 publication-title: J. Med. Virol. – volume: 24 start-page: 11960 year: 2020 end-page: 11963 article-title: Case report of COVID‐19 in an elderly patient: could SARS‐CoV2 trigger myositis? publication-title: Eur Rev Med Pharmacol Sci – volume: 39 start-page: 529 year: 2017 end-page: 539 article-title: Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology publication-title: Semin Immunopathol – start-page: 14 year: 2009 end-page: 36 – volume: 31 start-page: 256 year: 2002 end-page: 263 article-title: Viral infection and antiphospholipid antibodies publication-title: Semin Arthritis Rheum – volume: 79 start-page: 1661 year: 2020 end-page: 1663 article-title: Autoantibodies related to systemic autoimmune rheumatic diseases in severely ill patients with COVID‐19 publication-title: Ann Rheum Dis. – volume: 17 start-page: 733 year: 2018 end-page: 735 article-title: Autoimmune encephalitis after herpes simplex encephalitis: insights into pathogenesis publication-title: Lancet Neurol – article-title: Interleukin‐6 in Covid‐19: a systematic review and meta‐analysis publication-title: Rev Med Virol – volume: 56 start-page: 243 year: 2018 end-page: 248 article-title: Antinuclear antibodies in healthy people and non‐rheumatic diseases diagnostic and clinical implications publication-title: Reumatologia – volume: 22 start-page: 203 year: 2020 end-page: 210 article-title: Serological assays for SARS‐CoV‐2 infectious disease: benefits, limitations and perspectives publication-title: Isr Med Assoc J – start-page: 1 year: 2009 end-page: 13 – volume: 95 start-page: 103208 year: 2019 article-title: The REDCap consortium: building an international community of software partners publication-title: J Biomed Inform – volume: 13: start-page: 1077 end-page: 1086 article-title: Clinical and autoimmune characteristics of severe and clinical cases of COVID‐19 publication-title: Clin Transl Sci. – volume: 52 start-page: 177 year: 2020 end-page: 185 article-title: Antinuclear antibodies in infectious diseases publication-title: Infect Dis – volume: 50 start-page: 620 issue: SI‐1 year: 2020 end-page: 632 article-title: COVID‐19, immune system response, hyperinflammation and repurposing antirheumatic drugs publication-title: Turk J Med Sci – volume: 5 start-page: 109 year: 1999 end-page: 113 article-title: Atypical thyroiditis in Huelva, Spain publication-title: Endocr Pract – volume: 323 start-page: 1488 year: 2020 end-page: 1494 article-title: Epidemiologic features and clinical course of patients infected with SARS‐Cov2 in Singapore publication-title: JAMA – volume: 42 start-page: 377 year: 2009 end-page: 381 article-title: Research electronic data capture (REDCap) – a metadata‐driven methodology and workflow process for providing translational research informatics support publication-title: J Biomed Inform – volume: 369 start-page: m1936 year: 2020 article-title: Scope, quality, and inclusivity of clinical guidelines produced early in the covid‐19 pandemic: rapid review publication-title: BMJ – volume: 21 start-page: 3330 year: 2020 article-title: Cytokine release syndrome in COVID‐19 patients, a new scenario for old concern: the fragile balance between infection and autoimmunity publication-title: Int J Mol Sci – volume: 14 start-page: 107 year: 1993 end-page: 120 article-title: Infection, thyroid disease, and autoimmunity publication-title: Endocr Rev – article-title: Coagulopathy of COVID‐19 and antiphospholipid antibodies publication-title: J Thromb Haemost – volume: 155 start-page: 1 year: 2009 end-page: 15 article-title: The role of infections in autoimmune disease publication-title: Clin Exp Immunol – volume: 19 start-page: 102591 year: 2020 article-title: Molecular mimicry may explain multi‐organ damage in COVID‐19 publication-title: Autoimmun Rev – volume: 5 start-page: 84 year: 2020 article-title: Immune response in COVID‐19: addressing a pharmacological challenge by targeting pathways triggered by SARS‐CoV‐2 publication-title: Sig Transduct Target Ther – volume: 24 start-page: 11474 year: 2020 article-title: The first case of systemic lupus erythematous (SLE) trigger by COVID19 infection publication-title: Eur Rev Med Pharmacol Sci – volume: 6 start-page: 56 year: 2018 article-title: Cytokine release syndrome publication-title: J Immunother Cancer – ident: e_1_2_9_27_1 doi: 10.1007/s10067-018-4062-x – ident: e_1_2_9_22_1 article-title: Interleukin‐6 in Covid‐19: a systematic review and meta‐analysis publication-title: Rev Med Virol – ident: e_1_2_9_20_1 doi: 10.1002/jmv.26232 – volume: 24 start-page: 11960 year: 2020 ident: e_1_2_9_31_1 article-title: Case report of COVID‐19 in an elderly patient: could SARS‐CoV2 trigger myositis? publication-title: Eur Rev Med Pharmacol Sci – ident: e_1_2_9_19_1 doi: 10.3906/sag-2004-168 – ident: e_1_2_9_23_1 doi: 10.3389/fimmu.2020.01441 – ident: e_1_2_9_10_1 doi: 10.1016/S1474-4422(18)30279-5 – ident: e_1_2_9_17_1 doi: 10.1038/s41392-020-0191-1 – start-page: 1 volume-title: Il Laboratorio nelle malattie autoimmuni d’organo year: 2009 ident: e_1_2_9_6_1 – start-page: 14 volume-title: Il Laboratorio nelle malattie autoimmuni d’organo year: 2009 ident: e_1_2_9_7_1 – ident: e_1_2_9_9_1 doi: 10.4158/EP.5.3.109 – ident: e_1_2_9_5_1 doi: 10.1111/j.1365-2249.2008.03834.x – ident: e_1_2_9_16_1 doi: 10.1136/bmj.m1936 – ident: e_1_2_9_14_1 doi: 10.1016/j.jbi.2008.08.010 – ident: e_1_2_9_4_1 doi: 10.1186/s40425-018-0343-9 – ident: e_1_2_9_24_1 doi: 10.1111/cts.12805 – volume: 24 start-page: 11474 year: 2020 ident: e_1_2_9_32_1 article-title: The first case of systemic lupus erythematous (SLE) trigger by COVID19 infection publication-title: Eur Rev Med Pharmacol Sci – ident: e_1_2_9_13_1 doi: 10.1016/j.autrev.2020.102591 – ident: e_1_2_9_3_1 doi: 10.3390/ijms21093330 – volume: 14 start-page: 107 year: 1993 ident: e_1_2_9_8_1 article-title: Infection, thyroid disease, and autoimmunity publication-title: Endocr Rev – ident: e_1_2_9_21_1 doi: 10.1007/s00281-017-0629-x – ident: e_1_2_9_28_1 doi: 10.1111/j.1365-2036.2011.04932.x – volume: 22 start-page: 203 year: 2020 ident: e_1_2_9_18_1 article-title: Serological assays for SARS‐CoV‐2 infectious disease: benefits, limitations and perspectives publication-title: Isr Med Assoc J – ident: e_1_2_9_26_1 doi: 10.5114/reum.2018.77976 – ident: e_1_2_9_12_1 doi: 10.1136/annrheumdis-2020-218009 – ident: e_1_2_9_25_1 doi: 10.1080/23744235.2019.1690676 – ident: e_1_2_9_30_1 article-title: Coagulopathy of COVID‐19 and antiphospholipid antibodies publication-title: J Thromb Haemost – ident: e_1_2_9_11_1 doi: 10.1056/NEJMc2007575 – ident: e_1_2_9_29_1 doi: 10.1053/sarh.2002.28303 – ident: e_1_2_9_2_1 doi: 10.1001/jama.2020.3204 – ident: e_1_2_9_15_1 doi: 10.1016/j.jbi.2019.103208 |
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Snippet | Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we... Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID-19). In this study, we... Abstract Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this... |
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