Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.
Identifieur interne : 000081 ( PubMed/Corpus ); précédent : 000080; suivant : 000082Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.
Auteurs : Angela Ceribelli ; Francesca Motta ; Maria De Santis ; Aftab A. Ansari ; William M. Ridgway ; M Eric Gershwin ; Carlo SelmiSource :
- Journal of autoimmunity [ 1095-9157 ] ; 2020.
English descriptors
- KwdEn :
- Antibodies, Monoclonal, Humanized (therapeutic use), Antimalarials (therapeutic use), Antirheumatic Agents (therapeutic use), Azetidines (therapeutic use), Betacoronavirus (drug effects), Biological Therapy, Coronavirus Infections (complications), Coronavirus Infections (drug therapy), Coronavirus Infections (prevention & control), Cytokines (immunology), Humans, Immunosuppressive Agents (therapeutic use), Interleukin-1 (antagonists & inhibitors), Interleukin-6 (antagonists & inhibitors), Pandemics (prevention & control), Pneumonia, Viral (complications), Pneumonia, Viral (drug therapy), Pneumonia, Viral (prevention & control), Rheumatic Diseases (complications), Rheumatic Diseases (therapy), Sulfonamides (therapeutic use), Virus Internalization (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Interleukin-1, Interleukin-6.
- chemical , immunology : Cytokines.
- chemical , therapeutic use : Antibodies, Monoclonal, Humanized, Antimalarials, Antirheumatic Agents, Azetidines, Immunosuppressive Agents, Sulfonamides.
- complications : Coronavirus Infections, Pneumonia, Viral, Rheumatic Diseases.
- drug effects : Betacoronavirus, Virus Internalization.
- drug therapy : Coronavirus Infections, Pneumonia, Viral.
- prevention & control : Coronavirus Infections, Pandemics, Pneumonia, Viral.
- therapy : Rheumatic Diseases.
- Biological Therapy, Humans.
Abstract
The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.
DOI: 10.1016/j.jaut.2020.102442
PubMed: 32253068
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pubmed:32253068Le document en format XML
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Ansari</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ridgway, William M" sort="Ridgway, William M" uniqKey="Ridgway W" first="William M" last="Ridgway">William M. Ridgway</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gershwin, M Eric" sort="Gershwin, M Eric" uniqKey="Gershwin M" first="M Eric" last="Gershwin">M Eric Gershwin</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA. Electronic address: megershwin@ucdavis.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Selmi, Carlo" sort="Selmi, Carlo" uniqKey="Selmi C" first="Carlo" last="Selmi">Carlo Selmi</name><affiliation><nlm:affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy; Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy. Electronic address: carlo.selmi@hunimed.eu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32253068</idno><idno type="pmid">32253068</idno><idno type="doi">10.1016/j.jaut.2020.102442</idno><idno type="wicri:Area/PubMed/Corpus">000081</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000081</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.</title><author><name sortKey="Ceribelli, Angela" sort="Ceribelli, Angela" uniqKey="Ceribelli A" first="Angela" last="Ceribelli">Angela Ceribelli</name><affiliation><nlm:affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Motta, Francesca" sort="Motta, Francesca" uniqKey="Motta F" first="Francesca" last="Motta">Francesca Motta</name><affiliation><nlm:affiliation>Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="De Santis, Maria" sort="De Santis, Maria" uniqKey="De Santis M" first="Maria" last="De Santis">Maria De Santis</name><affiliation><nlm:affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Ansari, Aftab A" sort="Ansari, Aftab A" uniqKey="Ansari A" first="Aftab A" last="Ansari">Aftab A. Ansari</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ridgway, William M" sort="Ridgway, William M" uniqKey="Ridgway W" first="William M" last="Ridgway">William M. Ridgway</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gershwin, M Eric" sort="Gershwin, M Eric" uniqKey="Gershwin M" first="M Eric" last="Gershwin">M Eric Gershwin</name><affiliation><nlm:affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA. Electronic address: megershwin@ucdavis.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Selmi, Carlo" sort="Selmi, Carlo" uniqKey="Selmi C" first="Carlo" last="Selmi">Carlo Selmi</name><affiliation><nlm:affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy; Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy. Electronic address: carlo.selmi@hunimed.eu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of autoimmunity</title><idno type="eISSN">1095-9157</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antibodies, Monoclonal, Humanized (therapeutic use)</term><term>Antimalarials (therapeutic use)</term><term>Antirheumatic Agents (therapeutic use)</term><term>Azetidines (therapeutic use)</term><term>Betacoronavirus (drug effects)</term><term>Biological Therapy</term><term>Coronavirus Infections (complications)</term><term>Coronavirus Infections (drug therapy)</term><term>Coronavirus Infections (prevention & control)</term><term>Cytokines (immunology)</term><term>Humans</term><term>Immunosuppressive Agents (therapeutic use)</term><term>Interleukin-1 (antagonists & inhibitors)</term><term>Interleukin-6 (antagonists & inhibitors)</term><term>Pandemics (prevention & control)</term><term>Pneumonia, Viral (complications)</term><term>Pneumonia, Viral (drug therapy)</term><term>Pneumonia, Viral (prevention & control)</term><term>Rheumatic Diseases (complications)</term><term>Rheumatic Diseases (therapy)</term><term>Sulfonamides (therapeutic use)</term><term>Virus Internalization (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interleukin-1</term><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antibodies, Monoclonal, Humanized</term><term>Antimalarials</term><term>Antirheumatic Agents</term><term>Azetidines</term><term>Immunosuppressive Agents</term><term>Sulfonamides</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term><term>Rheumatic Diseases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term><term>Virus Internalization</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Coronavirus Infections</term><term>Pandemics</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Rheumatic Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Therapy</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32253068</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-9157</ISSN><JournalIssue CitedMedium="Internet"><Volume>109</Volume><PubDate><Year>2020</Year><Month>05</Month></PubDate></JournalIssue><Title>Journal of autoimmunity</Title><ISOAbbreviation>J. Autoimmun.</ISOAbbreviation></Journal><ArticleTitle>Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.</ArticleTitle><Pagination><MedlinePgn>102442</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0896-8411(20)30055-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jaut.2020.102442</ELocationID><Abstract><AbstractText>The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.</AbstractText><CopyrightInformation>Copyright © 2020. Published by Elsevier Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ceribelli</LastName><ForeName>Angela</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Motta</LastName><ForeName>Francesca</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Santis</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ansari</LastName><ForeName>Aftab A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ridgway</LastName><ForeName>William M</ForeName><Initials>WM</Initials><AffiliationInfo><Affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gershwin</LastName><ForeName>M Eric</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA. Electronic address: megershwin@ucdavis.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Selmi</LastName><ForeName>Carlo</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy; Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy. Electronic address: carlo.selmi@hunimed.eu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Autoimmun</MedlineTA><NlmUniqueID>8812164</NlmUniqueID><ISSNLinking>0896-8411</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D061067">Antibodies, Monoclonal, Humanized</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000962">Antimalarials</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018501">Antirheumatic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001384">Azetidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508600">IL6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007166">Immunosuppressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013449">Sulfonamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>I031V2H011</RegistryNumber><NameOfSubstance UI="C502936">tocilizumab</NameOfSubstance></Chemical><Chemical><RegistryNumber>ISP4442I3Y</RegistryNumber><NameOfSubstance UI="C000596027">baricitinib</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C000657245">COVID-19</SupplMeshName><SupplMeshName Type="Protocol" UI="C000705127">COVID-19 drug treatment</SupplMeshName><SupplMeshName Type="Organism" UI="C000656484">severe acute respiratory syndrome coronavirus 2</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D061067" MajorTopicYN="N">Antibodies, Monoclonal, Humanized</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000962" MajorTopicYN="N">Antimalarials</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018501" MajorTopicYN="N">Antirheumatic 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