Clozapine is strongly associated with the risk of pneumonia and inflammation.
Identifieur interne : 001315 ( Main/Exploration ); précédent : 001314; suivant : 001316Clozapine is strongly associated with the risk of pneumonia and inflammation.
Auteurs : Jose De Leon [États-Unis] ; Can-Jun Ruan [République populaire de Chine] ; Hélène Verdoux [France] ; Chuanyue Wang [République populaire de Chine]Source :
- General psychiatry [ 2517-729X ] ; 2020.
Abstract
Clinicians need to remember that (1) systemic inflammations can increase clozapine level; (2) clozapine, by itself, can cause inflammation, particularly during titration that is too rapid for that patient; (3) clozapine may increase the risk of infection; and (4) more specifically, clozapine may be particularly strongly associated with the risk of pneumonia. Pneumonia appears to be associated with high mortality in clozapine patients around the world. Clinicians who are alert to the risk of pneumonia in clozapine patients may significantly decrease mortality in clozapine patients. There is no data on COVID-19 infections in clozapine patients, but based on what we know about clozapine pharmacology, we can hypothesise that clozapine, possibly by impairing immunological mechanisms, may increase the risk of pneumonia in infected patients. More importantly, once fever and/or pneumonia develops, the clozapine dose should be cut in half to decrease the risk of clozapine intoxication. If there is any doubt that in spite of halving the dose there are still signs of clozapine intoxication, completely stopping clozapine may be indicated. Once the signs of inflammation and fever have disappeared, the clozapine dose can be increased to the prior dosage level.
DOI: 10.1136/gpsych-2019-100183
PubMed: 32420521
PubMed Central: PMC7199914
Affiliations:
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last="Wang">Chuanyue Wang</name><affiliation wicri:level="3"><nlm:affiliation>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32420521</idno><idno type="pmid">32420521</idno><idno type="doi">10.1136/gpsych-2019-100183</idno><idno type="pmc">PMC7199914</idno><idno type="wicri:Area/Main/Corpus">001240</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001240</idno><idno type="wicri:Area/Main/Curation">001240</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001240</idno><idno 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Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Verdoux, Helene" sort="Verdoux, Helene" uniqKey="Verdoux H" first="Hélène" last="Verdoux">Hélène Verdoux</name><affiliation wicri:level="1"><nlm:affiliation>Inserm, Bordeaux Population Health Research Center, University of Bordeaux Faculty of Medical Sciences, Bordeaux, Aquitaine, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Inserm, Bordeaux Population Health Research Center, University of Bordeaux Faculty of Medical Sciences, Bordeaux, Aquitaine</wicri:regionArea><wicri:noRegion>Aquitaine</wicri:noRegion><wicri:noRegion>Aquitaine</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Chuanyue" sort="Wang, Chuanyue" uniqKey="Wang C" first="Chuanyue" last="Wang">Chuanyue Wang</name><affiliation wicri:level="3"><nlm:affiliation>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">General psychiatry</title><idno type="ISSN">2517-729X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clinicians need to remember that (1) systemic inflammations can increase clozapine level; (2) clozapine, by itself, can cause inflammation, particularly during titration that is too rapid for that patient; (3) clozapine may increase the risk of infection; and (4) more specifically, clozapine may be particularly strongly associated with the risk of pneumonia. Pneumonia appears to be associated with high mortality in clozapine patients around the world. Clinicians who are alert to the risk of pneumonia in clozapine patients may significantly decrease mortality in clozapine patients. There is no data on COVID-19 infections in clozapine patients, but based on what we know about clozapine pharmacology, we can hypothesise that clozapine, possibly by impairing immunological mechanisms, may increase the risk of pneumonia in infected patients. More importantly, once fever and/or pneumonia develops, the clozapine dose should be cut in half to decrease the risk of clozapine intoxication. If there is any doubt that in spite of halving the dose there are still signs of clozapine intoxication, completely stopping clozapine may be indicated. Once the signs of inflammation and fever have disappeared, the clozapine dose can be increased to the prior dosage level.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32420521</PMID><DateRevised><Year>2020</Year><Month>05</Month><Day>22</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">2517-729X</ISSN><JournalIssue CitedMedium="Print"><Volume>33</Volume><Issue>2</Issue><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>General psychiatry</Title><ISOAbbreviation>Gen Psychiatr</ISOAbbreviation></Journal><ArticleTitle>Clozapine is strongly associated with the risk of pneumonia and inflammation.</ArticleTitle><Pagination><MedlinePgn>e100183</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1136/gpsych-2019-100183</ELocationID><Abstract><AbstractText>Clinicians need to remember that (1) systemic inflammations can increase clozapine level; (2) clozapine, by itself, can cause inflammation, particularly during titration that is too rapid for that patient; (3) clozapine may increase the risk of infection; and (4) more specifically, clozapine may be particularly strongly associated with the risk of pneumonia. Pneumonia appears to be associated with high mortality in clozapine patients around the world. Clinicians who are alert to the risk of pneumonia in clozapine patients may significantly decrease mortality in clozapine patients. There is no data on COVID-19 infections in clozapine patients, but based on what we know about clozapine pharmacology, we can hypothesise that clozapine, possibly by impairing immunological mechanisms, may increase the risk of pneumonia in infected patients. More importantly, once fever and/or pneumonia develops, the clozapine dose should be cut in half to decrease the risk of clozapine intoxication. If there is any doubt that in spite of halving the dose there are still signs of clozapine intoxication, completely stopping clozapine may be indicated. Once the signs of inflammation and fever have disappeared, the clozapine dose can be increased to the prior dosage level.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>de Leon</LastName><ForeName>Jose</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-7756-2314</Identifier><AffiliationInfo><Affiliation>University of Kentucky Mental Health Research Center, Eastern State Hospital, Lexington, Kentucky, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ruan</LastName><ForeName>Can-Jun</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verdoux</LastName><ForeName>Hélène</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Inserm, Bordeaux Population Health Research Center, University of Bordeaux Faculty of Medical Sciences, Bordeaux, Aquitaine, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Chuanyue</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Gen Psychiatr</MedlineTA><NlmUniqueID>101735271</NlmUniqueID><ISSNLinking>2517-729X</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Schizophr Bull. 2020 Jul 8;46(4):751</RefSource><PMID Version="1">32435811</PMID></CommentsCorrections></CommentsCorrectionsList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">psychopharmacology</Keyword><Keyword MajorTopicYN="N">schizophrenia</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>12</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>03</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>03</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>19</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32420521</ArticleId><ArticleId IdType="doi">10.1136/gpsych-2019-100183</ArticleId><ArticleId IdType="pii">gpsych-2019-100183</ArticleId><ArticleId IdType="pmc">PMC7199914</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Psychosomatics. 2020 Jan - 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