Treatments in Covid-19 patients with pre-existing metabolic dysfunction-associated fatty liver disease: A potential threat for drug-induced liver injury?
Identifieur interne : 000328 ( Main/Exploration ); précédent : 000327; suivant : 000329Treatments in Covid-19 patients with pre-existing metabolic dysfunction-associated fatty liver disease: A potential threat for drug-induced liver injury?
Auteurs : Pierre-Jean Ferron [France] ; Thomas Gicquel [France] ; Bruno Mégarbane [France] ; Bruno Clément [France] ; Bernard Fromenty [France]Source :
- Biochimie [ 1638-6183 ] ; 2020.
Abstract
Obese patients who often present metabolic dysfunction-associated fatty liver disease (MAFLD) are at risk of severe presentation of coronavirus disease 2019 (COVID-19). These patients are more likely to be hospitalized and receive antiviral agents and other drugs required to treat acute respiratory distress syndrome and systemic inflammation, combat bacterial and fungal superinfections and reverse multi-organ failure. Among these pharmaceuticals, antiretrovirals such as lopinavir/ritonavir and remdesivir, antibiotics and antifungal agents can induce drug-induced liver injury (DILI), whose mechanisms are not always understood. In the present article, we hypothesize that obese COVID-19 patients with MAFLD might be at higher risk for DILI than non-infected healthy individuals or MAFLD patients. These patients present several concomitant factors, which individually can favour DILI: polypharmacy, systemic inflammation at risk of cytokine storm, fatty liver and sometimes nonalcoholic steatohepatitis (NASH) as well as insulin resistance and other diseases linked to obesity. Hence, in obese COVID-19 patients, some drugs might cause more severe (and/or more frequent) DILI, while others might trigger the transition of fatty liver to NASH, or worsen pre-existing steatosis, necroinflammation and fibrosis. We also present the main mechanisms whereby drugs can be more hepatotoxic in MAFLD including impaired activity of xenobiotic-metabolizing enzymes, mitochondrial dysfunction, altered lipid homeostasis and oxidative stress. Although comprehensive investigations are needed to confirm our hypothesis, we believe that the current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of cases of DILI in COVID-19 patients, which may have participated in presentation severity and death.
DOI: 10.1016/j.biochi.2020.08.018
PubMed: 32891697
PubMed Central: PMC7468536
Affiliations:
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Electronic address: bernard.fromenty@inserm.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM, Univ Rennes, INRAE, Institut NUMECAN (Nutrition Metabolisms and Cancer) UMR_A 1341, UMR_S 1241, F-35000, Rennes</wicri:regionArea><placeName><region type="region" nuts="2">Région Bretagne</region><settlement type="city">Rennes</settlement></placeName></affiliation></author></analytic><series><title level="j">Biochimie</title><idno type="eISSN">1638-6183</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">Obese patients who often present metabolic dysfunction-associated fatty liver disease (MAFLD) are at risk of severe presentation of coronavirus disease 2019 (COVID-19). These patients are more likely to be hospitalized and receive antiviral agents and other drugs required to treat acute respiratory distress syndrome and systemic inflammation, combat bacterial and fungal superinfections and reverse multi-organ failure. Among these pharmaceuticals, antiretrovirals such as lopinavir/ritonavir and remdesivir, antibiotics and antifungal agents can induce drug-induced liver injury (DILI), whose mechanisms are not always understood. In the present article, we hypothesize that obese COVID-19 patients with MAFLD might be at higher risk for DILI than non-infected healthy individuals or MAFLD patients. These patients present several concomitant factors, which individually can favour DILI: polypharmacy, systemic inflammation at risk of cytokine storm, fatty liver and sometimes nonalcoholic steatohepatitis (NASH) as well as insulin resistance and other diseases linked to obesity. Hence, in obese COVID-19 patients, some drugs might cause more severe (and/or more frequent) DILI, while others might trigger the transition of fatty liver to NASH, or worsen pre-existing steatosis, necroinflammation and fibrosis. We also present the main mechanisms whereby drugs can be more hepatotoxic in MAFLD including impaired activity of xenobiotic-metabolizing enzymes, mitochondrial dysfunction, altered lipid homeostasis and oxidative stress. Although comprehensive investigations are needed to confirm our hypothesis, we believe that the current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of cases of DILI in COVID-19 patients, which may have participated in presentation severity and death.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32891697</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1638-6183</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Sep</Month><Day>03</Day></PubDate></JournalIssue><Title>Biochimie</Title><ISOAbbreviation>Biochimie</ISOAbbreviation></Journal><ArticleTitle>Treatments in Covid-19 patients with pre-existing metabolic dysfunction-associated fatty liver disease: A potential threat for drug-induced liver injury?</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0300-9084(20)30203-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biochi.2020.08.018</ELocationID><Abstract><AbstractText>Obese patients who often present metabolic dysfunction-associated fatty liver disease (MAFLD) are at risk of severe presentation of coronavirus disease 2019 (COVID-19). These patients are more likely to be hospitalized and receive antiviral agents and other drugs required to treat acute respiratory distress syndrome and systemic inflammation, combat bacterial and fungal superinfections and reverse multi-organ failure. Among these pharmaceuticals, antiretrovirals such as lopinavir/ritonavir and remdesivir, antibiotics and antifungal agents can induce drug-induced liver injury (DILI), whose mechanisms are not always understood. In the present article, we hypothesize that obese COVID-19 patients with MAFLD might be at higher risk for DILI than non-infected healthy individuals or MAFLD patients. These patients present several concomitant factors, which individually can favour DILI: polypharmacy, systemic inflammation at risk of cytokine storm, fatty liver and sometimes nonalcoholic steatohepatitis (NASH) as well as insulin resistance and other diseases linked to obesity. Hence, in obese COVID-19 patients, some drugs might cause more severe (and/or more frequent) DILI, while others might trigger the transition of fatty liver to NASH, or worsen pre-existing steatosis, necroinflammation and fibrosis. We also present the main mechanisms whereby drugs can be more hepatotoxic in MAFLD including impaired activity of xenobiotic-metabolizing enzymes, mitochondrial dysfunction, altered lipid homeostasis and oxidative stress. Although comprehensive investigations are needed to confirm our hypothesis, we believe that the current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of cases of DILI in COVID-19 patients, which may have participated in presentation severity and death.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ferron</LastName><ForeName>Pierre-Jean</ForeName><Initials>PJ</Initials><AffiliationInfo><Affiliation>INSERM, Univ Rennes, INRAE, Institut NUMECAN (Nutrition Metabolisms and Cancer) UMR_A 1341, UMR_S 1241, F-35000, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gicquel</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>INSERM, Univ Rennes, INRAE, Institut NUMECAN (Nutrition Metabolisms and Cancer) UMR_A 1341, UMR_S 1241, F-35000, Rennes, France; CHU Rennes, Laboratoire de toxicologie médico-légale, F-35000, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mégarbane</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Medical and Toxicological Critical Care, Lariboisière Hospital, University of Paris, INSERM, UMRS, 1144, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clément</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>INSERM, Univ Rennes, INRAE, Institut NUMECAN (Nutrition Metabolisms and Cancer) UMR_A 1341, UMR_S 1241, F-35000, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fromenty</LastName><ForeName>Bernard</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>INSERM, Univ Rennes, INRAE, Institut NUMECAN (Nutrition Metabolisms and Cancer) UMR_A 1341, UMR_S 1241, F-35000, Rennes, France. Electronic address: bernard.fromenty@inserm.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Biochimie</MedlineTA><NlmUniqueID>1264604</NlmUniqueID><ISSNLinking>0300-9084</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">Cytochrome P450</Keyword><Keyword MajorTopicYN="N">Drug hepatotoxicity</Keyword><Keyword MajorTopicYN="N">Fatty liver</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>06</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>08</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>9</Month><Day>6</Day><Hour>20</Hour><Minute>24</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32891697</ArticleId><ArticleId IdType="pii">S0300-9084(20)30203-0</ArticleId><ArticleId IdType="doi">10.1016/j.biochi.2020.08.018</ArticleId><ArticleId IdType="pmc">PMC7468536</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Région Bretagne</li><li>Île-de-France</li></region><settlement><li>Paris</li><li>Rennes</li></settlement></list><tree><country name="France"><region name="Région Bretagne"><name sortKey="Ferron, Pierre Jean" sort="Ferron, Pierre Jean" uniqKey="Ferron P" first="Pierre-Jean" last="Ferron">Pierre-Jean Ferron</name></region><name sortKey="Clement, Bruno" sort="Clement, Bruno" uniqKey="Clement B" first="Bruno" last="Clément">Bruno Clément</name><name sortKey="Fromenty, Bernard" sort="Fromenty, Bernard" uniqKey="Fromenty B" first="Bernard" last="Fromenty">Bernard Fromenty</name><name sortKey="Gicquel, Thomas" sort="Gicquel, Thomas" uniqKey="Gicquel T" first="Thomas" last="Gicquel">Thomas Gicquel</name><name sortKey="Megarbane, Bruno" sort="Megarbane, Bruno" uniqKey="Megarbane B" first="Bruno" last="Mégarbane">Bruno Mégarbane</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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