The role of drug-drug interactions in prostate cancer treatment: Focus on abiraterone acetate/prednisone and enzalutamide.
Identifieur interne : 000D72 ( PubMed/Curation ); précédent : 000D71; suivant : 000D73The role of drug-drug interactions in prostate cancer treatment: Focus on abiraterone acetate/prednisone and enzalutamide.
Auteurs : Marzia Del Re [Italie] ; Stefano Fogli [Italie] ; Lisa Derosa [France] ; Francesco Massari [Italie] ; Paul De Souza [Australie] ; Stefania Crucitta [Italie] ; Sergio Bracarda [Italie] ; Daniele Santini [Italie] ; Romano Danesi [Italie]Source :
- Cancer treatment reviews [ 1532-1967 ] ; 2017.
Descripteurs français
- KwdFr :
- 3-Phényl-2-thiohydantoïne (analogues et dérivés), 3-Phényl-2-thiohydantoïne (métabolisme), 3-Phényl-2-thiohydantoïne (pharmacologie), Acétate d'abiratérone (métabolisme), Acétate d'abiratérone (pharmacologie), Antinéoplasiques (pharmacologie), Cytochrome P-450 enzyme system (), Humains, Interactions médicamenteuses, Mâle, Polypharmacie, Prednisone (pharmacologie), Tumeurs de la prostate (traitement médicamenteux).
- MESH :
- analogues et dérivés : 3-Phényl-2-thiohydantoïne.
- métabolisme : 3-Phényl-2-thiohydantoïne, Acétate d'abiratérone.
- pharmacologie : 3-Phényl-2-thiohydantoïne, Acétate d'abiratérone, Antinéoplasiques, Prednisone.
- traitement médicamenteux : Tumeurs de la prostate.
- Cytochrome P-450 enzyme system, Humains, Interactions médicamenteuses, Mâle, Polypharmacie.
English descriptors
- KwdEn :
- Abiraterone Acetate (metabolism), Abiraterone Acetate (pharmacology), Antineoplastic Agents (pharmacology), Cytochrome P-450 Enzyme System (drug effects), Drug Interactions, Humans, Male, Phenylthiohydantoin (analogs & derivatives), Phenylthiohydantoin (metabolism), Phenylthiohydantoin (pharmacology), Polypharmacy, Prednisone (pharmacology), Prostatic Neoplasms (drug therapy).
- MESH :
- chemical , analogs & derivatives : Phenylthiohydantoin.
- chemical , drug effects : Cytochrome P-450 Enzyme System.
- chemical , metabolism : Abiraterone Acetate, Phenylthiohydantoin.
- chemical , pharmacology : Abiraterone Acetate, Antineoplastic Agents, Phenylthiohydantoin, Prednisone.
- drug therapy : Prostatic Neoplasms.
- Drug Interactions, Humans, Male, Polypharmacy.
Abstract
Elderly patients with cancer may have comorbidities, each requiring additional pharmacologic treatment. Therefore, the occurrence of pharmacokinetic (PK) and pharmacodynamic (PD) interactions is very likely, and the risk of adverse reactions (ADRs), due to the narrow therapeutic window of anticancer drugs, is increased. Drug-drug interactions (DDIs) may occur in prostate cancer patients due to inhibition by abiraterone of liver cytochrome P450 (CYP)-dependent enzymes CYP2C8 and 2D6, which are involved in the metabolism of approximately 25% of all drugs, and induction by enzalutamide of CYP3A4, 2C9 and 2C19, which metabolize up to 50% of medications. Therefore, abiraterone may increase plasma levels of CYP2D6 substrates, including amitriptyline, oxycodone and risperidone, as well as of CYP2C8 substrates including amiodarone and carbamazepine. Since enzalutamide is extensively metabolized by CYP2C8, its plasma levels are likely to be raised if coadministered with strong CYP2C8 inhibitors such as gemfibrozil or pioglitazone. Inducers of CYP2C8 (i.e., rifampin) may reduce the effectiveness of enzalutamide and hence should be avoided. Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. Growing awareness of the importance of DDIs in cancer patients is now reflected in the variety of web-based sources offering information and guidance. However, the evaluation of the clinical relevance of DDIs is the result of a comprehensive evaluation of many factors, including therapeutic index, amplitude of therapeutic range and presence of comorbidities, requiring a specific expertise in clinical pharmacology.
DOI: 10.1016/j.ctrv.2017.03.001
PubMed: 28340451
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Electronic address: romano.danesi@unipi.it.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Clinical and Experimental Medicine, University of Pisa</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cancer treatment reviews</title><idno type="eISSN">1532-1967</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abiraterone Acetate (metabolism)</term><term>Abiraterone Acetate (pharmacology)</term><term>Antineoplastic Agents (pharmacology)</term><term>Cytochrome P-450 Enzyme System (drug effects)</term><term>Drug Interactions</term><term>Humans</term><term>Male</term><term>Phenylthiohydantoin (analogs & derivatives)</term><term>Phenylthiohydantoin (metabolism)</term><term>Phenylthiohydantoin (pharmacology)</term><term>Polypharmacy</term><term>Prednisone (pharmacology)</term><term>Prostatic Neoplasms (drug therapy)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>3-Phényl-2-thiohydantoïne (analogues et dérivés)</term><term>3-Phényl-2-thiohydantoïne (métabolisme)</term><term>3-Phényl-2-thiohydantoïne (pharmacologie)</term><term>Acétate d'abiratérone (métabolisme)</term><term>Acétate d'abiratérone (pharmacologie)</term><term>Antinéoplasiques (pharmacologie)</term><term>Cytochrome P-450 enzyme system ()</term><term>Humains</term><term>Interactions médicamenteuses</term><term>Mâle</term><term>Polypharmacie</term><term>Prednisone (pharmacologie)</term><term>Tumeurs de la prostate (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Phenylthiohydantoin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Cytochrome P-450 Enzyme System</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Abiraterone Acetate</term><term>Phenylthiohydantoin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Abiraterone Acetate</term><term>Antineoplastic Agents</term><term>Phenylthiohydantoin</term><term>Prednisone</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>3-Phényl-2-thiohydantoïne</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Prostatic Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>3-Phényl-2-thiohydantoïne</term><term>Acétate d'abiratérone</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>3-Phényl-2-thiohydantoïne</term><term>Acétate d'abiratérone</term><term>Antinéoplasiques</term><term>Prednisone</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs de la prostate</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Drug Interactions</term><term>Humans</term><term>Male</term><term>Polypharmacy</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cytochrome P-450 enzyme system</term><term>Humains</term><term>Interactions médicamenteuses</term><term>Mâle</term><term>Polypharmacie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Elderly patients with cancer may have comorbidities, each requiring additional pharmacologic treatment. Therefore, the occurrence of pharmacokinetic (PK) and pharmacodynamic (PD) interactions is very likely, and the risk of adverse reactions (ADRs), due to the narrow therapeutic window of anticancer drugs, is increased. Drug-drug interactions (DDIs) may occur in prostate cancer patients due to inhibition by abiraterone of liver cytochrome P450 (CYP)-dependent enzymes CYP2C8 and 2D6, which are involved in the metabolism of approximately 25% of all drugs, and induction by enzalutamide of CYP3A4, 2C9 and 2C19, which metabolize up to 50% of medications. Therefore, abiraterone may increase plasma levels of CYP2D6 substrates, including amitriptyline, oxycodone and risperidone, as well as of CYP2C8 substrates including amiodarone and carbamazepine. Since enzalutamide is extensively metabolized by CYP2C8, its plasma levels are likely to be raised if coadministered with strong CYP2C8 inhibitors such as gemfibrozil or pioglitazone. Inducers of CYP2C8 (i.e., rifampin) may reduce the effectiveness of enzalutamide and hence should be avoided. Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. Growing awareness of the importance of DDIs in cancer patients is now reflected in the variety of web-based sources offering information and guidance. However, the evaluation of the clinical relevance of DDIs is the result of a comprehensive evaluation of many factors, including therapeutic index, amplitude of therapeutic range and presence of comorbidities, requiring a specific expertise in clinical pharmacology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28340451</PMID><DateCreated><Year>2017</Year><Month>03</Month><Day>24</Day></DateCreated><DateCompleted><Year>2017</Year><Month>08</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>08</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-1967</ISSN><JournalIssue CitedMedium="Internet"><Volume>55</Volume><PubDate><Year>2017</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Cancer treatment reviews</Title><ISOAbbreviation>Cancer Treat. Rev.</ISOAbbreviation></Journal><ArticleTitle>The role of drug-drug interactions in prostate cancer treatment: Focus on abiraterone acetate/prednisone and enzalutamide.</ArticleTitle><Pagination><MedlinePgn>71-82</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0305-7372(17)30038-5</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ctrv.2017.03.001</ELocationID><Abstract><AbstractText>Elderly patients with cancer may have comorbidities, each requiring additional pharmacologic treatment. Therefore, the occurrence of pharmacokinetic (PK) and pharmacodynamic (PD) interactions is very likely, and the risk of adverse reactions (ADRs), due to the narrow therapeutic window of anticancer drugs, is increased. Drug-drug interactions (DDIs) may occur in prostate cancer patients due to inhibition by abiraterone of liver cytochrome P450 (CYP)-dependent enzymes CYP2C8 and 2D6, which are involved in the metabolism of approximately 25% of all drugs, and induction by enzalutamide of CYP3A4, 2C9 and 2C19, which metabolize up to 50% of medications. Therefore, abiraterone may increase plasma levels of CYP2D6 substrates, including amitriptyline, oxycodone and risperidone, as well as of CYP2C8 substrates including amiodarone and carbamazepine. Since enzalutamide is extensively metabolized by CYP2C8, its plasma levels are likely to be raised if coadministered with strong CYP2C8 inhibitors such as gemfibrozil or pioglitazone. Inducers of CYP2C8 (i.e., rifampin) may reduce the effectiveness of enzalutamide and hence should be avoided. Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. Growing awareness of the importance of DDIs in cancer patients is now reflected in the variety of web-based sources offering information and guidance. However, the evaluation of the clinical relevance of DDIs is the result of a comprehensive evaluation of many factors, including therapeutic index, amplitude of therapeutic range and presence of comorbidities, requiring a specific expertise in clinical pharmacology.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Del Re</LastName><ForeName>Marzia</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical and Experimental Medicine, University of Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fogli</LastName><ForeName>Stefano</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, University of Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Derosa</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Oncology, Gustave Roussy Institute, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Massari</LastName><ForeName>Francesco</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Medical Oncology Unit, Policlinico S. Orsola-Malpighi, Bologna, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Souza</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Medical Oncology, University of Western Sydney, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crucitta</LastName><ForeName>Stefania</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Clinical and Experimental Medicine, University of Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bracarda</LastName><ForeName>Sergio</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Oncology, Azienda USL Toscana Sud Est, Arezzo, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Santini</LastName><ForeName>Daniele</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Oncology Unit, Campus Bio-Medico University Hospital, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Danesi</LastName><ForeName>Romano</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Clinical and Experimental Medicine, University of Pisa, Italy. Electronic address: romano.danesi@unipi.it.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>03</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Cancer Treat Rev</MedlineTA><NlmUniqueID>7502030</NlmUniqueID><ISSNLinking>0305-7372</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C540278">MDV 3100</NameOfSubstance></Chemical><Chemical><RegistryNumber>2010-15-3</RegistryNumber><NameOfSubstance UI="D010669">Phenylthiohydantoin</NameOfSubstance></Chemical><Chemical><RegistryNumber>9035-51-2</RegistryNumber><NameOfSubstance UI="D003577">Cytochrome P-450 Enzyme System</NameOfSubstance></Chemical><Chemical><RegistryNumber>EM5OCB9YJ6</RegistryNumber><NameOfSubstance UI="D000069501">Abiraterone Acetate</NameOfSubstance></Chemical><Chemical><RegistryNumber>VB0R961HZT</RegistryNumber><NameOfSubstance UI="D011241">Prednisone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000069501" MajorTopicYN="N">Abiraterone Acetate</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003577" MajorTopicYN="N">Cytochrome P-450 Enzyme System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004347" MajorTopicYN="N">Drug Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010669" MajorTopicYN="N">Phenylthiohydantoin</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019338" MajorTopicYN="N">Polypharmacy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011241" MajorTopicYN="N">Prednisone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011471" MajorTopicYN="N">Prostatic Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Abiraterone</Keyword><Keyword MajorTopicYN="N">CYP450</Keyword><Keyword MajorTopicYN="N">Drug-drug interactions</Keyword><Keyword MajorTopicYN="N">Enzalutamide</Keyword><Keyword MajorTopicYN="N">Metabolic clearance</Keyword><Keyword MajorTopicYN="N">Prostate cancer</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>07</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>02</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>03</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>3</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28340451</ArticleId><ArticleId IdType="pii">S0305-7372(17)30038-5</ArticleId><ArticleId IdType="doi">10.1016/j.ctrv.2017.03.001</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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