Interactions between antiepileptic and chemotherapeutic drugs
Cancer and epilepsy commonly co-occur, and concomitant administration of antiepileptic (AEDS) and chemotherapeutic drugs (CTDs) is necessary in many cases. Many drugs are metabolised by the hepatic cytochrome P450 (CYP) isoenzyme system, and coadministration of AEDs and CTDs can lead to clinically r...
Gespeichert in:
| Veröffentlicht in: | Lancet neurology 2003-07, Vol.2 (7), p.404-409 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 409 |
|---|---|
| container_issue | 7 |
| container_start_page | 404 |
| container_title | Lancet neurology |
| container_volume | 2 |
| creator | Vecht, Charles J Wagner, G Louis Wilms, Erik B |
| description | Cancer and epilepsy commonly co-occur, and concomitant administration of antiepileptic (AEDS) and chemotherapeutic drugs (CTDs) is necessary in many cases. Many drugs are metabolised by the hepatic cytochrome P450 (CYP) isoenzyme system, and coadministration of AEDs and CTDs can lead to clinically relevant interactions by induction or inhibition of enzymes in shared metabolic pathways. These interactions can cause insufficient tumour and seizure control or lead to unforeseen toxicity. Enzyme-inducing AEDs reduce the effects of taxanes, vinca alkaloids, methotrexate, teniposide, and camptothecin analogues. Inhibition of the metabolism of nitrosoureas or etoposide by valproic acid can lead to CTD toxicity. Poor seizure control may result from the combinations of phenytoin with cisplatin or corticosteroids, and valproic acid with methotrexate. Increased toxicity of AEDs can occur when phenytoin is combined with 5-fluorouracil. Use of enzyme-inducing AEDs should be avoided in patients with cancer, particularly in association with chemotherapy. Generally, valproic acid— although not free from interactions—would be the agent of first choice. Some of the newer AEDs not metabolised by the P450 system may prove to be good alternatives. |
| doi_str_mv | 10.1016/S1474-4422(03)00435-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_201490993</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1474442203004356</els_id><sourcerecordid>1661506851</sourcerecordid><originalsourceid>FETCH-LOGICAL-c454t-b0d1046aaf698aaac67a06331121e667a0e5a35d06e7927334c5d99124c50bbb3</originalsourceid><addsrcrecordid>eNqFkEtLAzEQgIMotlZ_glI86WE1r81uDiJSfBQKHtRzyCZTm9LurklW8d-bbYsePc2Db2aYD6FTgq8IJuL6hfCCZ5xTeoHZJcac5ZnYQ8NdW-T7vzmlA3QUwhJjSnhJDtGA0JJLQsohupnWEbw20TV1GFcQvwDqsa6jg9atoI3OpMqOzQLWTVwktIWub1rfvYdjdDDXqwAnuzhCbw_3r5OnbPb8OJ3czTLDcx6zCluCudB6LmSptTai0FgwRgglIPoCcs1yiwUUkhaMcZNbKQlNEVdVxUbofLu39c1HByGqZdP5Op1UFBMusZQsQfkWMr4JwcNctd6ttf9WBKvemdo4U70QhZnaOFMizZ3tlnfVGuzf1E5SAm63AKQXPx14FYyD2oB1HkxUtnH_nPgBkCt6yg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>201490993</pqid></control><display><type>article</type><title>Interactions between antiepileptic and chemotherapeutic drugs</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Vecht, Charles J ; Wagner, G Louis ; Wilms, Erik B</creator><creatorcontrib>Vecht, Charles J ; Wagner, G Louis ; Wilms, Erik B</creatorcontrib><description>Cancer and epilepsy commonly co-occur, and concomitant administration of antiepileptic (AEDS) and chemotherapeutic drugs (CTDs) is necessary in many cases. Many drugs are metabolised by the hepatic cytochrome P450 (CYP) isoenzyme system, and coadministration of AEDs and CTDs can lead to clinically relevant interactions by induction or inhibition of enzymes in shared metabolic pathways. These interactions can cause insufficient tumour and seizure control or lead to unforeseen toxicity. Enzyme-inducing AEDs reduce the effects of taxanes, vinca alkaloids, methotrexate, teniposide, and camptothecin analogues. Inhibition of the metabolism of nitrosoureas or etoposide by valproic acid can lead to CTD toxicity. Poor seizure control may result from the combinations of phenytoin with cisplatin or corticosteroids, and valproic acid with methotrexate. Increased toxicity of AEDs can occur when phenytoin is combined with 5-fluorouracil. Use of enzyme-inducing AEDs should be avoided in patients with cancer, particularly in association with chemotherapy. Generally, valproic acid— although not free from interactions—would be the agent of first choice. Some of the newer AEDs not metabolised by the P450 system may prove to be good alternatives.</description><identifier>ISSN: 1474-4422</identifier><identifier>EISSN: 1474-4465</identifier><identifier>DOI: 10.1016/S1474-4422(03)00435-6</identifier><identifier>PMID: 12849118</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Anticonvulsants - adverse effects ; Anticonvulsants - metabolism ; Anticonvulsants - therapeutic use ; Brain cancer ; Cancer therapies ; Convulsions & seizures ; Cytochrome ; Cytochrome P-450 Enzyme System - drug effects ; Drug dosages ; Drug Interactions ; Drug-Related Side Effects and Adverse Reactions ; Enzymes ; Epilepsy ; Epilepsy - complications ; Epilepsy - drug therapy ; Humans ; Metabolism ; Metabolites ; Neoplasms - complications ; Neoplasms - drug therapy ; Oxidation ; Pharmacodynamics ; Pharmacokinetics ; Polypharmacy ; Toxicity ; Tumors</subject><ispartof>Lancet neurology, 2003-07, Vol.2 (7), p.404-409</ispartof><rights>2003 Elsevier Ltd</rights><rights>Copyright Elsevier Limited Jul 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-b0d1046aaf698aaac67a06331121e667a0e5a35d06e7927334c5d99124c50bbb3</citedby><cites>FETCH-LOGICAL-c454t-b0d1046aaf698aaac67a06331121e667a0e5a35d06e7927334c5d99124c50bbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1474442203004356$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12849118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vecht, Charles J</creatorcontrib><creatorcontrib>Wagner, G Louis</creatorcontrib><creatorcontrib>Wilms, Erik B</creatorcontrib><title>Interactions between antiepileptic and chemotherapeutic drugs</title><title>Lancet neurology</title><addtitle>Lancet Neurol</addtitle><description>Cancer and epilepsy commonly co-occur, and concomitant administration of antiepileptic (AEDS) and chemotherapeutic drugs (CTDs) is necessary in many cases. Many drugs are metabolised by the hepatic cytochrome P450 (CYP) isoenzyme system, and coadministration of AEDs and CTDs can lead to clinically relevant interactions by induction or inhibition of enzymes in shared metabolic pathways. These interactions can cause insufficient tumour and seizure control or lead to unforeseen toxicity. Enzyme-inducing AEDs reduce the effects of taxanes, vinca alkaloids, methotrexate, teniposide, and camptothecin analogues. Inhibition of the metabolism of nitrosoureas or etoposide by valproic acid can lead to CTD toxicity. Poor seizure control may result from the combinations of phenytoin with cisplatin or corticosteroids, and valproic acid with methotrexate. Increased toxicity of AEDs can occur when phenytoin is combined with 5-fluorouracil. Use of enzyme-inducing AEDs should be avoided in patients with cancer, particularly in association with chemotherapy. Generally, valproic acid— although not free from interactions—would be the agent of first choice. Some of the newer AEDs not metabolised by the P450 system may prove to be good alternatives.</description><subject>Anticonvulsants - adverse effects</subject><subject>Anticonvulsants - metabolism</subject><subject>Anticonvulsants - therapeutic use</subject><subject>Brain cancer</subject><subject>Cancer therapies</subject><subject>Convulsions & seizures</subject><subject>Cytochrome</subject><subject>Cytochrome P-450 Enzyme System - drug effects</subject><subject>Drug dosages</subject><subject>Drug Interactions</subject><subject>Drug-Related Side Effects and Adverse Reactions</subject><subject>Enzymes</subject><subject>Epilepsy</subject><subject>Epilepsy - complications</subject><subject>Epilepsy - drug therapy</subject><subject>Humans</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Neoplasms - complications</subject><subject>Neoplasms - drug therapy</subject><subject>Oxidation</subject><subject>Pharmacodynamics</subject><subject>Pharmacokinetics</subject><subject>Polypharmacy</subject><subject>Toxicity</subject><subject>Tumors</subject><issn>1474-4422</issn><issn>1474-4465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkEtLAzEQgIMotlZ_glI86WE1r81uDiJSfBQKHtRzyCZTm9LurklW8d-bbYsePc2Db2aYD6FTgq8IJuL6hfCCZ5xTeoHZJcac5ZnYQ8NdW-T7vzmlA3QUwhJjSnhJDtGA0JJLQsohupnWEbw20TV1GFcQvwDqsa6jg9atoI3OpMqOzQLWTVwktIWub1rfvYdjdDDXqwAnuzhCbw_3r5OnbPb8OJ3czTLDcx6zCluCudB6LmSptTai0FgwRgglIPoCcs1yiwUUkhaMcZNbKQlNEVdVxUbofLu39c1HByGqZdP5Op1UFBMusZQsQfkWMr4JwcNctd6ttf9WBKvemdo4U70QhZnaOFMizZ3tlnfVGuzf1E5SAm63AKQXPx14FYyD2oB1HkxUtnH_nPgBkCt6yg</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Vecht, Charles J</creator><creator>Wagner, G Louis</creator><creator>Wilms, Erik B</creator><general>Elsevier Ltd</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0TZ</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8C2</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20030701</creationdate><title>Interactions between antiepileptic and chemotherapeutic drugs</title><author>Vecht, Charles J ; Wagner, G Louis ; Wilms, Erik B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-b0d1046aaf698aaac67a06331121e667a0e5a35d06e7927334c5d99124c50bbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Anticonvulsants - adverse effects</topic><topic>Anticonvulsants - metabolism</topic><topic>Anticonvulsants - therapeutic use</topic><topic>Brain cancer</topic><topic>Cancer therapies</topic><topic>Convulsions & seizures</topic><topic>Cytochrome</topic><topic>Cytochrome P-450 Enzyme System - drug effects</topic><topic>Drug dosages</topic><topic>Drug Interactions</topic><topic>Drug-Related Side Effects and Adverse Reactions</topic><topic>Enzymes</topic><topic>Epilepsy</topic><topic>Epilepsy - complications</topic><topic>Epilepsy - drug therapy</topic><topic>Humans</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Neoplasms - complications</topic><topic>Neoplasms - drug therapy</topic><topic>Oxidation</topic><topic>Pharmacodynamics</topic><topic>Pharmacokinetics</topic><topic>Polypharmacy</topic><topic>Toxicity</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vecht, Charles J</creatorcontrib><creatorcontrib>Wagner, G Louis</creatorcontrib><creatorcontrib>Wilms, Erik B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Pharma and Biotech Premium PRO</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Lancet Titles</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Lancet neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vecht, Charles J</au><au>Wagner, G Louis</au><au>Wilms, Erik B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions between antiepileptic and chemotherapeutic drugs</atitle><jtitle>Lancet neurology</jtitle><addtitle>Lancet Neurol</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>2</volume><issue>7</issue><spage>404</spage><epage>409</epage><pages>404-409</pages><issn>1474-4422</issn><eissn>1474-4465</eissn><coden>LANCAO</coden><abstract>Cancer and epilepsy commonly co-occur, and concomitant administration of antiepileptic (AEDS) and chemotherapeutic drugs (CTDs) is necessary in many cases. Many drugs are metabolised by the hepatic cytochrome P450 (CYP) isoenzyme system, and coadministration of AEDs and CTDs can lead to clinically relevant interactions by induction or inhibition of enzymes in shared metabolic pathways. These interactions can cause insufficient tumour and seizure control or lead to unforeseen toxicity. Enzyme-inducing AEDs reduce the effects of taxanes, vinca alkaloids, methotrexate, teniposide, and camptothecin analogues. Inhibition of the metabolism of nitrosoureas or etoposide by valproic acid can lead to CTD toxicity. Poor seizure control may result from the combinations of phenytoin with cisplatin or corticosteroids, and valproic acid with methotrexate. Increased toxicity of AEDs can occur when phenytoin is combined with 5-fluorouracil. Use of enzyme-inducing AEDs should be avoided in patients with cancer, particularly in association with chemotherapy. Generally, valproic acid— although not free from interactions—would be the agent of first choice. Some of the newer AEDs not metabolised by the P450 system may prove to be good alternatives.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>12849118</pmid><doi>10.1016/S1474-4422(03)00435-6</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1474-4422 |
| ispartof | Lancet neurology, 2003-07, Vol.2 (7), p.404-409 |
| issn | 1474-4422 1474-4465 |
| language | eng |
| recordid | cdi_proquest_journals_201490993 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Anticonvulsants - adverse effects Anticonvulsants - metabolism Anticonvulsants - therapeutic use Brain cancer Cancer therapies Convulsions & seizures Cytochrome Cytochrome P-450 Enzyme System - drug effects Drug dosages Drug Interactions Drug-Related Side Effects and Adverse Reactions Enzymes Epilepsy Epilepsy - complications Epilepsy - drug therapy Humans Metabolism Metabolites Neoplasms - complications Neoplasms - drug therapy Oxidation Pharmacodynamics Pharmacokinetics Polypharmacy Toxicity Tumors |
| title | Interactions between antiepileptic and chemotherapeutic drugs |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T13%3A23%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interactions%20between%20antiepileptic%20and%20chemotherapeutic%20drugs&rft.jtitle=Lancet%20neurology&rft.au=Vecht,%20Charles%20J&rft.date=2003-07-01&rft.volume=2&rft.issue=7&rft.spage=404&rft.epage=409&rft.pages=404-409&rft.issn=1474-4422&rft.eissn=1474-4465&rft.coden=LANCAO&rft_id=info:doi/10.1016/S1474-4422(03)00435-6&rft_dat=%3Cproquest_cross%3E1661506851%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=201490993&rft_id=info:pmid/12849118&rft_els_id=S1474442203004356&rfr_iscdi=true |