Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/32544
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dc.contributor.authorMuriel, J-
dc.contributor.authorEscorial, Mónica-
dc.contributor.authorCarratalá, C-
dc.contributor.authorMargarit, César-
dc.contributor.authorBarrachina, Jordi-
dc.contributor.authorLópez, A-
dc.contributor.authorKringen, Marianne K-
dc.contributor.authorPeiró, Ana-
dc.contributor.otherDepartamentos de la UMH::Farmacología, Pediatría y Química Orgánica-
dc.date.accessioned2024-07-18T10:26:59Z-
dc.date.available2024-07-18T10:26:59Z-
dc.date.created2024-06-14-
dc.identifier.citationBiomed Pharmacother. 2024 Jul:176:116882es_ES
dc.identifier.issn0753-3322-
dc.identifier.urihttps://hdl.handle.net/11000/32544-
dc.description.abstractBackground: Several opioids have pharmacogenetic and drug-drug interactions which may compromise their analgesic effectiveness, but are not routinely implemented into supportive pain management. We hypothesized that CYP2D6 phenotypes and concomitant use of CYP2D6 substrates or inhibitors would correlate with opioid analgesic outcomes. Materials and Methods: An observational cross-sectional study was conducted with 263 adult chronic non cancer pain (CNCP) patients from a real-world pain unit under long-term CYP2D6-related opioid treatment (tramadol, hydromorphone, tapentadol or oxycodone). Metabolizer phenotype (ultrarapid [UM], normal [NM], intermediate [IM] or poor [PM]) was determined by the CYP2D6 genotype. The socio-demographic (sex, age, employment status), clinical (pain intensity and relief, neuropathic component, quality of life, disability, anxiety and depression), pharmacological (opioid doses and concomitant pharmacotherapy) and safety (adverse events) variables were recorded. Results: The whole population (66 % female, 65 (14) years old, 70 % retired and 63 % attended for low back pain) were classified as PM (5 %), IM (32 %), NM (56 %) and UM (6 %). Multiple linear and logistic regressions showed higher pain intensity and neuropathic component at younger ages when using any CYP2D6 substrate (p = 0.022) or inhibitor (p = 0.030) drug, respectively, with poorer pain relief when CYP2D6 inhibitors (p=0.030) were present. Conclusion: The concomitant use of CYP2D6 substrates or inhibitors during opioid therapy for CNCP may result in lack of analgesic effectiveness. This aspect could be relevant for pharmacological decision making during CNCP management.es_ES
dc.formatapplication/pdfes_ES
dc.format.extent7es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAnalgesic opioidses_ES
dc.subjectPharmacogeneticses_ES
dc.subjectCYP2D6es_ES
dc.subjectDrug-drug interactionses_ES
dc.subjectChronic non cancer paines_ES
dc.subjectSubstrates/inhibitorses_ES
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::615 - Farmacología. Terapéutica. Toxicología. Radiologíaes_ES
dc.titleUse of CYP2D6 substrates and inhibitors during pain management with analgesic opioids: Drug-drug interactions that lead to lack of analgesic effectivenesses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.contributor.instituteInstitutos de la UMH::Instituto de Bioingenieríaes_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.biopha.2024.116882es_ES
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Artículos Farmacología, Pediatría y Química Orgánica


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