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dc.contributor.authorBech, Anne Berit
dc.contributor.authorClausen, Thomas
dc.contributor.authorWaal, Helge
dc.contributor.authorVindenes, Vigdis
dc.contributor.authorEdvardsen, Hilde Marie Erøy
dc.contributor.authorFrost, Joachim
dc.contributor.authorSkeie, Ivar
dc.date.accessioned2022-11-28T14:12:36Z
dc.date.available2022-11-28T14:12:36Z
dc.date.created2020-09-30T10:32:22Z
dc.date.issued2020
dc.identifier.citationAddiction. 2020:add.15211en_US
dc.identifier.issn0965-2140
dc.identifier.urihttps://hdl.handle.net/11250/3034537
dc.description.abstractAims: To present the substances and their concentrations detected postmortem in patients receiving opioid agonist treatment (OAT) stratified by cause of death, estimate the pooled opioid and benzodiazepine concentrations using established conversion factors for blood concentrations from the Norwegian Road Traffic Act and explore the association between drug‐induced cause of death and the pooled opioid and benzodiazepine concentrations. Design: Cross‐sectional nation‐wide study. Setting: Norway. Participants: One hundred and seven patients who died during OAT (i.e. within 5 days after the last intake of OAT medication) between 1 January 2014 and 31 December 2015, with postmortem femoral blood available for toxicology. Data were collected from hospital records, the Norwegian Cause of Death Registry and autopsy reports. Measurements: Presence of alcohol and non‐alcohol substances in the bloodstream postmortem, determined through records of toxicology of postmortem femoral blood. Findings: A median of four substances was detected across the causes of death. At least one benzodiazepine was detected in 81 (76%) patients. The median pooled opioid concentration was significantly higher in drug‐induced deaths compared with other causes of death (362 versus 182 ng/ml, P < 0.001), in contrast to the pooled benzodiazepine concentration (5466 versus 5701 ng/ml, P = 0.353). The multivariate regression analysis showed that only increasing pooled opioid concentration (ng/ml) was associated with increased odds of a drug‐induced cause of death (odds ratio = 1.003; 95% confidence interval = 1.001–1.006). Conclusions: In Norway, overall opioid concentration seems to play an important role in drug‐induced deaths during opioid agonist treatment in patients prescribed methadone or buprenorphine. Patients prescribed buprenorphine tend to replace their agonist with full agonists, while patients prescribed methadone tend to have high opioid concentrations from methadone as the only opioid.en_US
dc.language.isoengen_US
dc.publisherBlackwell Publishingen_US
dc.rightsNavngivelse-Ikkekommersiell 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/deed.no*
dc.titlePostmortem toxicological analyses of blood samples from 107 patients receiving opioid agonist treatment: substances detected and pooled opioid and benzodiazepine concentrationsen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.journalAddictionen_US
dc.identifier.doi10.1111/add.15211
dc.identifier.cristin1835335
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2


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Navngivelse-Ikkekommersiell 4.0 Internasjonal
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