Deaths involving serotonergic drugs

Pilgrim, Jennifer L.; Gerostamoulos, Dimitri; Drummer, Olaf H.

doi:10.1016/j.forsciint.2010.01.014

Cited by 38 publications

(13 citation statements)

References 63 publications

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“…Postmortem concentrations of VEN have been relatively well characterized previously and the VEN levels in our study (mean 0.93 µg/g, median 0.6 µg/g) are within the range reported by others [45,49,50,53]. A median VEN concentration of 1.05 mg/L (range 0.1-5.5 mg/L) was found in six deaths associated with serotonin toxicity [54]. In a compilation of reference concentrations of different antidepressants [49] the cases were divided into three groups (A, single drug intoxication; B, multiple drug intoxication; C, postmortem control) according to the strategy originally presented by Druid and Holmgren [35] (for further details, see Section 3.2).…”

Section: Discussionsupporting

confidence: 88%

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Influence of CYP2D6 genotype on the disposition of the enantiomers of venlafaxine and its major metabolites in postmortem femoral blood

Kingbäck

Karlsson

Zackrisson

et al. 2012

Forensic Science International

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However, a substantial variation in the relationship between the S-and R-enantiomers of VEN and metabolites was evident (S/R ratios ranging from 0.23-17.6). In six cases, a low S/R VEN ratio (mean 0.5) was associated with a high S/R ODV ratio (mean 11.9). Genotyping showed that these individuals carried two inactive CYP2D6 genes indicating a poor metabolizer phenotype. From these data we conclude that enantioselective analysis of VEN and ODV can predict if a person is a poor metabolizer genotype/phenotype for CYP2D6. Knowledge of the relationship between the S-and R-enantiomers of this antidepressant drug and its active metabolite is also important since the enantiomers display different pharmacodynamic profiles.

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Section: Discussionsupporting

confidence: 88%

“…Thus, drug interactions involving VEN may have occurred in several of the cases included in the present study. The combination of tramadol and VEN was found in five cases and the risk of serotonin syndrome, which can be fatal, cannot be negligible [54]. Other drugs found in our cases are inducers or inhibitors of CYP enzymes, e.g.…”

Section: Discussionmentioning

confidence: 58%

Influence of CYP2D6 genotype on the disposition of the enantiomers of venlafaxine and its major metabolites in postmortem femoral blood

Kingbäck

Karlsson

Zackrisson

et al. 2012

Forensic Science International

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“…No obvious reasons for this were found in necropsy. It is known that excess intrasynaptic serotonin in the CNS causes serious side effects termed serotonin syndrome or serotonin toxicity [30,31]. However, the reason for the higher mortality with the higher dose of fluoxetine remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine Promotes Remission in Acute Experimental Autoimmune Encephalomyelitis in Rats

Yuan

Qiu

Liu

et al. 2012

Neuroimmunomodulation

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Objective: This study was carried out to clarify the effects of the antidepressant fluoxetine, a selective serotonin reuptake inhibitor, for its potential use in autoimmune diseases like multiple sclerosis in a rat model of experimental autoimmune encephalomyelitis (EAE). Methods: The rat EAE model was induced by subcutaneous injection of guinea pig spinal cord homogenate. Rats received fluoxetine via daily intragastric administration, starting 2 weeks prior to immune induction (fluoxetine pretreatment). Clinical scores and pathological changes in EAE rats were analyzed. Changes in serum cytokine levels were assessed by ELISA. Results: Fluoxetine pretreatment significantly promoted remission in EAE. Histologically, fluoxetine-induced neuroprotection was accompanied by reductions in inflammatory foci and in the degree of demyelination in the spinal cord of EAE rats. The increase in serum IFN-γ in the EAE model was also suppressed by fluoxetine administration. Conclusions: These findings suggest that the prophylactic use of fluoxetine can relieve symptoms during remission in the acute EAE model, and these neuroprotective effects are associated with its anti-inflammatory effects.

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“…This ADR has been called 'serotonin syndrome' but is more properly called serotonin toxicity and is associated with a wide range of cognitive, autonomic and neuromuscular effects (Isbister et al 2007). This ADR can occur in people using prescribed doses of two or more drugs capable of interfering with the serotonin system as well as those misusing one serotonin active drug (Pilgrim et al 2010(Pilgrim et al , 2011a(Pilgrim et al , 2011b.…”

Section: Useful Websitementioning

confidence: 99%