Clinical toxicology : the official journal of the American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists
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Clin Toxicol (Phila) · Jul 2015
Pneumomediastinum predicts early mortality in acute paraquat poisoning.
In paraquat (PQ) poisoning, death often occurs after the appearance of pneumomediastinum (PM). However, the clinical features and eventual outcome of PM in PQ intoxication remains unclear. ⋯ Early PM, occurring within 8 days, is a specific predictor of mortality in PQ poisoning.
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Clin Toxicol (Phila) · Jul 2015
H2S induced coma and cardiogenic shock in the rat: Effects of phenothiazinium chromophores.
Hydrogen sulfide (H2S) intoxication produces an acute depression in cardiac contractility-induced circulatory failure, which has been shown to be one of the major contributors to the lethality of H2S intoxication or to the neurological sequelae in surviving animals. Methylene blue (MB), a phenothiazinium dye, can antagonize the effects of the inhibition of mitochondrial electron transport chain, a major effect of H2S toxicity. ⋯ MB can counteract NaHS-induced acute cardiogenic shock; this effect is also produced by azure B, but not by thionine, suggesting that the presence of methyl groups is a prerequisite for producing this protective effect.
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Clin Toxicol (Phila) · Jul 2015
ReviewCYP2D6 genetic polymorphisms and their relevance for poisoning due to amfetamines, opioid analgesics and antidepressants.
Cytochrome P450 2D6 (CYP2D6) is a member of the cytochrome P450 (CYP) superfamily involved in the biotransformation of drugs and substances of abuse encountered in clinical toxicology. Among the CYP superfamily, the CYP2D6 gene is considered as the most polymorphic as more than 105 different alleles have been identified so far. CYP2D6 genetic polymorphisms have the potential to affect the toxicity of their substrates. ⋯ Either poor or extensive/ultra-rapid CYP2D6 metabolisers may be exposed to toxic effects of amfetamines, opioid analgesics and antidepressants. In these three categories, the level of evidence is substance dependent, with differences within the same pharmacological class.
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Clin Toxicol (Phila) · Jul 2015
Observational StudyTramadol overdose causes seizures and respiratory depression but serotonin toxicity appears unlikely.
Tramadol is a commonly used centrally acting analgesic associated with seizures and suspected to cause serotonin toxicity in overdose. ⋯ Tramadol overdose is associated with seizures and respiratory depression, but is unlikely to cause serotonin toxicity.
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Clin Toxicol (Phila) · Jul 2015
Case ReportsCardiac sodium channel blockade after an intentional ingestion of lacosamide, cyclobenzaprine, and levetiracetam: Case report.
Lacosamide treats partial seizures by enhancing slow inactivation of voltage-gated sodium channels. The described cardiac toxicity of lacosamide in the literature to date includes atrioventricular blockade (PR prolongation), atrial flutter, atrial fibrillation, sinus pauses, ventricular tachycardia and a single cardiac arrest. We report a second case of cardiac arrest following an intentional lacosamide overdose. ⋯ The patient's lacosamide, cyclobenzaprine and levetiracetam overdose was associated with QRS prolongation and terminal right axis deviation--suggesting sodium channel blockade as a likely etiology for her cardiac arrest. Cyclobenzaprine has potential for sodium channel blockade and ventricular dysrhythmias although cardiac toxicity due to cyclobenzaprine alone is rare. The combination of cyclobenzaprine with lacosamide may have resulted in cardiovascular collapse. In conclusion, overdose of lacosamide combined with therapeutic concentrations of sodium channel blocking xenobiotics may cause cardiac conduction delays and cardiac arrest.