Journal of toxicology. Clinical toxicology
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Lamotrigine is an antiepileptic agent that has been shown to be an effective adjunctive treatment for refractory partial and generalized seizures. It is now licensed in more than 70 countries for this indication. There is very little published material about the effects of acute overdose with lamotrigine. ⋯ We describe the findings in a patient following the deliberate ingestion of a large amount of lamotrigine (stated 4.5 g, absorbed estimated 2.9 g), in excess of that previously described in the literature. The main clinical features were ataxia and rotary nystagmus. Electrocardiogram was unremarkable. Peak measured concentration of lamotrigine was 35.8 mg/L and half-life 19.5 hours, suggesting linear kinetics in overdose.
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J. Toxicol. Clin. Toxicol. · Jan 2000
ReviewMechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.
Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. FEATURES FOLLOWING INGESTION: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure. ⋯ While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.
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J. Toxicol. Clin. Toxicol. · Jan 2000
ReviewPyrethroid insecticides: poisoning syndromes, synergies, and therapy.
Pyrethroid insecticides are widely used, but there have been relatively few reports of systemic poisoning. These reports have, however, shown that pharmacotherapy is difficult and that the duration of poisoning can be unexpectedly long. Pyrethroids are ion channel toxins prolonging neuronal excitation, but are not directly cytotoxic. ⋯ Hence, the unauthorized pyrethroid/organophosphate mixtures marketed in some developing countries may precipitate human poisoning. Pyrethroid paresthesia can be treated by decontamination of the skin, but systemic poisoning is difficult to control with anticonvulsants. Pentobarbitone, however, is surprisingly effective as therapy against systemic type II pyrethroid poisoning in rats, probably due to its dual action as a chloride channel agonist and a membrane stabilizer.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Cardiac and hemodynamic assessment of patients with cocaine-associated chest pain syndromes.
Animal and human experimental studies have yielded conflicted data regarding the effects of cocaine on cardiovascular function. We studied the cardiac and hemodynamic profiles in emergency department chest pain patients following recent cocaine use. ⋯ Most emergency department patients with cocaine-associated chest pain have normal cardiac profiles at the time of presentation. The negative inotropic effects of high doses of cocaine observed in animal models do not appear to be present in patients who develop chest pain after using recreational doses of cocaine.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Fellowship training in medical toxicology: characteristics, perceptions, and career impact.
To determine the number of physicians who have received fellowship training in medical toxicology and to describe fellowship-trained medical toxicologists' perceptions of fellowship training and its career impact. ⋯ Most fellowship-trained toxicologists only work part-time in medical toxicology, but fellowship training has significant impact on choice of academic career and altering clinical responsibilities. Training concerns include limited bedside experiences, particularly outpatient, and uncertain job prospects.