A case series of patients with lamotrigine toxicity at one center from 2003 to 2012.

INTRODUCTION: Lamotrigine is a phenyltriazine compound that inhibits voltage-gated sodium channels, decreasing release of glutamate and aspartate, and inhibits serotonin, norepinephrine and dopamine reuptake. Reports of toxicity in the literature are limited to case reports and primarily involve coingestants. This case series is intended to report the clinical manifestations of lamotrigine toxicity. METHODS: This retrospective case series from 2003 to 2012 studies the effects of lamotrigine toxicity when not confounded by coingestants. Admission records at an inpatient toxicology center were reviewed for lamotrigine-only exposure based on history with supporting laboratory data when available. After identification, these charts were reviewed again to characterize vital signs, neurological examination findings, specific laboratory and electrocardiography parameters, and complications. RESULTS: Fifty-seven patients were identified with possible lamotrigine toxicity. Nine patients, including three toddlers, had lamotrigine-only ingestions. Three of these patients had seizures, four were hypertensive, five were tachycardic, and four experienced tachypnea. Mental status was altered in all nine (depressed (n = 4), agitated (n = 5) or both (n = 3)). Five patients were hyperreflexic and experienced intermittent myoclonus, and two had inducible clonus. On electrocardiogram, two patients experienced QRS prolongation (114-116 ms), and four had QTc prolongation (463-586 ms). No patient had life-threatening symptoms or signs. Serum levels of lamotrigine were available in seven patients, and averaged 35.4 mg/L (17-90 mg/L). The therapeutic range for sLTG is 3-14 mg/L. CONCLUSIONS: Lamotrigine toxicity manifested with minor-moderate neurologic and/or electrocardiographic effects. Toxicity reflects the known pharmacologic actions of lamotrigine: serotonin, norepinephrine and dopamine reuptake inhibition, and sodium channel blockade.

A retrospective review of California poison control system data of sibutramine exposures.

INTRODUCTION: Sibutramine is a centrally acting neurotransmitter reuptake inhibitor used for the treatment of obesity. In doses of 10-15 mg/day, sibutramine has been shown to promote modest weight loss; however, the literature devoted to characterizing overdoses and abuses of sibutramine is limited. METHODS: We queried and retrospectively reviewed the California Poison Control System database between January 1998 and August 1, 2008. This was an observational case series. RESULTS: A total of 62 cases were identified. Forty-four (71%) of our study subjects were females. Twenty-three patients (37%) were between 8 months and 2 years of age; 17 patients (27%) were between 31 and 50 years. The doses ranged from 2.5 to 75 mg. A total of 27 patients (44%) were referred to a medical center. In general, medical outcomes were minor. Twenty-five (40%) patients had no effects reported; 30 patients (48%) reported minor effects; and three patients (5%) had moderate effects. There were no major effects or deaths reported. In 58 (94%) patients, the ingestion was unintentional. Thirty-two (52%) cases resulted in the recommendation of observational therapy only as their management strategy. Of the patients who did experience adverse effects, cardiovascular side effects were the most common. In particular, tachycardia (nine patients, 14.5%) was the most notable, followed by chest pain (four patients, 6.5%). Six patients (10%) reported central nervous system side effects. Gastrointestinal side effects occurred in four patients (6.5%). The dose ingested did not appear to correlate with the clinical effects observed. DISCUSSION: Sibutramine ingestion resulted in no serious effects or deaths on our retrospective case series. Mild to moderate effects that were rarely reported included tachycardia, chest pain, agitation, irritation, dizziness, vertigo, nausea, and vomiting.

[Tiagabine overdose--report of two cases]. / Ostre zatrucia tiagabina--opis dwóch przypadków.

UNLABELLED: Tiagabine is a derivative of nipecotinic acid used in the therapy of partial seizures, partial seizures with secondary generalization, stress disorder, psychosis and cocaine dependence. The pharmacologic effect of the drug is achieved by inhibition of reuptake of gamma aminobutyric acid (GABA) into glial cells and neurons, without permanent increase in whole brain GABA concentration. Symptoms of acute tiagabine overdose include seizures, coma, respiratory depression ' and less often dystonias, involuntary movements, somnolence, agitation, tachycardia and increase or decrease of blood pressure. Two cases of acute tiagabine overdose have been described in the paper presenting with partial and generalized seizures which were managed with benzodiazepines. CONCLUSIONS: The onset of symptoms of acute tiagabine overdose is rapid with resolution within first 24 hours from exposure. Acute tiagabine poisoning may present with a wide variety of neurological symptoms. Administration of benzodiazepines may improve the outcome of overdose.

One fatal and seven non-fatal cases of 4-methylthioamphetamine (4-MTA) intoxication: clinico-pathological findings.

We present a case history involving one fatal and seven survived cases of intoxication with 4-methylthioamphetamine (4-MTA), also called para-methylthioamphetamine (p-MTA) or methylthioamphetamine (MTA), a relatively new amphetamine analogue. Two of the seven survivors required a 24-h-period of observation in hospital. This report proves once again that the new amphetamine designer drugs are not without danger, as is thought by many young people. In addition, individually different subjective reactions are described. Finally, the medico-legal implications of new, as yet unregistered drugs are discussed.

Para-methylthioamphetamine, a new amphetamine designer drug of abuse.

A case study is described of a patient who was intoxicated after the intake of so-called herbal stimulants. A visit to a physician after the intoxication prompted to this investigation and the case was examined for its direct cause. An interview with the patient revealed that the source of the herbal stimulants was a so-called 'S-5 tablet'. Information provided on the packings of the tablet only indicated the presence of natural alkaloids and vitamins. Toxicological analysis however proved that the 'S-5 tablet' contained para-methylthioamphetamine (MTA), mainly. MTA is a relative unknown amphetamine designer drug, which has only been studied as a model compound in some structure-activity relationship studies. The fact that MTA appeared in tablets was therefore completely unexpected. Not only the potential abuse of this new amphetamine designer drug is a serious matter of concern, but also the misleading information provided with the tablet.