Epidemiological description of an outbreak of dermatitis related to dimethylfumarate, France, 2008.

Following similar events in other European countries, some cases of dermatitis related to contact with China-imported furniture possibly treated with dimethyl(E)-butenedioate (dimethylfumarate [DMF]) were reported to the French institute for public health surveillance at the beginning of September 2008. An active multisource case collection was conducted in order to provide an epidemiological description of this outbreak. Results of this investigation show that, in France, mainly during the 4th quarter of 2008, a large number of people presented dermatological symptoms at least plausibly due to a contact with DMF-treated consumer products. The products involved were mostly shoes and sofa (94% of cases). This work offers an example of a multipartner investigation in the field of environmental health. It also shows how the results obtained contributed to decision-making and resulted in the limitation of DMF-treated products in France and in Europe.

Dysgeusia following consumption of pine nuts: more than 3000 cases in France.

INTRODUCTION: In March 2008, French poison centres (PCs) recorded the first calls reporting persistent bitterness following the ingestion of pine nuts. METHODS: The French toxic exposure surveillance system (French-Tess) was searched and a descriptive analysis of cases was performed on data recorded from 13 March 2008 to 31 January 2010. RESULTS: Some 3111 cases of bitterness were reported to PCs. The number of cases rose sharply from May 2009 to reach a peak in August 2009 with 697 cases. The median time to onset of dysgeusia was 24 hours and it lasted less than 14 days in 95% of cases. Raw as well as cooked or processed pine nuts were implicated. DISCUSSION: The delayed onset and persistence of dysgeusia suggest that the toxin may act via an unknown toxic mechanism on the receptor. The aetiological agent could be an unidentified toxin present in some varieties of non-edible pine nuts. CONCLUSION: The high incidence of the event and the lack of understanding of the nature of the toxin and its pathophysiological mechanism require continued monitoring of poison cases, botanical and biochemical analysis, and experimental studies.

Acute overdose with controlled-release levodopa-carbidopa.

INTRODUCTION: Reports of acute levodopa-carbidopa overdose are rare and no case of an acute overdose with a controlled-release formulation has been described. We describe such a case in which serial concentrations of catecholamines were measured. CASE REPORT: A 55-year-old man ingested 89 tablets of Sinemet 50/200 (17.8 g of levodopa, 4.45 g of carbidopa). Clinical effects and plasma concentrations of dopamine, noradrenaline and adrenalin were assessed over 66 hours. On admission 2.5 hours after the ingestion, his physical examination was normal except for mydriasis and urine retention. Five hours post-ingestion he had psychomotor agitation, delirium with logorrhea, joviality, visual hallucinations, regular sinus tachycardia and xerostomia. The clinical course included two episodes hypotension and four of transient tachycardia. Treatment was symptomatic and supportive. Clinical toxicity reappeared 48 hours after the intoxication. The patient was discharged at the end of the fourth day with amnesia for the event. DISCUSSION: Dopamine showed an initial plasma concentration peak 14 hours after the toxic ingestion, followed by a second peak 38 hours after the ingestion. The initial peak of noradrenaline occurred 20 hours post-ingestion with a second lower peak at 38 hours. There were no elevations in adrenalin concentrations. CONCLUSION: There appeared to be no correlation between the intensity of the clinical signs and the blood concentrations of dopamine and noradrenaline, although the resolution of the clinical signs did correspond to these catecholamines return to normal values. Patients who ingest controlled-release formulations need to be observed until after the second catecholamine peak.

Hair to document exposure to glibenclamide.

Among the drugs that are used to incapacitate victims such as kids or elderly for sedation or for criminal gain such as sexual offences or robberies, glibenclamide, an antidiabetic was never mentioned. To document the interest of hair testing in such forensic situations, we have developed an original method to test for glibenclamide. A 30-year-old man was admitted to the Emergency Unit for coma and seizures after a party with some members of his family. Blood glucose was 0.40 g/l. A hair specimen was collected several weeks after the event and divided into two segments of 2 cm. Twenty milligrams of each segment cut into small pieces were incubated overnight in a phosphate buffer (pH 5.5), in presence of gliclazide used as internal standard (IS). A liquid/liquid extraction was realized with a mixture of diethyl ether/methylene chloride, and hair extract was separated on a XTerra MS C18 column using a gradient of acetonitrile and formate buffer. Detection of glibenclamide was achieved using two transitions: m/z 493.9 to 168.9 and 493.9 to 368.8. Linearity was observed from 5 to 1000 pg/mg (r2 = 0.956) with a limit of quantification at 5 pg/mg and a clean-up recovery of about 61%. Within-batch precision and bias were 9.0 and 9.5%, respectively. Ion suppression tested on drug-free hair was about 50%. Glibenclamide tested positive in the two consecutive segments (root to 2 cm: 23 pg/mg and 2-4 cm: 31 pg/mg). These findings were in accordance with a repetitive exposure to the drug. The concentrations were compared with those obtained after a single and a daily dose administration. In the hair of a subject receiving a single 5mg dose and collected 4 weeks later, glibenclamide was detected in the proximal segment at 5 pg/mg. After a 20 mg/day dose, the hair concentration of a subject under glibenclamide therapy was 650 pg/mg.

[Acute higher funghi mushroom poisoning and its treatment]. / Intoxications aiguës par les champignons supérieurs et leur traitement.

PRINCIPLE: The various mushroom poisoning syndromes are summarised together with elements underlining uncertainty and lack of knowledge. For each of the classical syndromes concerned, classified in delays inferior or superior to 6 hours, the toxins and their mechanisms of action, the main mushrooms responsible, the symptoms and their treatment are all presented. EARLY SYNDROMES: Characterised by early onset within 6 hours, these represent the majority of intoxications. There are 6 syndromes: gastro-intestinal (resinoid), muscarine (sudorien, cholinergic), pantherine (myco-atropine, anticholinergic), coprine (similar to the antabuse syndrome), narcotine (psilocybin, hallucinatory) and paxillus syndrome (exceptional). LATE SYNDROMES: Characterised by an onset after six hours, they regroup the phalloid syndrome that is responsible for 90 to 95% of deaths due to higher funghi mushrooms, the orellanine and gyromitrin syndrome and new syndromes identified over the past decade concerning acute renal failure with shorter onset than during the orellanine syndrome (Amanita proxima), erythermalgia (Clitocybe amoenolens), rhabdomyolysis (Tricholoma equestre) and central nervous system failure (Hapalopilus rutilans).