Les intoxications avec le diméthylarsinate de sodium (expérience du centre antipoison de Paris de 1999 à 2004)

Les accidents domestiques sont fréquents et touchent particulièrement les enfants. Parmi les produits auxquels ils sont régulièrement exposés, il y a les formicides contenant du diméthylarsinate de sodium (DMA-Na) : sel d'un dérivé organique de l'arsenic qui semble avoir une faible toxicité clinique en cas d'ingestion aiguë même massive. Parmi tous les appels au Centre antipoison de Paris relatifs à une intoxication avec du DMA-Na entre 1999 et 2004, nous avons étudié 62 dossiers d'intoxications accidentelles ou volontaires. Dans de rares cas, il y eut des symptômes digestifs bénins et l'évolution a toujours été favorable. Mais les composés organoarsenicaux sont aussi suspects d'être cancérigènes. Le délai de prise en charge des cancers liés à l'arsenic étant de 40 ans, nous n'avons pas le recul nécessaire pour observer ces complications. Il convient donc de rester vigilant afin d'éviter les intoxications avec ce produit et de surveiller la survenue possible d'effets à long terme.Accidents in the home are frequent and affect children particularly. Among phytosanitary regulation products to which they are regularly exposed, there are formicides containing sodium dimethylarsinate (DMA-Na) : salt of an organic compound of arsenic which seems, unlike inorganic species, to have a low clinical toxicity in case of even massive acute ingestion. Among all calls to the poison control center of Paris relative to intoxication with DMA-Na between 1999 and 2004, we studied 62 files of accidental or voluntary poisonings. In rare cases, mild digestive symptoms were noted and the evolution was always favorable. But organoarsenical compounds are also suspected to be carcinogenic. Cancers related to an occupational exposure to inorganic arsenic occur about 40 years later so we do not have any necessary distance to observe these complications. It is thus advisable to remain vigilant in order to avoid poisonings with this product and to watch a possible onset of long-term effects.PARIS12-CRETEIL BU Médecine (940282101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Frontotemporal degeneration, the next therapeutic frontier: Molecules and animal models for frontotemporal degeneration drug development

Frontotemporal degeneration (FTD) is a common cause of dementia for which there are currently no approved therapies. Over the past decade, there has been an explosion of knowledge about the biology and clinical features of FTD that has identified a number of promising therapeutic targets as well as animal models in which to develop drugs. The close association of some forms of FTD with neuropathological accumulation of tau protein or increased neuroinflammation due to progranulin protein deficiency suggests that a drug's success in treating FTD may predict efficacy in more common diseases such as Alzheimer's disease. A variety of regulatory incentives, clinical features of FTD such as rapid disease progression, and relatively pure molecular pathology suggest that there are advantages to developing drugs for FTD as compared with other more common neurodegenerative diseases such as Alzheimer's disease. In March 2011, the Frontotemporal Degeneration Treatment Study Group sponsored a conference entitled "FTD, the Next Therapeutic Frontier," which focused on preclinical aspects of FTD drug development. The goal of the meeting was to promote collaborations between academic researchers and biotechnology and pharmaceutical researchers to accelerate the development of new treatments for FTD. Here we report the key findings from the conference, including the rationale for FTD drug development; epidemiological, genetic, and neuropathological features of FTD; FTD animal models and how best to use them; and examples of successful drug development collaborations in other neurodegenerative diseases