A review of 48 cases of acute ingestion-related poisoning with py

A review of 48 cases of acute ingestion-related poisoning with pyrethroids in Taiwan revealed

that gastrointestinal tract signs and symptoms were most common, found in 73% of cases [7]. Pulmonary abnormalities were found in 29% of cases, including aspiration pneumonitis and pulmonary edema [7], as evident in our second case. Central nervous system involvement, as demonstrated in the first case described here, was found in 33% cases and included confusion, coma and seizures [7]. The biodegradation of synthetic pyrethroidal compounds has been extensively studied [8], [9] and [10]. Permethrin is a synthetic Type I pyrethroid with a high selectivity http://www.selleckchem.com/products/azd5363.html for insects. It has four isomers with 1R cis-permethrin being the most insecticidal active isomer [11]. Pyrethroids kill insects by strongly exciting their nervous systems. They make the nervous system hypersensitive to stimuli from sensory organs. Permethrin-exposed nerves send a train of impulses, instead of a single impulse, in response to a stimulus. It does this by interacting with the voltage-dependent sodium channels and produces a prolongation of inward sodium current, and hence the channels remain open much longer, causing repetitive nerve impulses [11]. Permethrin has been shown in vitro

and in vivo to increase acetylcholine and acetylcholinesterase levels [12] and [13]. Monoamine oxidase and ATPase enzymes are inhibited by permethrin [1], [2] and [10]. It has been reported to inhibit the GABA receptor, producing excitability and convulsions INCB024360 [2] and [11]. At high doses, neurotoxic symptoms can include tremors, incoordination, hyperactivity, paralysis, and hyperthermia [14]. Some other effects are irritation to the eyes and skin. It is classified as a carcinogen and is a mutagen of human cell cultures [14]. The patients in this report were initially treated with atropine, which had no effect. An explanation for treatment failure could be that the atropine dose administered was not potent enough to overcome the permethrin toxin load. However, there is no

literature supporting treatment of permethrin toxicity with atropine. Permethrin is a very common and highly effective pesticide widely used around the world; however, reports of toxicity in 4-Aminobutyrate aminotransferase the pediatric literature are infrequent. The most common symptoms appear to be nausea and vomiting. Neurotoxicity appears to be most clinically significant. Permethrin toxicity may mimic organophosphate poisoning because of its cholinergic actions. Treatment for permethrin toxicity is mainly supportive, including protection of the airway due to the altered mental status and significant secretions, and involves reversal of GABA receptor dysfunction with benzodiazepines. Atropine is ineffective, and may have the undesired side effect of reducing seizure threshold in these patients.

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