In patients with thallium poisoning, treated with the chelating agent sodium diethyldithiocarbamate (dithiocarb), clinical deterioration and electroencephalographic disturbances have been observed coincident with the periods in which dithiocarb was given. Intravenous administration of dithiocarb to rats poisoned with thallium causes redistribution of thallium in the chelate form, with an increase of concentration in the brain. The chelate formed is rapidly decomposed again. These observations constitute a contraindication to the use of dithiocarb as an antidote in thallium poisoning.
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Kamerbeek et al. (1971) studied this question.
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