Treatment Guidelines for Lead Exposure in Children
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چکیده
The recent introduction of an effective oral chelating agent for the reduction of a body burden of lead and the changing standards of care for children exposed to lead prompted the Committee on Drugs to review the therapy for lead intoxication. This statement reviews the pharmacology of available chelating agents. Screening standards and detailed discussions of environmental control and nutritional management have been previously published by the American Academy of Pediatrics.1 Lead intoxication has been a problem throughout history. In the early i940s it was recognized that the amount of lead in the urban industrial environment had increased to the point at which a striking number of children demonstrated hematologic effects and clinical signs of acute lead intoxication. Blood lead levels in children in the United States on average have decreased, and rarely are children seen with blood lead levels of greater than 70 pg/dL. Even in patients with levels of greater than 50 pg/dL, “classic” laboratory and clinical findings of lead toxicity, such as basophilic stippling and encephalopathy, are rarely seen.2 In the past, therapy was based on the ability of chelators to reverse the hematologic effects of lead and halt the progression of lead encephalopathy. The efficacy of chelation therapy for children without the hematologic or neurologic findings has yet to be demonstrated; a decrease in blood lead concentration is the only discernible goal for chelation therapy in this setting. Eliminating the source of lead exposure also can accomplish this result. A recent study of moderately lead-exposed children receiving chelation therapy failed to demonstrate any additional benefit of CaNa2-ethylenediaminetetraacetic acid (EDTA) compared with abatement at improving cognitive function.3 Our understanding of the pharmacokinetics of lead and its alteration by chelating agents is mdimentary. Human lead pharmacokinetics has been studied in small series.4 Isotopic lead administered at low doses in adult human subjects revealed that lead has an extremely long terminal elimination half-life in blood of more than 30 days and similarly long rates of uptake into tissue. Rates of elimination from bone were so long that they could not be determined but are estimated in years. It is therefore extremely
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