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MeSH Review

Lead Poisoning

 
 
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Disease relevance of Lead Poisoning

 

Psychiatry related information on Lead Poisoning

  • The resultant mental incompetence and especially the rapidly declining birth rate among the ruling class are now believed to have been major factors in the decline of the Roman Empire. Epidemic outbreaks of lead poisoning have occurred repeatedly throughout history and still occur today [6].
  • However, coexposure to lead and ethanol could result in more serious depletion of calcium and magnesium, and this could be the cause of suspected synergism between alcohol consumption and lead poisoning [7].
 

High impact information on Lead Poisoning

 

Chemical compound and disease context of Lead Poisoning

  • The mean Kis of lead for glucose-6-phosphate and nicotinamide adenine dinucleotide phosphate (NADP) for G6PD were 1.5 microM and 2.1 microM, respectively, which is within the range of intraerythrocytic lead concentrations found in clinical lead poisoning [1].
  • In chronic demyelination caused by lead poisoning, the cellular and extracellular distribution of apolipoproteins was similar to Te neuropathy; the amount of apo E accumulation and the macrophage density were proportional to the prevalence of active demyelination in teased fibers [13].
  • Published recommendations (1985) for the management of childhood lead poisoning suggest the use of ethylenediaminetetraacetic acid (EDTA) provocation testing and chelation as the mainstay of treatment for blood lead levels between 25 and 55 micrograms/dL [14].
  • Effects of calcium disodium versenate (CaNa2EDTA) chelation in moderate childhood lead poisoning [15].
  • Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves [16].
 

Biological context of Lead Poisoning

 

Anatomical context of Lead Poisoning

 

Gene context of Lead Poisoning

 

Analytical, diagnostic and therapeutic context of Lead Poisoning

References

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  13. Macrophage apolipoprotein synthesis and endoneurial distribution as a response to segmental demyelination. Gelman, B.B., Goodrum, J., Bouldin, T.W. J. Neuropathol. Exp. Neurol. (1991) [Pubmed]
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