In acute severe anticholinesterase poisoning by organophosphate compounds, pralidoxime (P-2-AM, pyridine-2-aldoxime methiodide) used in the recommended doses, intravenously, has not been shown to reactivate the inhibited cholinesterase, as evidenced both clinically and biochemically. In vitro studies using pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by the organophosphate insecticide Bidrin (di-methyl-3-hydroxyl-N, N-dimethyl-crotonamide phosphate). This was even so despite prolonged exposure of the inhibited cholinesterases to the oxime. The value of pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate insecticides.
Surveys in a number of European and American populations have found the frequency of occurrence of the heterozygotes for the gene for the dibucaine-resistant variant of cholinesterase (E.C.3.1.1.8) to be relatively constant. Similar surveys in Oriental population have shown low incidence of the same gene. This study done on the multi-racial population consisting of 3 major groups shows an absence of the gene for the dibucaine resistant variant of cholinesterase. This is supported by the clinical experience in the use of suxamethonium as a single dose in more than 25,000 individuals.