Pesticide intoxications carry obvious risks of several secondary symptoms when drugs that are substrates to a target enzyme are administered.
Organophosphate pesticides and drugs act primarily by inhibiting irreversibly acetylcholinesterase enzymes.
The low levels of plasma acetylcholinesterase following acute or prolonged OP exposure changes the pharmacokinetics of drugs that are substrates for these enzymes. Thus, neuromuscular blocking agents such as succinylcholine (suxamethonium) and mivacurium, which are widely used in anaesthesia, will be slowly metabolized, thereby prolonging their pharmacological action.
A case is reported of a patient severely poisoned with parathion (an OP) given small doses of suxamethonium in an effort . . .
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