CHOLINESTERASES

Objective: To review current data on butyrylcholi-nesterase. Data sour ces: Search through Medline(R) data bases of articles in French or Eng lish. Study selection: Original articles and case reports were selecte d. Letters to editor were excluded. Data extraction: The articles were analyzed in order to obtain current data on biochemical structure, ac tion, major pathological variations, especially with regard to the rec ent informations obtained by molecular biology concerning the identifi cation of genetic variants. Data synthesis: Butyrylcholinesterase must be differentiated from acetylcholinesterase, which cannot hydrolyse s uccinylcholine. The physiological action of butyrylcholinesterase rema ins unknown, although it can hydrolyse many drugs. Excluding genetical mutations, several physiopathological situations alter butyryl-cholin esterase activity. Butyrylcholinesterase activity assessment does not allow the diagnosis of genetic variants. Whatever the origin, only def icits of more than 50% modify significantly the metabolism of succinyl choline or mivacurium. The diagnosis of a prolonged neuromuscular bloc kade is obtained with systematic monitoring of the neuromuscular funct ion in case of administration of mivacurium or succinylcholine. Mivacu rium should only be re-injected when one response at train of four is obtained. In case of prolonged neuromuscular blockade, the anticholine sterasic agent should not be administered when no response at train of four is obtained. The biochemical methods using inhibitors (dibucaine , fluoride) of the butyrylcholinesterase and a familial study lead to the diagnosis in mast cases because the atypical and fluoride variants are the most frequent. When results are doubtful, genetic molecular m ethods with the use of PCR and restriction enzymes allow a rapid diagn osis. (C) 1998 Elsevier, Paris.