Increased plasma cholinesterase activity and succinylcholine resistance: a genetic variant.

Abstract

Quantitative variations of plasma cholinesterase activity (also called serum cholinesterase, pseudocholinesterase, nonspecific cholinesterase, or cho- linesterase II) are associated with several diseases.Slightly elevated levels have been observed in thy- rotoxicosis (1), schizophrenia (2), hypertension (3), acute emotional disorders, and after concus- sion (4).Markedly elevated levels, two to three times normal, occur with the nephrotic syndrome (5).Plasma cholinesterase activity is decreased in various disorders of the liver (6), in carcinoma (7), and after anticholinesterase drugs (8).Low plasma cholinesterase activity may signify the presence of a qualitatively different enzyme.Some surgical patients develop prolonged apnea after succinylcholine, a muscle relaxant normally hydrolyzed rapidly by cholinesterase; their plasma hydrolyzes cholinesterase substrates more slowly than usual (9).Several cholinesterase inhibitors such as dibucaine, physostigmine, and hexametho- nium are weak inhibitors of the atypical cholines- terase from these patients (10).Under standard- ized conditions, dibucaine inhibits the usual en- zyme more than 70%o, but the atypical enzyme is inhibited only 20%o (11).The per cent inhibition by dibucaine has become known as the dibucaine number.People with dibucaine numbers of about 20 are very sensitive to succinylcholine.Kalow and Staron determined the dibucaine numbers of 1,556 healthy and mentally ill subjects (12) and demonstrated that two allelic, codomi- nant, autosomal genes control the presence of the usual and atypical cholinesterase.Ninety-seven per cent of the population have dibucaine num- bers higher than 70 and are homozygous for the usual cholinesterase; 0.03%o have dibucaine num-