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Discrimination of phenotypes in human serum cholinesterase deficiency.

Hereditary deficiency, of cholinesterase (pseudocholinesterase, acyicholine acylhydrolase) in human serum is easily demonstrated by the absence of measurable enzymatic activity, or by slight activity (<3% of normal), when benzoylcholine is used as a substrate. Deficient activity of the enzyme is under control of one genetic locus (the "silent" gene), and persons who are heterozygous for the deficiency have less activity than the average for normal people. The range of activity of the enzyme in normal persons is so great, however, that it has been considered impossible to define a level below which heterozygosity is assured. Deficiency of serum cholinesterase is found with a frequency of one in 100,000 in European populations (Hodgkin et al. 1965) but is found in about 1%0 of certain Eskimos in western Alaska (Gutsche et al. 1967). Genetic variants of cholinesterase, where the enzyme is resistant to inhibition by dibucaine or by fluoride (Kalow and Genest 1957; Harris and Whittaker 1961), have not been found in Eskimos, but the C5+ variant (Harris et al. 1963) is present. Serum obtained from all males 16 or more years old in two villages (Hooper Bay and Chevak) in this area gave a bimodal frequency distribution (fig. 1). This result suggested that it may be possible to discriminate between heterozygous and homozygous normal phenotypes. This study was designed to determine the extent to which such discrimination is possible.