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Eur J Intern Med. 2005 Nov;16(7):492-5. doi: 10.1016/j.ejim.2005.03.004.

Pseudocholinesterase polymorphism in an Irish population.

European journal of internal medicine

G I Adebayo, J Williams, S Healy

Affiliations

  1. Department of Medicine, Garavogue Centre, Level 3, Sligo General Hospital, The Mall, Sligo, Ireland.

PMID: 16275543 DOI: 10.1016/j.ejim.2005.03.004

Abstract

BACKGROUND: Pseudocholinesterase polymorphism, as an example of pharmacogenetics with important clinical implications, has been widely studied and documented. However, data on a sample Irish population is lacking. We sought to provide this.

METHOD: In an assay involving Ellman's reaction, pseudocholinesterase activity, alone and with dibucaine or fluoride as an inhibitor, was quantified using propionylthiocholine iodide as substrate.

RESULTS: Pseudocholinesterase activities of 1.13-12.71 U/ml (mean +/- SD 6.74 +/- 2.04 U/ml) showed a normal distribution among our 116 healthy, non-medicated volunteers, aged 11-80 years (30.7 +/- 10.5 years) and weighing 46-114.6 kg (66.8 +/- 11.4 kg). However, dibucaine numbers from an inhibition study yielded a trimodal pattern consistent with the hypothesis of two allelic genes. Using an established nomenclature, 92 (79.3%) of our volunteers were homozygous for the usual form of the enzyme (E1uE1u). Of the 13 genotyped as E1uE1a, it is possible that 3 were misclassified and are probably E1kE1a. Only one volunteer was homozygous for the atypical form of the enzyme, with activity of 1.13 U/ml and dibucaine and fluoride number of 18.2 and 82.8, respectively.

CONCLUSION: The continuous variation in pseudocholinesterase activity and the trimodal pattern of dibucaine numbers are both in accord with observations in other population groups. Although dibucaine number yields a trimodal pattern, its use could lead to misclassification of some E1kE1a as E1uE1a.

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