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UGT1A1*28 is associated with greater decrease in serum K⁺ levels following oral intake of procaterol.

Norihito Yokoe1, Etsuro Yamaguchi, Masaki Nishimura

  • 1Division of Respiratory Medicine and Allergology, Department of Internal Medicine, Aichi Medical University , Nagakute , Japan .

The Journal of Asthma : Official Journal of the Association for the Care of Asthma
|August 30, 2014
PubMed
Summary

Genetic variations in UGT1A1*28 may increase the risk of hypokalemia when using procaterol, a common asthma medication. This finding highlights potential personalized treatment approaches for beta-2 agonists.

Keywords:
cytochrome P450single nucleotide polymorphismuridine diphosphate glucuronosyltransferase 1A1β2-adrenergic receptor

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Area of Science:

  • Pharmacogenetics
  • Clinical Pharmacology
  • Respiratory Medicine

Background:

  • Procaterol is a widely used beta-2 agonist for asthma and COPD.
  • Individual responses to beta-2 agonists vary due to genetic differences.
  • Genetic polymorphisms in drug-metabolizing enzymes and receptors may influence these variations.

Purpose of the Study:

  • To investigate the relationship between gene polymorphisms and the physiological effects of procaterol in healthy individuals.
  • To identify genetic factors influencing procaterol metabolism and response.

Main Methods:

  • Ninety-two healthy volunteers received procaterol (1 µg/kg).
  • Serum procaterol concentrations, serum potassium (K+), and physical responses were monitored.
  • Genotyping was performed for ADRB2, CYP3A4, and UGT1A1 polymorphisms.

Main Results:

  • No studied gene polymorphisms affected serum procaterol concentrations.
  • UGT1A1*28 carriers showed significantly lower serum K+ levels post-administration.
  • No other polymorphisms were associated with serum K+ levels or physical responses.

Conclusions:

  • UGT1A1*28 genotype is associated with a higher risk of procaterol-induced hypokalemia.
  • This suggests potential for personalized medicine in beta-2 agonist therapy.
  • Liver metabolism of beta-2 agonists may be influenced by UGT1A1 polymorphisms.