Prolonged clonazepam-induced withdrawal symptoms in an NAT2 ultraslow acetylator.
PHARMACOGENOMICS(2019)
Abstract
Clonazepam undergoes nitroreduction to 7-amino-clonazepam via CYP3A4/5, followed by acetylation to 7-acetamido-clonazepam via NAT2 enzyme. While no pharmacological activity is attributed to the metabolites of clonazepam, 7-amino-clonazepam has some affinity for the benzodiazepine receptor as a partial agonist for the gamma aminobutyric acid-A receptor and can compete with clonazepam. Interindividual variability in the incidence of adverse events in patients may, in part, be attributable to differences in clonazepam metabolism. Here, we report on a case of a 70-year-old Caucasian female with insomnia and difficulty weaning off long-term use of clonazepam suggesting that a slow acetylator phenotype contributing to patient's presentation. This hypothesis was confirmed by NAT2 gene sequencing. NAT2 genotyping may play a role in guiding clonazepam therapy.
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Key words
clonazepam,NAT2 genotype,NAT2 pharmacogenomics,personalized clonazepam therapy
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