Even when handed information on whether each clopidogrel-treated patient was a
poor metabolizer of the drug, treating physicians usually did not switch them to a different antiplatelet drug, ticagrelor, that would be fully effective despite the patient's reduced-metabolizer status.
The findings of this case represent therapeutic failure of primaquine due to an allele mutation of CYP2D6 rendering the individual a
poor metabolizer. While primaquine remains the therapeutic treatment for P.
Genotyping revealed the subject has CYP2D6 (*4/* 5; 1 gene copy) and CYP2C19 (*2/*2) which corresponded to
poor metabolizer phenotype for both enzymes.
Moreover, only one admixed subject was a CYP2C9 predicted
poor metabolizer (gPMs).
The activity of CYP2D6 is largely determined by genetic variability and common sequence variants exist in human populations that lead to
poor metabolizer (PM) phenotypes [72].
Four phenotypic categories have been assigned to individuals according to enzyme function:
poor metabolizer (PM), intermediate metabolizer (IM), extensive metabolizer (EM), and ultra-fast metabolizer (10,11).
When patients undergo pharmacogenetic testing, they are categorized into one of four phenotypes: ultra-rapid metabolizer (UM), extensive metabolizer (EM), intermediate metabolizer (IM), or
poor metabolizer (PM).
([section]) BMI, body mass index; ([parallel]) EM, extensive metabolizer; ([paragraph]) PM,
poor metabolizer; (a) one patient in RA group refused the drug sensitivity test; (b) four patients (two in RAL group and two in RA group) refused the analysis of CYP2C19 polymorphism; * unpaired f-test; ** chi-square test.
The traditional assignment of phenotype is as follows: extensive metabolizer (EM), intermediate metabolizer (IM),
poor metabolizer (PM), and ultrarapid metabolizer (UM).