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The genetic basis for extensive and poor metaboliser variability is the CYP2D6 allele, located on chromosome 22.
The report in Nature noted that a person would not be a "poor metabolizer" of drugs unless he had two copies of the abnormal gene.
Senna-induced hepatitis in a poor metabolizer.
The results showed that she was a poor metabolizer in using the 2C19 enzyme and somewhat slower than normal for the 2D6 enzyme.
Thus an extensive metabolizer may have adverse effects from a rapid buildup of codeine metabolites while a poor metabolizer may get little or no pain relief.
Polymorphism within this gene is associated with variable ability to metabolize mephenytoin, known as the poor metabolizer and extensive metabolizer phenotypes.
There are four possible categories for each marker: poor metabolizer, intermediate metabolizer, extensive metabolizer, or ultra-extensive metabolizer.
In theory, by using pure esomeprazole the effects on the proton pump will be equal in all patients, eliminating the "poor metabolizer effect" of the racemate omeprazole.
CYP2C8*1 is characterized as the wild-type allele, which shows an acceptable safety profile, while CYP2C8*2, *3 and *4 all show a range of "poor metabolizer" phenotypes.
Codeine is more commonly used; however, as codeine is, in essence, a prodrug that requires in vivo metabolism for efficacy, it is ineffective for some individuals with the "poor metabolizer" genotype of the liver cytochrome P450 enzyme CYP2D6.