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- Mar 16, 2016
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Any of you do genetic testing to determine what psychotropic meds may work best for a patient? What are the benefits of doing this?
Prozac DONT CARE BOUT YOUR METABOLISM with a giant arm with biceps bursting through it is the take home message. This is particularly important in CAP where Prozac is frequently a first line medication and/or should be the second line medication after failing Zoloft/Lexapro. Prozac is also not effected by the p-glycoprotein pump and thus any failure on the medication is due to the effects of the medication and not pharmacokinetics (**if adequately dosed and given time to respond, I punch the air every time I hear about a PCP seeing someone back for a 2 week f/u on Prozac initiation and changing meds when it "doesn't work").Agreed. I remember digging into the fluoxetine package insert and finding this:
Variability in Metabolism – A subset (about 7%) of the population has reduced activity of the drug metabolizing enzyme cytochrome P450 2D6 (CYP2D6). Such individuals are referred to as “poor metabolizers” of drugs such as debrisoquin, dextromethorphan, and the TCAs. In a study involving labeled and unlabeled enantiomers administered as a racemate, these individuals metabolized S-fluoxetine at a slower rate and thus achieved higher concentrations of S-fluoxetine. Consequently, concentrations of S-norfluoxetine at steady state were lower. The metabolism of R-fluoxetine in these poor metabolizers appears normal. When compared with normal metabolizers, the total sum at steady state of the plasma concentrations of the 4 active enantiomers was not significantly greater among poor metabolizers. Thus, the net pharmacodynamic activities were essentially the same. Alternative, nonsaturable pathways (non-2D6) also contribute to the metabolism of fluoxetine. This explains how fluoxetine achieves a steady-state concentration rather than increasing without limit.
Way more complex than a red label that says "don't use."