Genetic Testing

[painballer27]

Advertisement - Members don't see this ad

Any of you do genetic testing to determine what psychotropic meds may work best for a patient? What are the benefits of doing this?

 

[UTsksk]

I kind of follow what my boss taught me. Genetic testing is used in situations where patient is on a high dose with no effects and has failed multiple adequate trials. Or they are on a low dose and have a ton of side effects.

 

[SmallBird]

'Work best' isn't really how I'd think of this information. It seems to mostly tell you about how the liver will metabolize the medication. Any clinical implication is really a hypothesis I think.

 

[Sushirolls]

They are pointless.
Liver metabolic rates don't determine side effects experienced or not experienced by patients.
Being a slow or rapid metabolizer doesn't determine clinical efficacy.
"go low, go slow" still applies.
Save your patients money. Same insurance companies money.
When patients hand them to me from their previous nurse practitioner who used it as some sort of gospel prescribing guide for the meds in the "green column" I only look to see if they are a rapid metabolizer of anything. This could be useful to support higher than FDA dosing maximums.

Pointless tests.

 

[tr]

Generally agree with most of what's been said above.

I will usually go to pharmacogenetic testing for patients who have failed 3 medication trials (either ineffective or not tolerated).

If they turn out to be a slow metabolizer that can suggest trying lower than standard doses; if they are a rapid metabolizer then I feel more comfortable going over FDA ranges.

The other thing that can be useful is the SLC6A4 genotype. If they are s/s then I won't waste my time on multiple trials of different serotonergic medications.

I find that Genomind has a more scientifically accurate style to their report than Genesight. Genesight's formatting is designed to mislead people to believe that the results comprise some kind of personalized medication efficacy holy grail.

Most patients will get the testing covered by insurance these days if you document 3 failed med trials.

 

[Liquid8]

Agree with most of what’s been already said.

These tests are expensive for patients, and often don’t add much. For what it’s worth, rapid metabolisers can usually be identified based on their clinical presentation, often exhibiting classic withdrawal symptoms in an earlier than expected timeframe. When suspected, a trial of a split dose regime is often worth considering.

The other thing to keep in mind for the OP, is that patient generally like it when you can save them money. As an added benefit, it also means they can keep afford to seeing you when you raise your fees.

 

[Stagg737]

Agree with everything said above.

I'll add that I would occasionally order testing in certain individuals with autism or rare genetic conditions if they didn't already have it done as I've seen some pretty wild reactions to meds in some of those individuals (full-blown tonic clinic seizures leading to status in a 30ish yo started on 3.75mg of mirtazapine). Results have been mixed for me. Mostly it's just helpful with guiding target dose and potential rate of increase in individuals who have had significant problems with previous meds, though the "start low, go slow" method sushi mentioned is probably just as effective anyway.

 

[romanticscience]

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."

 

[Merovinge]

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."

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").

 

[comp1]

Please don't order these tests. You're increasing the cost of healthcare without benefit.