Thoughts on Abilify LAI

[Not_a_psychic]

At my program, most attendings essentially scoff at starting Abilify Aristada or Maintena for patients with schizophrenia. Not because of the cost, but because they consistently feel that the binding affinity for the partial agonist at dopamine is stronger than other antipsychotics, thus if a patient becomes psychotic while on either of the Abilify LAIs, no amount of alternative antipsychotic will have effect until the Abilify is out of the patient's system (meaning the patients stay psychotic longer). I couldn't find any definite answers about this online, and I know that antipsychotic preference varies seemingly from hospital to hospital, so I was wondering if anyone else had any thoughts on this issue? Do you use either of the Abilify LAI in your residency/practice?

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[deleted736562]

You could always devise nice "hypotheses" how antipsychotics would behave in practice based on how they supposedly work in theory, but they remain just that. At the end of the day you need hard data to support whatever you're saying and it seems like in this case it's lacking.

There's a good amount of "urban myths" that circulate in our field due to the paucity of good data, a lot of it is based on practice culture and ideas that could possibly make sense but are not well supported. They get passed from clinician to clinician without the necessary questioning. Usually a pubmed search is good enough to bust them.

 

[wolfvgang22]

I concur with fpsychdoc. Best practice is to trial patients on oral antipsychotic first, and if the patient responds start the depot formulation. Patients can stop responding to medications sometimes, but most often non adherence to medication is the culprit. You have to weigh the risks and benefits of each medication for the individual patient, keeping the side effect profile of the medications in mind.

I have two or three patients on Abilify Maintena. They do fine.

 

[splik]

Abilify does have the highest affinity for dopamine receptors. As a partial agonist, it can potentially act as a dopamine agonist in the presence of a dopamine antagonist. This is one reason it can be very effective at treating antipsychotic induced hyperprolactinemia. However, the notion that one should not use depot abilify because of fears an antipsychotic switch would not work are someone foolish for a number of reasons. Firstly, if someone is on depot abilify, it is because they have tolerated and responded to po abilify. if they are having breakthrough symptoms, the first thing you would do would be to increase the dose of the depot abilify. The second thing you would do would be to increase the frequency of the shots (e.g. to q3.5 weeks or q3 weeks as opposed to monthly). I have found where people do have breakthrough symptoms on abilify it is often related to the waning of the effects/dose in the last week of treatment so dosing more frequently can help. Thirdly, on a patient on a depot, treatment failure is more likely to be due to non-adherence than anything else (with substance abuse a close second). Fourthly, there are non-antipsychotic options for psychosis including psychotherapies (e.g. supportive psychotherapy, CBT, family work) and benzodiazepines (which are under-utilized). Typically, by the time someone has got on abilify maintenana or aristada they have failed several antipsychotics. Thus, if a new medication is required, the best choice is likely clozapine, which can be combined safely and effectively with abilify. In fact the abilify/clozapine combo is one of the strategies used in refractory schizophrenia.

Abilify gets a bad rap primarily because of its long half-life which means it takes much longer to work than some other antipsychotics. Because of its heavy marketing for mood disorders, many psychiatrists mistakenly belief it is less powerful for psychosis. However, I have found it to be a useful drug in psychosis if you are prepared to wait for it to work. It is also often well tolerated compared to some other neuroleptics.

 

[hamstergang]

Abilify does have the highest affinity for dopamine receptors.

I've heard this elsewhere before, but when I looked for actual D2 Ki values, this didn't seem to be true. Do you have some sources for numbers that back this up?

Edit: doing some more research again just after posting this, and I'm finding different Ki values in different sources, so I'm not sure what to make of this.

 

[Bartelby]

If a patient does well on oral Abilify but has breakthrough symptoms due to noncompliance (for whatever reason), then depot Abilify sounds like a better option than trying a different antipsychotic. I agree with others here that factors such as noncompliance or substance abuse are more likely culprits than Abilify's suddenly losing its efficacy for a patient who has responded well.

 

[whopper]

My problems about the med from a marketing viewpoint, not against the medication itself in terms of clinical effectiveness.

LAIs are in general given to patients with compliance problems. Such patients usually are on the worse end of the spectrum with their psychosis or bipolar disorder.

And Abilify is not quite as clinically effective for psychosis or mania vs heavier duty antipsychotics such as Olanzapine, Risperidone, or Invega. Of course this is a generalized statement. Some patients some meds, even the ones known to not be as effective for most, work better.

Also it's price is higher and the other ones mentioned above, some of them are now available as generic.