vivitrol

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kumar28

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Hey all,
Whats ur experiences with the use of vivitrol? Does it work with the pts that you have used it on? Most common side effects?? Are pts usually satisfied with it...I know that there is a risk of respiratory depression with the use of opiates/alcohol/benzos so pts have to wear a bracelet and have a card..is it still risky though...thoughts??

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Hey all,
Whats ur experiences with the use of vivitrol? Does it work with the pts that you have used it on? Most common side effects?? Are pts usually satisfied with it...I know that there is a risk of respiratory depression with the use of opiates/alcohol/benzos so pts have to wear a bracelet and have a card..is it still risky though...thoughts??

vivitrol is an opiate ANTAGONIST. never heard of anybody wearing bracelets or being respiratory depressed for it.
 
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actually it is an opiate antagonist..and one of the common warnings is the risk of respiratory depression due to someone taking opiates who do not feel the effects of the opiates and may take alot as a result. Unfortunately the side effects are still evident and resp depression and death are the most severe
 
actually it is an opiate antagonist..and one of the common warnings is the risk of respiratory depression due to someone taking opiates who do not feel the effects of the opiates and may take alot as a result. Unfortunately the side effects are still evident and resp depression and death are the most severe

That sucks<-- professional opinion.
 
yeah, thats the major problem with this medication-hence people wear bracelets or have cards to prevent ERs giving them opiate medications if they happen to get into an accident and need painkillers
 
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anyone any experience with this injection??
 
Hey all,
Whats ur experiences with the use of vivitrol? Does it work with the pts that you have used it on? Most common side effects?? Are pts usually satisfied with it...I know that there is a risk of respiratory depression with the use of opiates/alcohol/benzos so pts have to wear a bracelet and have a card..is it still risky though...thoughts??

None of the FDA approved medications are very compelling for the treatment of Alcohol dependence. Naltrexone has never been found to be effective for African Americans. Naltrexone when combined with 12-steps doesn't separate from placebo with 12-steps. That said, Naltrexone is possibly the most supported medication for alcohol dependence and a placebo affect seems to have a robust effect in addiction patients. The literature supporting the use for Naltrexone/Vivitrol mostly shows a reduction in 'heavy days' of drinking, not complete abstinence.
Vivitrol is an expensive medication, almost a grand a month. Most insurance companies will require a pre-authorization and documentation of failure of PO Naltrexone, so you may get an idea of what the patient behaves like while on an Alcohol/Opioid Dependent medication.
Yes, Alkermes provides bracelets or necklaces for patients who receive Vivitrol, most of the time the nurse who administers the injection will offer the patient either one.

Side effect wise, it's usually well tolerated, however it resembles a very mild opiate withdrawal initially - with nausea, GI distress, and increased depression/irritability which gets better quickly. Respiratory depression is more linked to using alcohol/opiates on top of the naltrexone rather than a direct effect. The unicorn side effect that you should be aware of is eosinophilic pneumonia. More serious and common effects are local injection site infections, and hepatotoxicity. The consensus with LFTs is that less than 3x of normal (AST/ALT <150) should be safe to use PO Naltrexone of 50mg daily. Vivitrol of 380mg monthly is a lower daily dose than the recommended Naltrexone, so don't be afraid to use IM if they can afford it.

I think it would be wise to always start a short trial of PO Naltrexone to see if they tolerate it before going straight into a monthly injection.
 
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anyone any experience with this injection??


I've acquired 2 patients on it.

One was a late 30s female who refrained from alcohol for the entire time I was following her (6 months), but she also was probably in the action phase at this point and was also going to AA, had inpatient rehab twice, and this was her second attempt at quitting--first time did last a month or two without any medication. Aside from pain at the injection site and on one occasion about 3 months into using it developed "muscle/bone pain" which I was not too sure what to make of since she denied any opiate exposure that she knew of and it would have been a little late for withdrawal, she had no side effects.

The other was a male in his early 20s who really was not ready to quit drinking and it had no effect. Followed him for a few months until he moved, but stopped the medication.

This is the only personal experience ive had with vivitrol. I've seen inpatients who had been on Revia, Campral, etc., but had not followed and saw mixed results. There was a talk at the APA about certain genes being linked to better responses with Campral, but I don't remember the specifics...then there was also that time I decided it was a good idea to give a heroin addict revia while inpatient because he wanted something to stop him from using heroin on the unit. He went into rapid withdrawal since he had actually shot up the previous day (while inpatient). This was before he decided to piss on everything in his room as a goodbye present once we finally got him off the unit.
 
I've acquired 2 patients on it.

One was a late 30s female who refrained from alcohol for the entire time I was following her (6 months), but she also was probably in the action phase at this point and was also going to AA, had inpatient rehab twice, and this was her second attempt at quitting--first time did last a month or two without any medication. Aside from pain at the injection site and on one occasion about 3 months into using it developed "muscle/bone pain" which I was not too sure what to make of since she denied any opiate exposure that she knew of and it would have been a little late for withdrawal, she had no side effects.

The other was a male in his early 20s who really was not ready to quit drinking and it had no effect. Followed him for a few months until he moved, but stopped the medication.

This is the only personal experience ive had with vivitrol. I've seen inpatients who had been on Revia, Campral, etc., but had not followed and saw mixed results. There was a talk at the APA about certain genes being linked to better responses with Campral, but I don't remember the specifics...then there was also that time I decided it was a good idea to give a heroin addict revia while inpatient because he wanted something to stop him from using heroin on the unit. He went into rapid withdrawal since he had actually shot up the previous day (while inpatient). This was before he decided to piss on everything in his room as a goodbye present once we finally got him off the unit.

Pure class
 
Naltrexone's evidence for effectiveness are when patients are sober for a minimum of 3-7 days, so not a good option for acute Psych inpatients. Naltrexone has no benefits for opiate cravings, and minimal for alcohol.
That adverse consequence should be a learning experience, and a testament to Psych general residencies needing more training in addictions.
 
in the right clinical setting, it can work for folks. i've had serious heroin dependence patients on monthly injections, now achieving the longest periods of their sobriety (were not candidates for agonist therapy given also benzo abuse etc). however have to be motivated and in comprehensive therapeutic program simult. tend to be my multidrug, and had serious consequences (unintentional overdoses) and multiple failed treatment.

they tell me it wears off the last few days of the month, so give extra po naltrexone to cover those 3 days. for alcohol, can also help, but not as dramatic; though some patients swear by it.

Agree w/ above, starting po naltrexone for alcohol in inpatient setting is usually not effective (pt usually not committed and don't follow through transitioning to injection)

Disadvantages: insurance approval; liver, (gi w/ po); have to have an injection clinic set up, can precipitate withdrawal, more difficult to manage pain if in emergency
 
Naltrexone's evidence for effectiveness are when patients are sober for a minimum of 3-7 days, so not a good option for acute Psych inpatients. Naltrexone has no benefits for opiate cravings, and minimal for alcohol.

This is kind of a controversial point. There are ongoing trials for detox -> antagonist maintenance as an abstinence only treatment for opiates, and the jury is still out, as compared to bup/methadone. As for alcohol, there is fairly good evidence for potential craving curbing effects. The problem is the NNT is large-ish for naltrexone in alcohol, likely in the 6-10 range, which is why often you don't see an obvious effect. Looks from the latest data that naltrexone for alcohol is gonna have to be guided by pharmacogenetics. But maybe this is gonna be the first personalized treatment and laboratory guided treatment in psychiatry!
 
This is kind of a controversial point. There are ongoing trials for detox -> antagonist maintenance as an abstinence only treatment for opiates, and the jury is still out, as compared to bup/methadone. As for alcohol, there is fairly good evidence for potential craving curbing effects. The problem is the NNT is large-ish for naltrexone in alcohol, likely in the 6-10 range, which is why often you don't see an obvious effect. Looks from the latest data that naltrexone for alcohol is gonna have to be guided by pharmacogenetics. But maybe this is gonna be the first personalized treatment and laboratory guided treatment in psychiatry!

Maybe I'm not understanding your post, but Naltrexone for detox opiate treatment is cruel and unscientific, you would just precipitate opiate withdrawal.

To address several of your points, yes, you can find some smaller effects in different trials suggesting that Naltrexone helps with Alcohol cravings (I even tell alcoholics that naltrexone may help with this), however if you look at the original studies that established effectiveness for Naltrexone in Alcohol Dependence, leading to the FDA approval, it showed NO craving benefits. In fact, the biggest difference between Naltrexone vs Placebo was that Naltrexone caused a much bigger increase in Depression. For Alcohol Dependence, if you actually look at the numbers between a lead-in abstinence of 7 days vs 3 days vs no lead in abstinence, the effect size is much larger for the 7-day lead-in abstinence period.

(Naltrexone in alcohol dependence: a randomized controlled trial of effectiveness in a standard clinical setting. Noeline C Latt, Stephen Jurd, Jennie Houseman and Sonia E Wutzke)

FDA approvals require Safety and Effectiveness data, and the Safety trials showed a small effect for cravings in alcohol dependence, however the Effectiveness trial contradicted this finding.

I do agree that genetic testing may help with Naltrexone, however, it is unlikely that insurance companies or the Affordable Healthcare Act will pay for a thousand dollar lab test to search for a modest 19% improvement in Heavy Drinking Days (24% improvement for Vivitrol), keeping in mind that Naltrexone does not improve overall abstinence or alcohol free days.
Instead of relying on an expensive genetic test, what may be just as helpful is knowing that Naltrexone's effectiveness in Women and African Americans are not proven/effective.

In conclusion, I think Steve Balt, the editor of the Carlat Psychiatry Report says it nicely...

"If science continues to look at addictions through the lens of neurotransmitters and “reward pathways” in the brain, then we will achieve nothing more than partial success in treating substance dependence.”
 

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Maybe I'm not understanding your post, but Naltrexone for detox opiate treatment is cruel and unscientific, you would just precipitate opiate withdrawal.

No, I'm talking about detox first, then transition patients to naltrexone only as a strategy for opiate dependent patients. This is considered an "abstinence only" treatment because there's no agonist in the system.

There's no treatment published trial for this strategy compared to standard buprenorphine/methadone maintenance strategy. All trials are on-going.

I do agree that genetic testing may help with Naltrexone, however, it is unlikely that insurance companies or the Affordable Healthcare Act will pay for a thousand dollar lab test to search for a modest 19% improvement in Heavy Drinking Days (24% improvement for Vivitrol), keeping in mind that Naltrexone does not improve overall abstinence or alcohol free days.

The cost effectiveness of genetic testing is unclear, and without advocacy the test itself may not be paid for, and it's not clear that it will continued to be so costly. Thinking in terms of what's going on now in policy instead of what SHOULD happen is somewhat shortsighted, in my mind.

Your second point is somewhat politically driven. Why is overall abstinence or alcohol free days a better outcome measure than heavy drinking days? Are you arguing that all drinking behavior is ipso facto bad? Also, the second result is not as simplistic as you say. While Naltrexone is generally not believed to increase the total days of abstinent days in the long run, it increases the time it takes to get to the first relapse (COMBINE). The total alcohol free days is also a poor measure because the noise is much larger in that signal by survey methodology. I would argue survival analysis is the better measure.


Instead of relying on an expensive genetic test, what may be just as helpful is knowing that Naltrexone's effectiveness in Women and African Americans are not proven/effective.

I disagree. Because, it's very possible that in SOME women and SOME African Americans it IS effective. It's just that in some current trials, there's suggestion that this effect over placebo is less than in white male population. It's incorrect to approach clinical practice by using potentially incorrect subgroup analysis. The correct clinical practice is to give it to everyone because don't know who's going to benefit and the side effect is small. This is, in fact, the current evidence based guideline.

By the way, this is the same way antidepressant effectiveness trials are being misused to argue an incorrect point. Antidepressants are OFTEN shown to be less effective in minority populations, and these results are distorted to mean that minorities don't benefit from antidepressants, which is false--they do sometimes, it's just that there is a larger variance in the effect in minority subjects, and usually it's a smaller sample, and therefore the signal doesn't reach statistical significance.

Absence of evidence is not evidence of absence.

"If science continues to look at addictions through the lens of neurotransmitters and "reward pathways" in the brain, then we will achieve nothing more than partial success in treating substance dependence."

While I agree that the approach of using neuroscience to treat addiction is not the entire story, the general principle of using evidence and the scientific method instead of political axe grinding is a much better approach than the faith based method various interest groups propound. PROJECT MATCH, for instance, showed that there's no superiority for any specific psychotherapeutic paradigm (i.e. intense AA is NOT better than CBT) and no easy way to match patients to the right therapy. Things are very complex, and to simplistically say this works or not work for this or that person is, in my opinion, not responsible.

Both vivitrol and naltrexone are backed up by solid evidence in terms of overall group effect for treatment of alcohol dependence. The fact that it's possible to develop a MEDICATION for treatment alcohol, to me, strongly argues that there is at least a component of substance abuse that is NOT just a "human weakness" or "social injustice," but actually driven by biology.

Addiction is a complex, multifaceted phenomenon, which makes it fascinating and a great field to go into. But I caution against simplistic, and politically motivated ways of approaching data.
 
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No, I'm talking about detox first, then transition patients to naltrexone only as a strategy for opiate dependent patients. This is considered an "abstinence only" treatment because there's no agonist in the system.

There's no treatment published trial for this strategy compared to standard buprenorphine/methadone maintenance strategy. All trials are on-going.



The cost effectiveness of genetic testing is unclear, and without advocacy the test itself may not be paid for, and it's not clear that it will continued to be so costly. Thinking in terms of what's going on now in policy instead of what SHOULD happen is somewhat shortsighted, in my mind.

Your second point is somewhat politically driven. Why is overall abstinence or alcohol free days a better outcome measure than heavy drinking days? Are you arguing that all drinking behavior is ipso facto bad? Also, the second result is not as simplistic as you say. While Naltrexone is generally not believed to increase the total days of abstinent days in the long run, it increases the time it takes to get to the first relapse (COMBINE). The total alcohol free days is also a poor measure because the noise is much larger in that signal by survey methodology. I would argue survival analysis is the better measure.




I disagree. Because, it's very possible that in SOME women and SOME African Americans it IS effective. It's just that in some current trials, there's suggestion that this effect over placebo is less than in white male population. It's incorrect to approach clinical practice by using potentially incorrect subgroup analysis. The correct clinical practice is to give it to everyone because don't know who's going to benefit and the side effect is small. This is, in fact, the current evidence based guideline.

By the way, this is the same way antidepressant effectiveness trials are being misused to argue an incorrect point. Antidepressants are OFTEN shown to be less effective in minority populations, and these results are distorted to mean that minorities don't benefit from antidepressants, which is false--they do sometimes, it's just that there is a larger variance in the effect in minority subjects, and usually it's a smaller sample, and therefore the signal doesn't reach statistical significance.

Absence of evidence is not evidence of absence.



While I agree that the approach of using neuroscience to treat addiction is not the entire story, the general principle of using evidence and the scientific method instead of political axe grinding is a much better approach than the faith based method various interest groups propound. PROJECT MATCH, for instance, showed that there's no superiority for any specific psychotherapeutic paradigm (i.e. intense AA is NOT better than CBT) and no easy way to match patients to the right therapy. Things are very complex, and to simplistically say this works or not work for this or that person is, in my opinion, not responsible.

Both vivitrol and naltrexone are backed up by solid evidence in terms of overall group effect for treatment of alcohol dependence. The fact that it's possible to develop a MEDICATION for treatment alcohol, to me, strongly argues that there is at least a component of substance abuse that is NOT just a "human weakness" or "social injustice," but actually driven by biology.

Addiction is a complex, multifaceted phenomenon, which makes it fascinating and a great field to go into. But I caution against simplistic, and politically motivated ways of approaching data.

Alright, you are confusing me because you are contradicting your previous statements.

You said that Naltrexone may be the first genetically driven treatment, however when I stated that African Americans and Women do not benefit from Naltrexone based on them not having the receptors that Naltrexone antagonizes, you seem to agree, but you say that SOME may benefit, which disproves your statement that addictions can be biologically determined, which was my whole point in the first place.

I personally believe Naltrexone is the best pharmacological alternative for White or Asian Male alcoholics, however it's not very effective overall. The desire to be sober has to be stronger than the desire to get high. Only 15% of people who consent to take Naltrexone ever fill more than one prescription.
Thus addictions treatment will only be partially successful if you rely solely on pharmacogenetics. Addictions is more about empathy, motivation, and persuasion, not opioid receptors.
 
You said that Naltrexone may be the first genetically driven treatment, however when I stated that African Americans and Women do not benefit from Naltrexone based on them not having the receptors that Naltrexone antagonizes, you seem to agree, but you say that SOME may benefit, which disproves your statement that addictions can be biologically determined, which was my whole point in the first place.

Things are not as dichotomous as you say. In order to understand this you might need a bit of math. Think, simplistically, of a linear regression, where the probability of quitting (P) depends on naltrexone(N - say mostly representing biological factors) and race (R - i.e. say mostly representing environmental factors)

P ~ N + R + N*R (model 1) This third term is often called gene cross environment interaction

The tilda sign here means correlated to

The reality of the trial results indicate that this is probably the best model

A 100% "biological" model says

P ~ N (model 2)

A 100% "social" model says

P ~ R (model 3)

Clinical trial data suggest that model 1 is better than model 2 or 3. There is no contradiction at all.

As to your second point, you say addiction is MOSTLY this or MOSTLY that. What you really mean is that when you do the regression you have some coefficients

P = a * N + b * R

and b>>a. Is this true? I'm too lazy to go back to the naltrexone meta-analysis papers to check this. Did they even do this analysis?
 
Wow, that may be the weirdest response I've gotten from a post on SDN.

Here's a link to a recent abstract concerning African Americans with Naltrexone. If you read the whole article, the authors suggest that only rarely do African Americans have the OPRM1 receptor which Naltrexone targets in addiction, thus NTX is not very promising for African Americans.
If this gene is only "rarely" present in African Americans, why would you routinely order an expensive genetic test for this population?
http://www.ncbi.nlm.nih.gov/pubmed/21679264

I never said (or even view) that "Abstinent days" is a better treatment goal compared to "less heavy drinking days". What I was implying is that Naltrexone's effects are limited, and it's important to know what the evidence points to instead of giving it to anyone with Alcohol Use Disorders. If Naltrexone was a magic bullet, it would also decrease total alcohol consumption (due to less euphoria when drinking), and also increase abstinent days (due to possible craving benefits), but it does neither.

I actually feel you know quite a bit about Naltrexone and that we are seeing things from different view points concerning the real-world use of Naltrexone. I feel I'm more of a skeptic than you concerning the generalization of Naltrexone in Alcoholics. But like I've said before, Naltrexone does seem to have the best overall evidence for Alcohol Dependence. However, Randomized Trials and Probability Equations don't account for things such as non-compliance or wanting to get drunk, because if they didn't matter then Disulfiram would in theory work very well.
 
No, vivitrol doesnt work very well. Never was the slightest bit of evidence that it does.
 
ive probably put about 10 pts of mine on it thus far and the results are pretty good. I would say that about 7 responded well, meaning cravings decreased and remained abstinent
 
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