Comments on
Side Effects II

By J.T. Junig, MD, PhD

In my last post, I wrote about the work-up of a patient …

6 Comments to
Side Effects II

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  1. While I know you’re trying to find the cause, in the meantime could you have them switch to subutex, at least to test the theory that the symptoms are caused by nalaxone at all? Just a thought from a fan of your articles & also a lint time sub patient.

  2. *long time! Not lint ;)

  3. Suboxone (as a form of addiction maintenance), is not the answer to opiate addiction. It may have some use as a detox drug in furtherance of abstinence. This is an important distinction. This is a complicated subject.

    • Detox with Suboxone was discredited years ago— I recommend that you read the literature, or at least spend some time working with opioid addicts– over time. Several large studies looking into ‘detox’ showed very clearly that relapse after suboxone detox is similar to relapse after residential treatment– 95% if people are on Suboxone for a year, 97% of they are on Suboxone for a couple months. Those numbers– over 95%– are relapse within ONE YEAR; anyone who follows opioid addiction over years, as I have, knows that relapse occurs after 1,5,10, or more years. Over 95% of the people who decide to ‘detox’ off opioids, after a period of opioid dependence, will only end up ‘detoxing’ over and over again– if they stay alive.

  4. Interesting problem. Given that the effects only last an hour it’s a safe bet to stick with the presumption that it’s the naloxone somehow interfering. Is the patient taking any OTC medications like Tagamet, st johns wart or eating foods like grapefruit juice that would interfere with CYP450 or others? Has he had problems with medications in the past not “breaking down”?
    An easy solution would be to prescribe Subutex if there is no history of IV drug abuse in the patient.
    That’s not to say it wouldn’t be worthwhile to investigate more drug interactions since if the naloxone isn’t being properly metabolized then I’d be willing to bet the buprenorphine isnt either, maybe take a look at their plasma concentration levels after dosing and compare to what’s a normal range x hours after dose would be helpful (if the patient has insurance that is)
    Hope you can share a follow up here

    • All very good thoughts– and more evidence that my readers are some of the brightest blog readers out there.

      When I look up the metabolism of naloxone, I am disappointed to see that there is no critical process that might be blocked by other meds. I was hoping to find that the specific cytochrome was blocked by the antihistamine he is taking… but naloxone seems to be broken down by ubiquitous emzymes that add a glucoronide molecule that then alllows for excretion at the keys.

      The quantitavie tests for buprenorphine give a wide range for ‘normal levels’ after a certain dose. I think that is in part because of the change in efficiency of dosing, from one person to another.

      I think I’ll end up putting him ono buprenorphine without Naloxone ans see how that works. But I have great respect for the placebo respect, so even significant improvement using a med without naloxone won’t amswer the questopms intirely. Thanks for the suggestions!

      J
      J
      J

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