Psycho-Babble Medication Thread 87847

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Low Dose (~20 mg) Anafranil ??

Posted by rod on December 25, 2001, at 13:13:11

I am taking 40 mg of Citalopram (does not help me much). A few days ago I started anafranil (37,5 mg), quick response at the first 3 days (really started feeling good), then got worse again. After 1 week dosage of anafranil up to 75 mg - > very bad (anxious, confused) - > reduced to ~20 (a quater of the pill)- > felt better again. 1 week quater of pill - > felt good the time, and increased it to 37,5 - > bad again.
Question: Should I listen to my body or my Doc (he wants me to take 75 mg). I do not believe that the path to relief goes through hell at the first few steps. Too many times I believed Doctors and then the medication directed me into a dead end. But my Doctors opinion is that treatment of anxiety disorders (I have GAD, social phobia and thereby caused depression), with medication fist leads to an increase of anxiety, panic until the "counter-reaction" of the body "heals" the illness. I dont know if I should believe him (he does a lot of research in hospital and university, so he is indeed a specialist, in some way). If anyone tells me that his way of treating anxiety patients is right (incuding ignoring patients personal opinion), I might obey his orders.

thanks
rod

 

Re: Low Dose (~20 mg) Anafranil ??

Posted by edward602 on December 25, 2001, at 15:19:12

In reply to Low Dose (~20 mg) Anafranil ??, posted by rod on December 25, 2001, at 13:13:11

> I am taking 40 mg of Citalopram (does not help me much). A few days ago I started anafranil (37,5 mg), quick response at the first 3 days (really started feeling good), then got worse again. After 1 week dosage of anafranil up to 75 mg - > very bad (anxious, confused) - > reduced to ~20 (a quater of the pill)- > felt better again. 1 week quater of pill - > felt good the time, and increased it to 37,5 - > bad again Question: Should I listen to my body or my Doc (he wants me to take 75 mg). I do not believe that the path to relief goes through hell at the first few steps. Too many times I believed Doctors and then the medication directed me into a dead end. But my Doctors opinion is that treatment of anxiety disorders (I have GAD, social phobia and thereby caused depression), with medication fist leads to an increase of anxiety, panic until the "counter-reaction" of the body "heals" the illness. I dont know if I should believe him (he does a lot of research in hospital and university, so he is indeed a specialist, in some way). If anyone tells me that his way of treating anxiety patients is right (incuding ignoring patients personal opinion), I might obey his orders.
>
> thanks
> rod


My pdoc has the same opinion and again he has lots of experience at a major teaching hospital. He treats my anxiety, which is often just awful, as a symptom of depression that will often et worse on ssri's before it gets better. At first I did not complain enough at how bad the anxiety was but now I am more ready for it. Currently on 60 mg. celexa and taking ativan for the anxiety. My pdoc seems pretty confident -- he usually is -- treat the underlying depression and the anxiety will resolve itself. Now I am going to steel myself and try to make it to a holiday party. But first I'll take an ativan. Demand a benzo so you can eliminate the anxiety in the short-term and better figure out how you are reacting to the anafranil.

Edward

 

SSRI + TCA Interaction (isozyme P450 2D6)

Posted by rod on December 27, 2001, at 7:01:51

In reply to Re: Low Dose (~20 mg) Anafranil ??, posted by edward602 on December 25, 2001, at 15:19:12

Now I know, why I felt bad on Prozac + Elavil (both full dose) and why my current med combo Celexa + Anafranil is not good.So I might be right taking Anafranil at a very low dosage. My Doctor is a JERK!

http://www.rxlist.com/cgi/generic/clomipr_ad.htm

excerpt:

Drugs Metabolized by P450 2D6: The biochemical activity of the drug metabolizing isozyme cytochrome P450 2D6 (debrisoquin hydroxylase) is reduced in a subset of the Caucasian population (about 7%-10% of Caucasians are so-called ?poor metabolizers"); reliable estimates of the prevalence of reduced P450 2D6 isozyme activity among Asian, African and other populations are not yet available. Poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants (TCAs) when given usual doses. Depending on the fraction of drug metabolized by P450 2D6, the increase in plasma concentration may be small or quite large (8 fold increase in plasma AUC of the TCA). In addition, certain drugs inhabit the activity of this isozyme and make normal metabolizers resemble p.o. metabolizers. An individual who is stable on a given dose of TCA may become abruptly toxic when given one of these inhibiting drugs as concomitant therapy. The drugs that inhibit cytochrome P450 2D6 include some that are not metabolized by the enzyme (quinidine: cimetidine) and many that are substrates for P450 2D6 (many other antidepressants phenothiazines and the Type 1C antiarrythmics propafenone and flecainide) while all the selective serotonin reuptake inhibitors (SSRIs), e.g fluoxetine, sertraline, and paroxetine, inhabit P450 2D6. They may vary in the extent of inhibition. The extent to which SSRI-TCA interactions may pose clinical problems will depend on the degree of inhibition and the pharmacokinetics of the SSRI involved. Nevertheless, caution is indicated in the co-administration of T.A. with any of the SSRIs and also in switching from one class to the other. Of particular importance, sufficient time must elapse before initiating TCA treatment in a patient being withdrawn from fluoxetine, given the long half-life of the parent and active metabolite (at least 5 weeks may be necessary). Concomitant use of tricyclic antidepressants with drugs that can inhibit cytochrome P450 2D6 may require lower doses than usually prescribed for either the tricyclic antidepressant or the other drug. Furthermore, whenever one of these drugs is withdrawn from co-therapy, an increased dose of tricyclic antidepressant may be required. It is desirable to monitor TCA plasma levels whenever a TCA is going to be co-administered with another drug known to be an inhibitor of P450 2D6.


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