Jabberwocky
Frumious Bandersnatch
TRAMADOL MEGATHREAD
1. What is Tramadol ?
2. Pharmacology of Tramadol.
3. The two main characteristcs and ways of action.
4. Routes of administration and bioavailability.
5. Side effects.
6. Withdrawal.
7. Potentiation.
8. Interaction with other medicines and other forms of interaction.
1. What is Tramadol?
Tramadol is an opioid pain medication used to treat moderate to moderately severe pain.
Tramadol is a fully synthetic opioid unlike opiates like Morphine or Codeine which are found in the poppy plant ( Papaverus Somniferum ) or semi-synthethic opioids like Diamorphine (Heroin) .
Tramadol acts by binding to the μ-opioid receptor of the neuron and is also a serotonin–norepinephrine reuptake inhibitor.
Beside the medical uses, it has recreational uses with similar and also unique characteristics as other opioids.
It's usage is mainly limited by the lowered seizure threshold or defficiency of the CYP2D6 enzyme.
2. Pharmacology of Tramadol
Tramadol itself is not as active as you would believe and the binding affinity of the substance itself is lower than those of its metabolites.
The metabolism of tramadol is liver-mediated demethylation and glucuronidation via CYP2D6 & CYP3A4.
The two active metabolites resulted are desmetramadol (O-desmethyltramadol), which is the major active metabolite, and nortramadol which adds to its uniqueness compared to other opiates/opioids due to the amplified SNRI/SRI activity it has.
Tramadol acts on the opioid receptors through its major active metabolite desmetramadol, which has as much as 700-fold higher affinity for the MOR relative to tramadol. Moreover, tramadol itself has been found to possess no efficacy in activating the MOR in functional activity assays, whereas desmetramadol activates the receptor with high intrinsic activity (Emax equal to that of morphine). As such, desmetramadol is exclusively responsible for the opioid effects of tramadol.
Other properties:
Agonist of the μ-opioid receptor (MOR) and to a far lesser extent of the δ-opioid receptor (DOR) and κ- opioid receptor (KOR)
Serotonin reuptake inhibitor (SRI) and norepinephrine reuptake inhibitor); hence, an SNRI
Serotonin 5-HT2C receptor antagonist
M1 and M3 muscarinic acetylcholine receptor antagonist
α7 nicotinic acetylcholine receptor antagonist
NMDA receptor antagonist (very weak)
TRPA1 inhibitor
The difference in the affinity is not the only one, as the halflife of Tramadol has an aprox value of 6 hours while desmetramadol aprox. 9 hours. ( PLEASE TAKE IN CONSIDERATION THAT THIS VARRIES FROM PERSON TO PERSON, AND FROM INSTANT RELEASE TO EXTENDED RELEASE, AS SOME OF YOU MIGHT TAKE OTHER MEDICATION CONTRAINDICATED IN COMBINATION OF TRAMADOL PLEASE DON'T TAKE THESE HALF LIFE VALUES FOR GRANTED AND CONSULT YOUR DOCTOR ).
3. The two main ways of action.
Normally this subject would be and is partially covered in the Pharmacology section.
But considering that some of you use it in self medicating purposes which are not related to pain and don't know why it has such a "positive" (this is subjective) effect on your mood, it will be covered shortly.
So we all know that the main action of it is in its opioid-like properties, but due to the SNRI/SRI activity it has an antidepressant, anti-anxiety and mood enhancing activity. It tends to be more prominent than in other opiates and feel kinda weird that's why people describe the "high"/effect dirty.
Although it is structurally similar to Effexor and other such compounds I advise against using it as an antidepressant due to the seizure risk, double withdrawal ( beside the SNRI withdrawal you will feel the main part of its withrawal arsenal which is very opiate/semi-syntethic opioid/fully syntethic opioid like ).
So if you hate the brain zaps, mood swings and enhanced angryness avoid!
Another short note which is not fully medically sustained but by my own experience, some psyhiatrist tend to misdiagnose tramadol addicts with bipolar disorder, had couple of friends diagnosed with it when they went to rehab because of tramadol and I assure you they are not bipolar at all, compared to legit bipolar people I also know. My guess would be the cause of this misdiagnose is due to the major mood swings experienced at high dosages or in tramadol withdrawal.
4. Routes of administration, bioavailability and dosage.
Dosage:
BIG WARNING: Tramadol causes seizures, saw a lot of them at low doses, mid doses, high doses so please take caution, if you are predisposed please use another opioid/opiate or seek an alternative treatment approved by your doctor.
The maximum dosage per day approved by doctors would be 400mg per day.
For a begginer I would suggest starting with 100 mg and add 50 mg until you reach the level you want,
it has excelent re-dosing potential unlike other substances ( for example codeine which has a ceiling effect and re-dosing can be tricky without the ceiling also.
BIGGEST LESSON LEARNED HERE ON BLUELIGHT: YOU CAN ALWAYS AND MORE BUT YOU CAN'T DROP THE DOSAGE AFTER YOU TOOK IT. JUST LIKE WITH SALT ADDED TO FOOD.
The effects with the immediate release formula can kick in between 30-45 minutes while the extend ones start to kick in between 1-3 hours. So before re-dosing please consider this.
WARNING: If you have a formulation that includes something else than Tramadol too, like Ultram which has APAP or here in Romania Dorretta, please consider doing a cold water extraction exactly like when you do with codeine and APAP products, the solubility varies but the tramadol already does some damage and combined with APAP it is rough on the liver.
Routes of administration and biovailability:
Oral: 70% to 75%
This is the ROA I recommend the most due to the liver-mediated demethylation talked about in section 2, the simplicity of the administration and the less risks associated with it ( for example: IV has lots of risks like infections, abscesses etc.)
Rectal: 77%
This ROA can be done by plugging or suppositories sold by pharmacies.
For details about plugging substances please search for the plugging thread through the search engine located in the upper left corner of the forum or on google by typing site::bluelight.com after the keyword.
IM: 100%
For this ROA please use ampoules (vials) directly bought from the pharmacy, IM''ing pills is even more dangerous than IV'ing them as the binders and fillers get stuck in the tissue and can cause an abcess.
IV: 100 %
As for the IM ROA vials must be used too and not pills ( it does not matter if they are legit, pressed, instant release or extended release, IV'ing pills is a plain NO NO. )
5. Side Effects.
Its properties of lowering the seizure threshold are the biggest risk factor.
Chemical unbalance in the brain is another one which can result in depression, anxiety, mood swings, angryness etc. ( so don't be fooled by its antidepressant properties as those can take a big U Turn and surprise you)
The most common adverse effects of tramadol include nausea, dizziness, dry mouth, indigestion, abdominal pain, vertigo, vomiting, constipation, drowsiness, and headache. Compared to other opioids, respiratory depression and constipation are considered less of a problem with tramadol.
Another big one would be the addiction potential, some doctors might say that is less addictive than other opioids or not at all, well this is not true at all as I've been addicted to it for 6 years + and even prefered it over morphine, oxycodone, fentanyl, codeine etc. Even when I would use one of the substances stated I would always use tramadol also that''s how addictive it can be . ( please don't take other opioids or benzos with tramadol it won't become more magical than it is, only the side effects become more "magical" ).
Avoid using it in combination with MAOis and other SNRI, SRI substances, if you are so desperate to due so please ask about this issue the psychiatrist that prescribed you the MAOI/SNRI/SRI.
6. Withdrawal.
Now this is a very unique part of it, as I said in other sections it is an opioid and SNRI/SRI working substance so the withdrawal will always have dual properties, that's why I for example found it hard to quit because the SNRI/SRI part would result in brain zaps, mood swings and crippling depression/anxiety.
Combine the withdrawal symptoms from above with the typical ones resulted from other opiod withdrawals nausea, diarheea , stomach pain, muscle pain, insomnia and restless leg syndrome and it will result in a typical tramadol withdrawal.
The addiction can be stopped by two ways of quitting : Cold Turkey ( you stop taking it all at once ) or tappering where you titrate the dosage by an amount which you found comfortable.
Real life example: I was addicted to a huge dosage between 1000-1500 mg which is stupidly dangerous and would do big damage to anyone without a tolerance and even with one (don't think that cross- tolerance works as between oxy and morphine for example due to the nortramadol thing).
My tappering plan ( APPROVED BY A PSYCHIATRIST ) was to go 100mg down per week so this kind of tappering in my case took about 10-11 weeks.
Withdrawal can be defeated in Cold Turkey with OTC medications such as Immodiun, Non-Steroidal Anti-Inflamatorry Drugs as ie. Ibuprofen, benzos ( I advise against benzos due to their abuse and addiction potential, but if you find yourself having seizures which is possible in tramadol withdrawal I would recommend taking them but only after consulting your DOCTOR as I am not qualified as one by any degree).
7.Potentiation
Tramadol can be potentiated by :
Nicotine
Caffeine
Grapefruit Juice
Other CY2PD6 enzyme function enhancers beside Grapefruit Juice.
Benzos ( Not a big difference, I would take them only at mega high doses to prevent seizures)
Other Opiates/Opiods (If you are in position to do this, just switch to a stronger opiate you feel comfortable with as the respiraty depression can become more prevalent than with using only tramado, plus it's good to avoid a double opiate additction as I had for some time).
FINAL NOTES:
This megathread was created due to frequently asked questions about tramadol usage, I'm no chemist, doctor or anything related, just had a long love affair with it as a kid and big curiosities about psyhoactive substances, all these elements resulting in my knowledge.
Any modifications, edits, additional knowledge are welcomed.
KK edit:
8. Interaction with other medicines and other forms of interaction.
Copied from https://www.medsafe.govt.nz/profs/Datasheet/t/TramalcapSRtabinjoraldrops.pdf
Use with Benzodiazepines and other Central Nervous System (CNS) Depressants:
Due to additive pharmacologic effect, the concomitant use of benzodiazepines or other CNS-depressants including alcohol, increases the risk of respiratory depression, profound sedation, coma, and death.
Tramadol should be used with caution and in reduced dosages when administered to patients receiving Benzodiazepines and CNS-depressants such as sedative/hypnotics, anxiolytics, tranquillisers, muscle relaxants, general anaesthetics, drugs with antihistaminesedating actions such as antipsychotics, phenothiazines, alcohol, other opioids.
The combination of tramadol with mixed opiate agonists/antagonists (eg. buprenorphine, pentazocine) is not advisable because the analgesic effect of a pure agonist may be theoretically reduced in such circumstances.
Use with other serotonergic agents:
The presence of another drug that increases serotonin by any mechanism should alert the treating physician to the possibility of aninteraction.
Concomitant therapeutic use of tramadol and serotonergic medicines such as selective serotonin re-uptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors
(SNRIs), MAO inhibitors (see 4.3 Contraindications), tricyclic antidepressants and mirtazapine may cause serotonin toxicity. Serotonin syndrome is likely when one of the
following is observed:
- Spontaneous clonus
- Inducible or ocular clonus with agitation or diaphoresis
- Tremor and hyperreflexia
- Hypertonia and body temperature >38?C
Check out this thread for more information on Serotonin Syndrome/Serotonin toxicity
Use with coumarin derivatives -> caution should be exercised during concomitant treatment with tramadol and coumarin derivatives (eg. warfarin) due to reports of increasedinternational normalised ratio (INR) with major bleeding and ecchymoses in some patients.
Drugs which reduce the seizure threshold -> tramadol can induce convulsions and increase the potential for selective serotonin re-uptake inhibitors(SSRIs), serotoninnorepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, antipsychotics and other seizure threshold lowering agents (such as bupropion, mirtazapine, tetrahydrocannabinol) to cause convulsions.
Use with MAO inhibitors -> tramadol should not be used in patients who are taking MAO inhibitors or who have taken them within the last fourteen days, as tramadol inhibits the uptake of noradrenaline and serotonin.
Concomitant administration of tramadol with carbamazepine causes a significant increase in tramadol metabolism, presumably through metabolic induction by carbamazepine.
Tramadol is metabolised to M1 by the CYP2D6 P450 isoenzyme. Drugs that selectively inhibit that isoenzyme (quinidine, phenothiazines, antipsychotic agents) may cause increased concentrations of tramadol and decreased concentrations of M1.
Concomitant administration of tramadol with cimetidine does not result in clinically significant changes in tramadol pharmacokinetics.
Other drugs known to inhibit the CYP3A4 isoenzyme of cytochrome P450, such as ketoconazole and erythromycin, may inhibit the metabolism of tramadol (via Ndemethylation) and probably the metabolism of the active O-demethylated metabolite (M1). The clinical importance of such an interaction has not been studied.
1. What is Tramadol ?
2. Pharmacology of Tramadol.
3. The two main characteristcs and ways of action.
4. Routes of administration and bioavailability.
5. Side effects.
6. Withdrawal.
7. Potentiation.
8. Interaction with other medicines and other forms of interaction.
1. What is Tramadol?
Tramadol is an opioid pain medication used to treat moderate to moderately severe pain.
Tramadol is a fully synthetic opioid unlike opiates like Morphine or Codeine which are found in the poppy plant ( Papaverus Somniferum ) or semi-synthethic opioids like Diamorphine (Heroin) .
Tramadol acts by binding to the μ-opioid receptor of the neuron and is also a serotonin–norepinephrine reuptake inhibitor.
Beside the medical uses, it has recreational uses with similar and also unique characteristics as other opioids.
It's usage is mainly limited by the lowered seizure threshold or defficiency of the CYP2D6 enzyme.
2. Pharmacology of Tramadol
Tramadol itself is not as active as you would believe and the binding affinity of the substance itself is lower than those of its metabolites.
The metabolism of tramadol is liver-mediated demethylation and glucuronidation via CYP2D6 & CYP3A4.
The two active metabolites resulted are desmetramadol (O-desmethyltramadol), which is the major active metabolite, and nortramadol which adds to its uniqueness compared to other opiates/opioids due to the amplified SNRI/SRI activity it has.
Tramadol acts on the opioid receptors through its major active metabolite desmetramadol, which has as much as 700-fold higher affinity for the MOR relative to tramadol. Moreover, tramadol itself has been found to possess no efficacy in activating the MOR in functional activity assays, whereas desmetramadol activates the receptor with high intrinsic activity (Emax equal to that of morphine). As such, desmetramadol is exclusively responsible for the opioid effects of tramadol.
Other properties:
Agonist of the μ-opioid receptor (MOR) and to a far lesser extent of the δ-opioid receptor (DOR) and κ- opioid receptor (KOR)
Serotonin reuptake inhibitor (SRI) and norepinephrine reuptake inhibitor); hence, an SNRI
Serotonin 5-HT2C receptor antagonist
M1 and M3 muscarinic acetylcholine receptor antagonist
α7 nicotinic acetylcholine receptor antagonist
NMDA receptor antagonist (very weak)
TRPA1 inhibitor
The difference in the affinity is not the only one, as the halflife of Tramadol has an aprox value of 6 hours while desmetramadol aprox. 9 hours. ( PLEASE TAKE IN CONSIDERATION THAT THIS VARRIES FROM PERSON TO PERSON, AND FROM INSTANT RELEASE TO EXTENDED RELEASE, AS SOME OF YOU MIGHT TAKE OTHER MEDICATION CONTRAINDICATED IN COMBINATION OF TRAMADOL PLEASE DON'T TAKE THESE HALF LIFE VALUES FOR GRANTED AND CONSULT YOUR DOCTOR ).
3. The two main ways of action.
Normally this subject would be and is partially covered in the Pharmacology section.
But considering that some of you use it in self medicating purposes which are not related to pain and don't know why it has such a "positive" (this is subjective) effect on your mood, it will be covered shortly.
So we all know that the main action of it is in its opioid-like properties, but due to the SNRI/SRI activity it has an antidepressant, anti-anxiety and mood enhancing activity. It tends to be more prominent than in other opiates and feel kinda weird that's why people describe the "high"/effect dirty.
Although it is structurally similar to Effexor and other such compounds I advise against using it as an antidepressant due to the seizure risk, double withdrawal ( beside the SNRI withdrawal you will feel the main part of its withrawal arsenal which is very opiate/semi-syntethic opioid/fully syntethic opioid like ).
So if you hate the brain zaps, mood swings and enhanced angryness avoid!
Another short note which is not fully medically sustained but by my own experience, some psyhiatrist tend to misdiagnose tramadol addicts with bipolar disorder, had couple of friends diagnosed with it when they went to rehab because of tramadol and I assure you they are not bipolar at all, compared to legit bipolar people I also know. My guess would be the cause of this misdiagnose is due to the major mood swings experienced at high dosages or in tramadol withdrawal.
4. Routes of administration, bioavailability and dosage.
Dosage:
BIG WARNING: Tramadol causes seizures, saw a lot of them at low doses, mid doses, high doses so please take caution, if you are predisposed please use another opioid/opiate or seek an alternative treatment approved by your doctor.
The maximum dosage per day approved by doctors would be 400mg per day.
For a begginer I would suggest starting with 100 mg and add 50 mg until you reach the level you want,
it has excelent re-dosing potential unlike other substances ( for example codeine which has a ceiling effect and re-dosing can be tricky without the ceiling also.
BIGGEST LESSON LEARNED HERE ON BLUELIGHT: YOU CAN ALWAYS AND MORE BUT YOU CAN'T DROP THE DOSAGE AFTER YOU TOOK IT. JUST LIKE WITH SALT ADDED TO FOOD.
The effects with the immediate release formula can kick in between 30-45 minutes while the extend ones start to kick in between 1-3 hours. So before re-dosing please consider this.
WARNING: If you have a formulation that includes something else than Tramadol too, like Ultram which has APAP or here in Romania Dorretta, please consider doing a cold water extraction exactly like when you do with codeine and APAP products, the solubility varies but the tramadol already does some damage and combined with APAP it is rough on the liver.
Routes of administration and biovailability:
Oral: 70% to 75%
This is the ROA I recommend the most due to the liver-mediated demethylation talked about in section 2, the simplicity of the administration and the less risks associated with it ( for example: IV has lots of risks like infections, abscesses etc.)
Rectal: 77%
This ROA can be done by plugging or suppositories sold by pharmacies.
For details about plugging substances please search for the plugging thread through the search engine located in the upper left corner of the forum or on google by typing site::bluelight.com after the keyword.
IM: 100%
For this ROA please use ampoules (vials) directly bought from the pharmacy, IM''ing pills is even more dangerous than IV'ing them as the binders and fillers get stuck in the tissue and can cause an abcess.
IV: 100 %
As for the IM ROA vials must be used too and not pills ( it does not matter if they are legit, pressed, instant release or extended release, IV'ing pills is a plain NO NO. )
5. Side Effects.
Its properties of lowering the seizure threshold are the biggest risk factor.
Chemical unbalance in the brain is another one which can result in depression, anxiety, mood swings, angryness etc. ( so don't be fooled by its antidepressant properties as those can take a big U Turn and surprise you)
The most common adverse effects of tramadol include nausea, dizziness, dry mouth, indigestion, abdominal pain, vertigo, vomiting, constipation, drowsiness, and headache. Compared to other opioids, respiratory depression and constipation are considered less of a problem with tramadol.
Another big one would be the addiction potential, some doctors might say that is less addictive than other opioids or not at all, well this is not true at all as I've been addicted to it for 6 years + and even prefered it over morphine, oxycodone, fentanyl, codeine etc. Even when I would use one of the substances stated I would always use tramadol also that''s how addictive it can be . ( please don't take other opioids or benzos with tramadol it won't become more magical than it is, only the side effects become more "magical" ).
Avoid using it in combination with MAOis and other SNRI, SRI substances, if you are so desperate to due so please ask about this issue the psychiatrist that prescribed you the MAOI/SNRI/SRI.
6. Withdrawal.
Now this is a very unique part of it, as I said in other sections it is an opioid and SNRI/SRI working substance so the withdrawal will always have dual properties, that's why I for example found it hard to quit because the SNRI/SRI part would result in brain zaps, mood swings and crippling depression/anxiety.
Combine the withdrawal symptoms from above with the typical ones resulted from other opiod withdrawals nausea, diarheea , stomach pain, muscle pain, insomnia and restless leg syndrome and it will result in a typical tramadol withdrawal.
The addiction can be stopped by two ways of quitting : Cold Turkey ( you stop taking it all at once ) or tappering where you titrate the dosage by an amount which you found comfortable.
Real life example: I was addicted to a huge dosage between 1000-1500 mg which is stupidly dangerous and would do big damage to anyone without a tolerance and even with one (don't think that cross- tolerance works as between oxy and morphine for example due to the nortramadol thing).
My tappering plan ( APPROVED BY A PSYCHIATRIST ) was to go 100mg down per week so this kind of tappering in my case took about 10-11 weeks.
Withdrawal can be defeated in Cold Turkey with OTC medications such as Immodiun, Non-Steroidal Anti-Inflamatorry Drugs as ie. Ibuprofen, benzos ( I advise against benzos due to their abuse and addiction potential, but if you find yourself having seizures which is possible in tramadol withdrawal I would recommend taking them but only after consulting your DOCTOR as I am not qualified as one by any degree).
7.Potentiation
Tramadol can be potentiated by :
Nicotine
Caffeine
Grapefruit Juice
Other CY2PD6 enzyme function enhancers beside Grapefruit Juice.
Benzos ( Not a big difference, I would take them only at mega high doses to prevent seizures)
Other Opiates/Opiods (If you are in position to do this, just switch to a stronger opiate you feel comfortable with as the respiraty depression can become more prevalent than with using only tramado, plus it's good to avoid a double opiate additction as I had for some time).
FINAL NOTES:
This megathread was created due to frequently asked questions about tramadol usage, I'm no chemist, doctor or anything related, just had a long love affair with it as a kid and big curiosities about psyhoactive substances, all these elements resulting in my knowledge.
Any modifications, edits, additional knowledge are welcomed.
KK edit:
8. Interaction with other medicines and other forms of interaction.
Copied from https://www.medsafe.govt.nz/profs/Datasheet/t/TramalcapSRtabinjoraldrops.pdf
Use with Benzodiazepines and other Central Nervous System (CNS) Depressants:
Due to additive pharmacologic effect, the concomitant use of benzodiazepines or other CNS-depressants including alcohol, increases the risk of respiratory depression, profound sedation, coma, and death.
Tramadol should be used with caution and in reduced dosages when administered to patients receiving Benzodiazepines and CNS-depressants such as sedative/hypnotics, anxiolytics, tranquillisers, muscle relaxants, general anaesthetics, drugs with antihistaminesedating actions such as antipsychotics, phenothiazines, alcohol, other opioids.
The combination of tramadol with mixed opiate agonists/antagonists (eg. buprenorphine, pentazocine) is not advisable because the analgesic effect of a pure agonist may be theoretically reduced in such circumstances.
Use with other serotonergic agents:
The presence of another drug that increases serotonin by any mechanism should alert the treating physician to the possibility of aninteraction.
Concomitant therapeutic use of tramadol and serotonergic medicines such as selective serotonin re-uptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors
(SNRIs), MAO inhibitors (see 4.3 Contraindications), tricyclic antidepressants and mirtazapine may cause serotonin toxicity. Serotonin syndrome is likely when one of the
following is observed:
- Spontaneous clonus
- Inducible or ocular clonus with agitation or diaphoresis
- Tremor and hyperreflexia
- Hypertonia and body temperature >38?C
Check out this thread for more information on Serotonin Syndrome/Serotonin toxicity
Use with coumarin derivatives -> caution should be exercised during concomitant treatment with tramadol and coumarin derivatives (eg. warfarin) due to reports of increasedinternational normalised ratio (INR) with major bleeding and ecchymoses in some patients.
Drugs which reduce the seizure threshold -> tramadol can induce convulsions and increase the potential for selective serotonin re-uptake inhibitors(SSRIs), serotoninnorepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, antipsychotics and other seizure threshold lowering agents (such as bupropion, mirtazapine, tetrahydrocannabinol) to cause convulsions.
Use with MAO inhibitors -> tramadol should not be used in patients who are taking MAO inhibitors or who have taken them within the last fourteen days, as tramadol inhibits the uptake of noradrenaline and serotonin.
Concomitant administration of tramadol with carbamazepine causes a significant increase in tramadol metabolism, presumably through metabolic induction by carbamazepine.
Tramadol is metabolised to M1 by the CYP2D6 P450 isoenzyme. Drugs that selectively inhibit that isoenzyme (quinidine, phenothiazines, antipsychotic agents) may cause increased concentrations of tramadol and decreased concentrations of M1.
Concomitant administration of tramadol with cimetidine does not result in clinically significant changes in tramadol pharmacokinetics.
Other drugs known to inhibit the CYP3A4 isoenzyme of cytochrome P450, such as ketoconazole and erythromycin, may inhibit the metabolism of tramadol (via Ndemethylation) and probably the metabolism of the active O-demethylated metabolite (M1). The clinical importance of such an interaction has not been studied.
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