Right off the bat, I would give this a huge, gigantor, massive, fucking NO!!!!!!!!!!!
However...here's a little research. This is NOT CONDONING MIXING THESE TWO DRUGS. I would highly advise you NOT TO MIX THESE. NO NO NO!
Moclobemide has less interactions than the irreversible MAOI's. There is little increase in the effects of alcohol when combined with moclobemide and, in fact, moclobemide causes a reduction in alcohol related impairments. Moclobemide also interacts with pethidine/meperidine,and dextropropoxyphene. Ephedrine in combination with moclobemide increases the risk of cardiovascular adverse effectsMoclobemide also like to interact with warfarin.
Serotonin syndrome has been reported when moclobemide has been taken in combination with other serotonin enhancing drugs; however, due to moclobemide's reversible MAO inhibition, serotonin syndrome is significantly less likely to occur with moclobemide than with the dangerous older irreversible MAOIs. Serotonin syndrome, a potentially fatal syndrome, has been reported when trazadone was abruptly replaced with moclobemide. Taking at the same time or starting moclobemide too soon after discontinuing clomipramine, or other serotonin reuptake inhibitors, such as SSRI's may result in the development of a serotonin syndrome. SNRIs, such as venlafaxine in combination with moclobemide have also been associated with serotonin syndrome. Cimetidine, causes a doubling of the blood plasma levels of moclobemide. Blood plasma levels of trimipramine and maprotiline and possibly other tricyclic antidepressants increase when used in combination with moclobemide and may require dosage adjustments if the combination is used for treatment resistant depression. The elimination of zolmitriptan is reduced by moclobemide and if the combination is used, a dosage reduction of zolmitriptan is recommended. Moclobemide reduces the metabolism of dextromethorphan.
- wikipedia
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The Serotonin Syndrome
Concurrent administration of an MAOI with agents that increase serotonin availability may, in rare instances, result in a specific toxic reaction termed the 'serotonin syndrome.' The serotonin syndrome is characterized by a constellation of at least three of the following symptoms present in the setting of a recent addition or increase in dosage of a serotonergic agent: mental status changes, agitation, myoclonus, hyperreflexia, fever, shivering, diaphoresis, ataxia and diarrhea. Hypertension need not occur. In rare, severe cases, a progression to seizures, hyperthermia (>40.5oC, 104oF), rhabdomyolysis, ventricular arrhythmia, respiratory arrest and death can be seen.
Most case reports of the serotonin syndrome have come from patients who received a simultaneous combination of an MAOI with a specific serotonin reuptake inhibitor (SSRI) or tricyclic antidepressant (TCA). The combination of inhibition of MAO with inhibition of reuptake may result in a flood of 5-HT and NE into the synapse, exceeding its capacity for enzymatic catabolism. The only effective route of catabolism for excess 5-HT is through MAO; catecholamines, on the other hand, can be catabolized also by catechol-o-methyl transferase (COMT). Thus, when combined with inhibition of MAO, the blockade of 5-HT reuptake may have greater potential for CNS toxicity than the blockade of catecholamine reuptake. Accentuation of serotonergic neurotransmission has been implicated in this syndrome, possibly as a result of activation or modification of the 5-HT1A receptor in the brainstem and spinal cord. The importance of 5-HT in the serotonin syndrome is underscored by the fact that in animals this syndrome can be blocked by pretreatment with p-chlorophenylalanine, an inhibitor of 5-HT synthesis, and by methysergide, a 5-HT receptor antagonist.
Toxicity is seen more often when TCAs and SSRIs are added to MAOIs rather than vice versa, although reactions may occur at any time, as well as when switching between MAOIs. To avoid potentiation, most manufacturers recommend a drug-free period when switching a patient either from a TCA or SSRI to an MAOI or vice versa. The duration of this drug free period is determined by considerations of the half-life of the drug and how long it takes the body to regenerate an adequate supply of the enzyme. Thus, 4–5 weeks are recommended when initiating an MAOI in a patient who previously received fluoxetine. The active metabolite of fluoxetine, norfluoxetine, has a half-life of seven days. For other SSRIs or TCAs with shorter half lives, a 1–2 week washout may be adequate.
Concomitant administration of TCAs and MAOIs has been safely used in the past. At present, however, there is insufficient evidence documenting a clear clinical advantage of combining these drugs over using them separately to justify the additional risk. TCA/MAOI or SSRI/MAOI combinations are not recommended, except in severely refractory patients in a monitored inpatient setting. Although the RIMAs may present a lower risk, moclobemide has been implicated in eliciting the serotonin syndrome in two patients receiving concomitant TCAs, as well as in patients receiving SSRIs. Selegiline in rare instances has been reported to cause the serotonin syndrome in combination with SSRIs. In subjects receiving serotonergic agents, caution is advised in dispensing doses of selegiline greater than 10 mg/day, above which it begins to lose its selectivity for MAO-B.
Other agents with serotonin-potentiating properties have been implicated, as well, in the serotonin syndrome, including meperidine, other phenyl-piperidine analgesics, pentazocine, dextromethorphan, buspirone, clomipramine, lithium, tryptophan, fenfluramine, and methylenedioxymethamphetamine (MDMA, 'ecstasy'). Administration of meperidine to a patient receiving MAOIs is absolutely contraindicated. Plant-derived narcotics such as codeine or morphine may elicit fewer adverse reactions than meperidine and may be initiated if agents such as acetaminophen, aspirin or nonsteroidal anti-inflammatory drugs fail. Dosage reduction of these narcotics is advisable, since MAOIs often magnify their effects, including analgesia.
Most cases of the serotonin syndrome are mild and resolve within 6–24 hours. Nevertheless, hospitalization of the patient for observation is prudent. Optimal treatment generally is conservative and entails discontinuation of the suspected medication and providing supportive measures when necessary. Hyperreflexia and myoclonus may respond to benzodiazepines and possibly propranolol. Patients who develop hyperthermia unresponsive to acetaminophen should be treated aggressively with external cooling and paralysis, which may diminish the risk of complications (rhabdomyolysis and disseminated intravascular coagulation) developing later. Other agents, such as methysergide and cyproheptadine, both nonspecific 5-HT1 and 5-HT2 receptor antagonists, are useful adjuncts in treating the serotonin syndrome.
source - http:// www . acnp .org/g4/gn401000046/ ch046.html (without the spaces, of course)
Even though the above reports don't EXACTLY list dexedrine, the drugs it does react with are way too close to it for comfort. I truly think you should avoid taking these two drugs together.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
