Monoamine oxidase inhibitors fluoxetine with

Monoamine Oxidase Inhibitors (MAOIs). Controlled trials comparing the M AOl phenelzine to clomipramine or fluoxetine have produced mixed results. Given the limited data regarding any efficacy of MAOIs in the treatment of OCD coupled with their potentially dangerous interactions, we cannot recommend MAOIs in the treatment of OCD until other approaches have been tried. 

Hypersensitivity to SSRIs in combination with a monoamine oxidase inhibitor (MAOl), or within 14 days of discontinuing an MAOl administration of thioridazine with fluoxetine or within a minimum of 5 weeks after fluoxetine has been discontinued coadministration of fluvoxamine with cisapride, thioridazine or pimozide concomitant use of thioridazine with paroxetine concomitant use of pimozide with sertraline coadministration of sertraline oral concentrate and disulfiram. 

Although behavioral treatments for social phobia have been well studied, there are very limited data on its pharmacological management, b- Blockers (propranolol, atenolol) have been recommended, but available evidence indicates their effect may be no different than that of placebo ( 78). In a controlled study, the monoamine oxidase inhibitor (MAOl) phenelzine has been shown to be more effective than placebo (78, 79). Anecdotal reports have also described efficacy with alprazolam, clonidine, and fluoxetine, but systematic data are lacking (80, 81, 82 and 83). 

A growing number of drugs are used that affect the many neurotransmitters in the brain benzodiazepines and others act on GABAergic transmission antidepressants, such as monoamine oxidase inhibitors and tricyclic antidepressants, are thought to increase the concentration of transmitter amines in the brain and so elevate mood—these will also act at peripheral nerve terminals, so interactions with them are a combination of peripheral and central actions. Levodopa (L-dopa) increases central as well as peripheral dopamine, and the newer class of psychoactive drugs, the selective serotonin reuptake inhibitors (SSRIs) of which the ubiquitous fluoxetine (Prozac) is best known, act in a similar way on serotonergic pathways. 

The depressive phase of manic-depressive disorder often requires concurrent use of an antidepressant drug (see Chapter 30). Tricyclic antidepressant agents have been linked to precipitation of mania, with more rapid cycling of mood swings, although most patients do not show this effect. Selective serotonin reuptake inhibitors are less likely to induce mania but may have limited efficacy. Bupropion has shown some promise but—like tricyclic antidepressants—may induce mania at higher doses. As shown in recent controlled trials, the anticonvulsant lamotrigine is effective for many patients with bipolar depression. For some patients, however, one of the older monoamine oxidase inhibitors may be the antidepressant of choice. Quetiapine and the combination of olanzapine and fluoxetine has been approved for use in bipolar depression. 

Newer antidepressants (eg, fluoxetine, paroxetine, citalopram, venlafaxine) are mostly SSRIs and are generally safer than the tricyclic antidepressants and monoamine oxidase inhibitors, although they can cause seizures. Bupropion (not an SSRI) has caused seizures even in therapeutic doses. Some antidepressants have been associated with QT prolongation and torsade de pointes arrhythmia. SSRIs may interact with each other or especially with monoamine oxidase inhibitors to cause the serotonin syndrome, characterized by agitation, muscle hyperactivity, and hyperthermia (see Chapter 16). 

Stroll et al. (1994), from Harvard s McLean Hospital, compared the blinded charts of 49 consecutive inpatient admissions with antidepressant-induced mania with 49 matched cases of spontaneous mania over a 1-year period, from March 1, 1990, to February 28, 1991. The patients had been exposed to tricyclics (n = 19), fluoxetine (n = 13), monoamine oxidase inhibitors (n = 8), bupropion (n = 6), and mixed antidepressants (n = 3). (It is striking that these doctors were already aware of the risk of Prozac-induced mania approximately 2 years after the January 1988 introduction of Prozac into the market. Meanwhile, too many health care providers remain in denial about this significant risk.)... 

The symptoms described here resemble the 5HT toxicity syndrome (SEDA-25,16) and suggest that pethidine can provoke this reaction when combined with SSRIs, as it can with monoamine oxidase inhibitors. The report is also a useful reminder that the active metabolite of fluoxetine, norfluoxetine, has a half-life of about 1 week and would still have been present at the time of endoscopy, even though fluoxetine had been stopped 14 days before. 

The problem of the long half-life of fluoxetine, leading to interactions with monoamine oxidase inhibitors, even after withdrawal, has been discussed previously (SEDA-13, 12), and caused the manufacturer to circulate a warning to that effect. 

In the 1980s an entirely new class of antidepressant arrived with the SSRIs, firstly fluvoxamine immediately followed by fluoxetine (Prozac). Within 10 years, the SSRI class accounted for half of antidepressant prescriptions in the United Kingdom. Further developments in the evolution of the antidepressants have been novel compounds such as venlafaxine, reboxetine, nefazodone and mirtazapine, and a reversible monoamine oxidase inhibitor, moclobemide. 

All SSRIs have common 5-HT agonistic effects and because of this, SSRIs have common interactions and side effects. SSRIs are potent inhibitors of serotonin reuptake by CNS neurons and may interact with other drugs such as monoamine oxidase inhibitors (MAOIs) or circumstances which cause serotonin release. A minimum 2 weeks wash-out period should be observed between stopping a MAOI and starting an SSRI. Conversely, a MAOI should not be started for at least 1 week after an SSRI has been stopped, 5 weeks after fluoxetine, and 2 weeks for paroxetine and sertraline. Escitalopram and citalopram are hypersensitive to each other. 

The bulk of literature examining antidepressant use in AD is made up of case reports and uncontrolled studies. Most of these report a favorable response to antidepressants, but several placebo-controlled trials have demonstrated mixed results. Of the antidepressants studied, citalopram, sertraline, clomipramine, and moclobe-mide (a monoamine oxidase inhibitor not marketed in the U.S.) were considered efficacious in at least one study but fluoxetine and imipramine were no better than placebo. It should be noted that citalopram and sertraline have both been studied in other placebo-controlled trials in this population with no difference over placebo. ... 

Antidepressant drugs A major class of psychotropic drugs with diverse chemical configurations including the monoamine oxidase inhibitors (MAOIs), the heterocyclic drugs (composed of mono-, di-, tri-, and hetero-cyclics), the serotonin reuptake inhibitors (fluoxetine, paroxetine, sertraline, trazodone, and venlafaxine), and bupropion are more recent innovations. Antidepressants usually must be taken for several weeks to have the desired effect and they often have a low therapeutic index, so they must be closely monitored. 

Traditionally, dysthymic disorder has not been the focus of pharmacotherapeutic interventions, given its chronicity and the presumed non-biological personality variables associated with it. Psychotherapy and psychoanalysis were generally considered the first-choice treatment options, although these treatment modalities have not been well studied in controlled trials. However, as a result of a series of placebo-controlled medical trials, this attitude has been changed. Among the antidepressants found to be superior to placebo are the selective serotonin reuptake inhibitors (SSRIs, with results being evident so far with fluoxetine and sertraline), the tricyclic antidepressants (TCAs) amitriptyline, desipramine, and imipramine (with a 40-60% favorable response), and the reversible and irreversible monoamine oxidase inhibitors (MAOIs) moclobemide and phenelzine, respectively. 

Selective serotonin reuptake inhibitors (SSRIs) are the first-line therapy for PTSD. Efficacy for fluoxetine, paroxetine, and sertraline has been demonstrated in well-designed double-blind placebo-controlled studies to reduce all symptom domains (intrusive recollection, avoidance/numbness, and hyperarousal). - Other treatment options include the tricyclic antidepressants (TCAs) amitriptyline and imipramine and the irreversible monoamine oxidase inhibitor (MAOl) phenelzine, which have been shown to reduce re-experiencing. However, in comparison with SSRIs, TCAs and phenelzine are associated with a higher incidence of side-effects, risk of overdose, and poor compliance. Alprazolam has demonstrated anecdotal efficacy however, regular use of benzodiazepines is not recommended. Benzodiazepines can be used on an as-needed basis for specific symptoms (e.g. sleep disturbances). CBT has shown beneficial effects in relatively well-controlled studies, while the results with exposure therapy are... 

Psychiatric evaluation of a patient after 6 weeks of treatment with a monoamine oxidase inhibitor (MAOI) shows no improvement. The psychiatrist now writes a prescription for fluoxetine which the patient starts two days after her final dose of the MAOI. Since the MAOIs used as antidepressants continue to exert effects for 2 or more weeks after discontinuance, the most likely result of the administration of fluoxetine now will be to cause (A) A rapid amelioration of her depressive symptoms Electrocardiographic abnormalities Extrapyramidal dysfunction The serotonin syndrome Weight gain... 

S X d X o Half-life is 48-72 hrs, thus onedose/day. Takes weeks to achieve equilibrium blood levels. Life-threatening reaction possible with monoamine oxidase inhibitors. Do not use within 2 weeks. Increased suicide rate reported in patients taking fluoxetine. 

Antidepressants can be crudely divided into three classes the monoamine oxidase inhibitors (MAOIs), the tricylic antidepressants (TCAs) and related compounds, and the selective serotonin reuptake inhibitors (SSRIs). HPLC-ED did not feature in a review of methods for five leading SSRIs citalopram, fluoxetine, fluvoxa-mine, paroxetine and sertraline. More recently, Clement et measured venlafaxine (Figure 6.17) and 0-desmethylvenlafaxine by HPLC with coulometric... 

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