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Venlafaxine SSRIs

Panic disorder SSRIs Venlafaxine XR Alprazolam Clomipramine Clonazepam Imipramine Phenelzine... [Pg.755]

Many commonly used medications also contain substances that are eliminated by the MAOIs and must not be taken by these patients. The list of medications to be avoided inclndes the narcotic pain reliever meperidine (Demerol), and many over-the-connter cold remedies containing dextromethorphan or pseudoephedrine. Finally, patients taking MAOIs must also avoid medications that elevate serotonin levels. This inclndes certain appetite snppressants and antidepressants including the SSRIs, venlafaxine, duloxetine, mirtazapine, nefazodone, and trazodone. Medications that interact with the MAOIs cannot be taken until at least 2 weeks after the MAOI has been stopped. [Pg.51]

Treatment of choice - mood stabilizer with or without an antidepressant (e.g. lithium, valproate, carbamazepine, lamotrigine). Antidepressants include an SSRI, venlafaxine, mirtazepine as possibilities but few controlled trials to substantiate choice. [Pg.210]

Unlike SSRIs, venlafaxine shows a positive dose-response relation patients with mild depression may respond to lower doses, whereas patients with more severe or recurrent depression may respond better to higher doses. [Pg.31]

The side-effect profile of venlafaxine is similar to that of SSRIs and includes gastrointestinal symptoms, sexual dysfunction, and transient discontinuation symptoms. Like the SSRIs, venlafaxine does not affect cardiac conduction or lower the seizure threshold. In most patients, venlafaxine is not associated with sedation or weight gain. Side effects that differ from those of SSRIs are hypothesized to be related to the increased noradrenergic activity of this drug at higher doses these side effects are dose-dependent anxiety (in some patients) and dose-dependent hypertension. [Pg.31]

In contrast to the SSRIs, venlafaxine has an ascending dose-response curve consistent with its sequential, concentration (and hence dose) dependent effects on serotonin and NE uptake pumps (Table 7-9). At 225 mg per day, the magnitude of the antidepressant effect is 50% higher than that seen with the SSRIs. Also consistent with its dual mechanism of action at higher concentrations, venlafaxine at a dose of 225 mg per day produced an antidepressant response in hospitalized patients with melancholia superior to both placebo and fluoxetine (114, US, 116, H7, H8, H9, 120, 121, 122, 123, 124,125, 126,127, 128,129, 130,131, 132,... [Pg.121]

In psychomotorically retarded patients, many clinicians prefer to use a less sedating drug (e.g., an SSRI, venlafaxine, bupropion, or desipramine), but definitive evidence is lacking. [Pg.130]

Optimal dosing with venlafaxine differs from that of both TCAs and SSRIs. Venlafaxine is like the SSRIs and different from the TCAs in that a therapeutic dose (i.e., 75 mg per day) can be started from the beginning. Unlike the SSRIs, however, dose escalation with venlafaxine does increase the magnitude of the antidepressant effect, which supports increasing the dose in the event of an inadequate response to the initial trial ( Table 7-9). Venlafaxine in its sustained release formulation can be given once a day, just like the SSRIs and TCAs. [Pg.131]

Given their design differences, no direct comparison can be made between the relative relapse efficacy of SSRIs, venlafaxine, and nefazodone. The bottom line, however, is that both designs demonstrated that maintenance therapy for up to 1 year is important in reducing the risk of a depressive relapse after an initial response. [Pg.135]

Two major problems complicating the question of treatment-resistant depression are inappropriate diagnosis and inadequate treatment (355). Studies have found only a small proportion (< 15%) of newly diagnosed depressed patients receive adequate antidepressant treatment as defined by dose and duration criteria (356, 357). Hence, a substantial number of treatment-resistant cases are actually the result of inadequate therapy (i.e., relative resistance). For example, in the MacEwan and Remick (358) study, 70% of those defined as treatment-unresponsive achieved complete remission with an adequate trial of an HCA, MAOl, or ECT. Patients who do not receive sufficient benefit from a trial of one antidepressant now have the option of newer agents whose activity does not necessarily overlap with earlier generation compounds (e.g., SSRIs, venlafaxine, nefazodone). [Pg.141]

The combination of an MAOl plus an SSRI, venlafaxine, or nefazodone should not be attempted because of the risk of a serotonin syndrome. [Pg.143]

Although more stimulating antidepressants (e.g., bupropion, SSRIs, venlafaxine, or certain MAOIs) do not potentiate alcohol, they can produce insomnia. To minimize this problem, the dose may be given earlier in the day. TCAs may cause episodes of excitement (rare), confusion, or mania, usually in patients with an underlying psychotic illness, suggesting that a preexisting disorder must be present for these drugs to exert any psychotomimetic effects. [Pg.147]

In addition to buspirone and the non-barbituate, non-BZP hypnotics, selective serotonin reuptake inhibitors (SSRIs), venlafaxine, and other new antidepressants all represent attempts to achieve anxiolytic and hypnotic effects seen with the BZDs, while avoiding their unwanted properties. [Pg.229]

The adverse effects of SSRIs, venlafaxine, and nefazodone in children and adolescents are comparable with those in adults (see Chapter 7) and have been documented in both clinical trials and practice ( 35, 36, 119, 120 and 121 123). As in adults, isolated case reports have described behavioral activation in children and adolescents given SSRIs (133, 134). The significance of such reports in terms of a causal link to the drug is difficult because of their rare and anecdotal nature and because the patients are at increased risk for such behavioral disturbances relative to the general population as a result of their underlying psychiatric disorder. [Pg.280]

The SSRIs, venlafaxine, or nefazodone may be reasonable alternatives to earlier generation antidepressants because of their less problematic side effect profiles (486). The propensity to increase activity, the lack of sedation, gastrointestinal symptoms, and alterations in blood pressure are potential complications, however. Given AIDS-induced altered metabolism, for many of these agents, TDM may be helpful in establishing an effective, nontoxic dose. [Pg.301]

The SNRIs have relatively fewer CYP450 interactions than the SSRIs. Venlafaxine is a substrate but not an inhibitor of CYP2D6 or other isoenzymes, whereas desvenlafaxine is a minor substrate for CYP3A4. Duloxetine is a moderate inhibitor of CYP2D6 and so may elevate TCA and other CYP2D6 substrate levels. Like all serotonergic antidepressants, SNRIs are contraindicated in combination with MAOIs. [Pg.669]

This report confirms that, like SSRIs, venlafaxine can cause galactorrhea and also suggests, as has been observed with other drugs, that the symptom of lactation is not necessarily closely linked to plasma prolactin concentrations. This suggests that other mechanisms could be involved in the production of drug-induced galactorrhea. [Pg.647]

In a prospective cohort study of over 450 patients who had attempted suicide by antidepressant ingestion the risk of seizures after venlafaxine overdose (14%) was significantly greater than that of SSRIs (1.3%) and similar to that seen with dosulepin (11%) (12). Rates of 5HT toxicity did not differ significantly between venlafaxine and SSRIs (29% versus 19%) but were greater than with tricyclic antidepressants (1.2%). Unlike SSRIs, venlafaxine was associated with significant prolongation of the QT interval tricyclic antidepressants had a similar effect. [Pg.4]

The analgesic drug tramadol can cause 5HT toxicity in association with SSRIs. Venlafaxine is also a potent reuptake inhibitor, and perhaps not surprisingly has been reported to cause features of the 5HT syndrome in a patient taking tramadol (49). [Pg.120]

NSAIDs SSRIs, VENLAFAXINE Slight t risk of bleeding Unknown Warn patients to watch for early signs of bleeding... [Pg.464]

Masand PS, Gupta S. Long-term side effects of newer-generafion anfidepressanfs SSRIs, venlafaxine, nefazodone, bupropion, and mirtazapine. Ann Clin Psychiafry 2002 14(3) 175-82. [Pg.42]

SSRIs, venlafaxine, bupropion, phentermine, or stimulants may mitigate mirtazapine-induced weight gain... [Pg.304]

Combining agents (e.g. tricyclic and SSRI venlafaxine and mirtazepine). [Pg.81]

The manufacturers of duloxetine contraindicate the concurrent use of MAOIs because of the theoretical risk of the serotonin syndrome. Similarly they recommend caution with other serotonergic drugs, including the SSRIs, venlafaxine, and tryptophan. Fluvoxamine should not be used with duloxetine, because it markedly increases duloxetine levels. Low-dose paroxetine caused a modest increase in the duloxetine ATJC, and fluoxetine is predicted to interact similarly. [Pg.1212]


See other pages where Venlafaxine SSRIs is mentioned: [Pg.617]    [Pg.310]    [Pg.323]    [Pg.12]    [Pg.124]    [Pg.132]    [Pg.147]    [Pg.148]    [Pg.664]    [Pg.310]    [Pg.120]    [Pg.354]    [Pg.245]    [Pg.3617]    [Pg.93]    [Pg.310]    [Pg.322]    [Pg.14]   
See also in sourсe #XX -- [ Pg.748 ]




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Venlafaxine

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