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Fluoxetine dosing

Initial 10 mg/day. After 1 week, increase the dose to 20 mg/day. Fluoxetine doses above 60 mg/day have not been systematically evaluated. [Pg.1078]

A 71-year-old woman who had taken fluoxetine (dose unspecified) for a number of weeks noted unilateral galactorrhea and had a raised prolactin of 37 ng/ml (reference range 1.2-24 ng/ml) (419). She was also taking estrogen hormonal replacement therapy, benaza-pril, and occasional alprazolam. Withdrawal of the fluoxetine led to normalization of the prolactin concentration and resolution of the galactorrhea. [Pg.602]

Hcrvas I, Vilaid MT, Romero L, Scorza MC, Mengod G, Artigas F. Desensitization of 5-HT(lA) autoreceptors by a low chronic fluoxetine dose effect of the concurrent administration of WAY-100635. Neuropsychopharmacology 2001 24 11-20. [Pg.391]

For some patients A/ith severe problems discontinuing paroxetine, it may be useful to add an SSRI A/ith a long half-life, especially fluoxetine, prior to taper of paroxetine A/hile maintaining fluoxetine dosing, first slo A/ly taper paroxetine and then taper fluoxetine... [Pg.354]

A case of serotonin syndrome in a woman taking fluoxetine coincided with the start of a new antiretroviral regimen including efavirenz. Symptoms resolved when the fluoxetine dose was halved. It was suggested that efavirenz inhibited the metabolism of fluoxetine. Until further information is available, caution may be warranted if both drugs are given. [Pg.1220]

Two cases of serotonin syndrome were attributed to adding ritonavir to established fluoxetine treatment. In one patient this was managed by halving the fluoxetine dose, and in the other ritonavir was withdrawn. Other cases of the serotonin syndrome have been seen in patients taking ritonavir or indinavir with fluoxetine. One involved the additional use of trazodone , (p.l229), and the other involved large quantities of grapefruit , (p.1217). [Pg.1223]

Differences exist in primary care between the patterns of prescribing fluoxetine, paroxetine or sertraline, which may influence cost outcomes. Sertraline-treated patients are more likely to have their dose increased (Sclar et al, 1995 Donoghue, 1998), and to drop out of treatment prematurely (Donoghue, 1998). The apparent need to titrate doses upwards with sertraline may require more involvement by the clinician and may delay response to treatment, with resultant increases in direct health costs (Sclar et al, 1995). However, these economic findings are retrospective, may suffer from selection bias, and being derived from HMO patients may not be generalizable to other populations confirmation in further studies is required. [Pg.50]

It is perhaps not surprising that, even after taking into account pharmacokinetic differences between these drugs, the therapeutic doses of the SSRIs do not parallel their Ki for inhibition of 5-HT reuptake. For instance, citalopram is about a thousand times more selective than fluoxetine for inhibition of 5-HT uptake, and yet their clinically effective doses are similar. In short, not only is their selectivity for the 5-HT transporter in vitro a poor predictor of their efficacy in vivo but it has to be questioned whether any of these compounds actually work by blocking 5-HT uptake alone. [Pg.441]

However, the specific serotonin uptake inhibitor fluoxetine failed to produce an MBDB-like cue and failed to block the stimulus effects of MBDB when it was given prior to a training dose of MBDB. Table 3 summarizes results of fluoxetine testing in MBDB-trained rats. In other exploratory studies, pretreatment of MDMA-trained rats with either methysergide or ketanserin failed to block completely the MDMA-discriminative stimulus. [Pg.12]

Dose of Fluoxetine N Percentage Selecting Drug Lever... [Pg.13]

We have not explored all of the dose-response relationships. And with respect to the nature of the cue, we have studies underway now with a variety of serotonin agonists and antagonists, for example, fluoxetine. And have looked at MDMA. We eannot bloek the cue with fluoxetine. We are also looking at 8-hydroxy-DPAT, buspirone. PCPA pretreatment is on the way. So there are a variety of manipulations that we have in process. [Pg.21]

Fluoxetine 94 4-6 days with chronic dosing 4-1 6 days (active metabolite) Yes... [Pg.575]

The initial dose of SSRI is similar to that used in depression. Patients should be titrated as tolerated to response. Many patients will require maximum recommended daily doses. Patients with comorbid panic disorder should be started on lower doses (Table 37-4). When discontinuing SSRIs, the dose should be tapered slowly to avoid withdrawal symptoms, with the possible exception of fluoxetine. Relapse rates may be as high as 50%, and patients should be monitored closely for several weeks.58 Side effects of SSRIs in SAD patients are similar to those seen in depression and most commonly include nausea, sexual dysfunction, somnolence, and sweating. [Pg.617]

SSRIs Citalopram 10-30 mg fluoxetine 10-20 mg fluvoxamine 50 mg paroxetine 10-30 sertraline 25-150 mg all agents are given by mouth daily and can be dosed continuously or during the luteal phase only26 Sexual dysfunction (reduced libido, anorgasmia), insomnia sedation, hypersomnia, nausea, diarrhea... [Pg.759]

Risperidone Aripiprazole 2D6 > 3A4 2D6, 3A4 Carbamazepine and phenytoin topiramate hypericum (St. John s Wort). Paroxetine, fluoxetine, sertraline (high dose) grapefruit juice 2D6 or 3A4 substrates acting as competitive inhibitors. [Pg.49]

Quetiapine 3A4 2D6, 2C9 Carbamazepine and phenytoin topiramate prednisolone. Fluvoxamine fluoxetine sertraline (high dose) CYP3A4 substrates grapefruit juice. [Pg.49]

Figure 7.3 Dose-response effects of MDMA on the release of preloaded [3H]5-HT (left panel) and [3H]DA (right panel) from synaptosomes in vitro. [3H]Transmitter release is expressed as percent of tritium retained in tissue. Various concentrations of MDMA were incubated with or without the 5-HT uptake blocker fluoxetine (10 n/W) in [3H]5-HT assays, whereas various concentrations of MDMA were incubated with or without the DA uptake blocker GBR12909 (10 n/W) in [3H]DA assays. Data are mean SD for three separate experiments, each performed in triplicate. See Baumann et al.39 for methods. Figure 7.3 Dose-response effects of MDMA on the release of preloaded [3H]5-HT (left panel) and [3H]DA (right panel) from synaptosomes in vitro. [3H]Transmitter release is expressed as percent of tritium retained in tissue. Various concentrations of MDMA were incubated with or without the 5-HT uptake blocker fluoxetine (10 n/W) in [3H]5-HT assays, whereas various concentrations of MDMA were incubated with or without the DA uptake blocker GBR12909 (10 n/W) in [3H]DA assays. Data are mean SD for three separate experiments, each performed in triplicate. See Baumann et al.39 for methods.

See other pages where Fluoxetine dosing is mentioned: [Pg.1084]    [Pg.516]    [Pg.516]    [Pg.516]    [Pg.517]    [Pg.517]    [Pg.301]    [Pg.72]    [Pg.248]    [Pg.1084]    [Pg.516]    [Pg.516]    [Pg.516]    [Pg.517]    [Pg.517]    [Pg.301]    [Pg.72]    [Pg.248]    [Pg.250]    [Pg.290]    [Pg.76]    [Pg.92]    [Pg.105]    [Pg.63]    [Pg.208]    [Pg.440]    [Pg.444]    [Pg.291]    [Pg.295]    [Pg.575]    [Pg.577]    [Pg.628]    [Pg.49]    [Pg.76]    [Pg.96]    [Pg.121]    [Pg.31]    [Pg.32]    [Pg.77]    [Pg.181]   
See also in sourсe #XX -- [ Pg.131 , Pg.1168 , Pg.1240 , Pg.1250 , Pg.1296 ]




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