Research and Clinical Trials on Fluvoxamine (Luvox, Faverin)

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This list of current clinical research trials on Fluvoxamine (Luvox, Faverin) is followed by a short set of abstracts from the most recent research articles published on the drug.

Fluvoxamine (Luvox, Faverin) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Fluvoxamine (Luvox, Faverin).

 

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Current Research Literature on Fluvoxamine (Luvox, Faverin)

Here are abstracts for some of the latest research articles to have appeared on Fluvoxamine (Luvox, Faverin):

Observation of QTc prolongation in an adolescent girl during fluvoxamine pharmacotherapy.

J Child Adolesc Psychopharmacol. 2009 Oct; 19(5): 591-2
Brzozowska A, Werner B

Brugada syndrome ECG provoked by the selective serotonin reuptake inhibitor fluvoxamine.

Europace. 2009 Oct 29;
Stirnimann G, Petitprez S, Abriel H, Schwick NG
A patient with an SCN5A p.W822X nonsense mutation, localized in the transmembrane region DII-S4 of the Na(v)1.5 sodium channel and leading to a non-expression of the mutant allele, was prescribed the selective serotonin reuptake inhibitor (SSRI) fluvoxamine (Floxyfral((R))), 100 mg per day. His normal baseline ECG changed to a characteristic Brugada-Type-1-ECG pattern. To investigate whether fluvoxamine may reduce the cardiac sodium current, the effect of this drug was studied on the wild-type voltage-gated cardiac sodium channel Na(v)1.5 stably expressed in HEK293 cells. Patch-clamp recording showed a 50% inhibition of the current at a concentration of 57.3 microM. In our patient, no arrhythmia occurred but the proarrhythmic potential of SSRI in patients with SCN5A mutations cannot be excluded. Therefore, we advise 12-lead ECG control after administering SSRI in these patients.

Use of antidepressants for management of hot flashes.

Pharmacotherapy. 2009 Nov; 29(11): 1357-74
Carroll DG, Kelley KW
A growing body of evidence suggests that antidepressant therapies, particularly selective serotonin reuptake inhibitors and venlafaxine, are effective in the management of hot flash symptoms. Several of these agents have the support of the American College of Obstetricians and Gynecologists and the North American Menopause Society. To review the literature on antidepressants for the treatment of hot flashes in women, we searched the PubMed, International Pharmaceutical Abstracts, and MEDLINE databases from inception through May 2009. All publication types that included human participants and that were published in English were eligible for review. These articles, relevant abstracts, and additional references were used to collect pertinent data. Although initial small pilot trials were conducted solely in breast cancer survivors, additional studies have been conducted both in breast cancer survivors and in relatively healthy menopausal women. Data on the benefits with many of these agents are conflicting. Venlafaxine and paroxetine have been studied more extensively than any of the other antidepressants and are more consistent in effectively reducing the frequency and severity of hot flashes, based on these study results. Desvenlafaxine, sertraline, fluoxetine, and citalopram should be considered second- or third-line options if patients fail therapy with or cannot tolerate venlafaxine or paroxetine, based on the current published data. Duloxetine, escitalopram, fluvoxamine, and mirtazapine should be reserved as last-line therapy until more rigorous studies are conducted assessing their use in the management of hot flashes.

[Comparative efficacy and acceptability of new-generation antidepressants. Synthesis meta-analysis "Cipriani"]

Encephale. 2009 Oct; 35(5): 499-504
Gaillard R
Conventional meta-analyses have shown inconsistent results for efficacy of new-generation antidepressants. The authors therefore did a multiple-treatments meta-analysis, which accounts for both direct and indirect comparisons, to assess the effects of 12 of these antidepressants. They systematically reviewed 117 randomised controlled trials (25,928 participants), which compared any of the following antidepressants for the acute treatment of unipolar major depression in adults: bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirtazapine, paroxetine, reboxetine, sertraline, and venlafaxine. The main outcomes were the proportion of patients who responded to or dropped out of the allocated treatment. Analysis was done on an intention-to-treat basis. Mirtazapine, escitalopram, venlafaxine, and sertraline were significantly more efficacious than duloxetine, fluoxetine, fluvoxamine, paroxetine, and reboxetine. Escitalopram and sertraline showed the best profile of acceptability, leading to significantly fewer discontinuations than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine. Clinically important differences exist between commonly prescribed antidepressants for both efficacy and acceptability in favour of escitalopram and sertraline.

In vitro and in vivo evaluation of the inhibition potential of risperidone toward clozapine biotransformation.

Br J Clin Pharmacol. 2009 Oct; 68(4): 574-9
Chetty M, d'Esposito F, Zhang WV, Glen J, Dore G, Stankovic Z, Edwards RJ, Ramzan I, Murray M
AIMS: To study the impact of risperidone (RISP) on clozapine (CLZ) biotransformation in vitro in microsomal fractions containing varying expression of CYP oxidases and in vivo in patients. METHODS: Human liver microsomes (n= 11) were assessed for expression of CYPs 1A2, 2D6 and 3A4, because these enzymes mediate RISP and CLZ oxidation. Inhibition of CLZ oxidation by RISP was assessed. Plasma CLZ elimination was estimated in patients with schizophrenia who received either CLZ alone or the CLZ-RISP combination (n= 10 per group). RESULTS: (i) The CYP3A4 and CYP1A2 inhibitors ketoconazole and fluvoxamine inhibited CLZ oxidation to varying extents in individual microsomal fractions. (ii) RISP did not inhibit CLZ oxidation, regardless of variations in CYP expression. (iii) RISP co-administration did not impair CLZ clearance. CONCLUSIONS: No evidence was found for CYP-mediated inhibitory or pharmacokinetic interactions between RISP and CLZ. Occasional literature reports of such interactions may involve other pathways that participate in CLZ disposition.

 

This page was last reviewed by Dr Greg Mulhauser, Monday, 1 June 2009.

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