Disease relevance of fluvoxamine

• Toxic epidermal necrolysis after fluvoxamine [1].
• Fluvoxamine in the treatment of binge-eating disorder: a multicenter placebo-controlled, double-blind trial [2].
• Neuroleptic malignant syndrome induced by quetiapine and fluvoxamine [3].
• Treatment of irritable bowel syndrome with fluvoxamine [4].
• The additional effect of two types of treatment for panic attacks--pharmacological (fluvoxamine) and psychological (repeated hyperventilation provocations and respiratory training)--was examined [5].

Psychiatry related information on fluvoxamine

• Fluvoxamine for the treatment of anxiety disorders in children and adolescents [6].
• Efficacy of fluvoxamine in obsessive-compulsive disorder. A double-blind comparison with placebo [7].
• A comparison of fluvoxamine, cognitive therapy, and placebo in the treatment of panic disorder [8].
• Fluvoxamine-induced improvement in symptoms of obsessive-compulsive disorder was not correlated with the severity of baseline depressive symptoms [9].
• Fluvoxamine also produced improvement earlier than cognitive therapy [8].

High impact information on fluvoxamine

• Fluvoxamine and epilepsy [10].
• CONCLUSIONS: Clinical doses of clomipramine and fluvoxamine occupied approximately 80% of 5-HTT, and dose escalation would have minimal effect on 5-HTT blockade [11].
• A double-blind, placebo-controlled study of fluvoxamine in adults with autistic disorder [12].
• Haloperidol addition in fluvoxamine-refractory obsessive-compulsive disorder. A double-blind, placebo-controlled study in patients with and without tics [13].
• Eight of eight patients with comorbid chronic tic disorders, such as Tourette's disorder, responded to double-blind haloperidol addition to ongoing fluvoxamine treatment [13].

Chemical compound and disease context of fluvoxamine

• METHODS: Thirty adults with autistic disorder completed a 12-week double-blind, placebo-controlled trial of the potent and selective serotonin uptake inhibitor fluvoxamine maleate [12].
• In a 4-week double-blind crossover design, the serotonin-uptake blocker fluvoxamine maleate (100 to 200 mg/d) was found to improve episodic memory in only the patients with alcohol amnestic disorder [14].
• CONCLUSIONS: These findings suggest that fluvoxamine or fluoxetine prescriptions adjusted for dose/mass are an acceptable treatment approach for medicating children with autistic disorder or other pervasive developmental disorders [15].
• Limited therapeutic effect of addition of buspirone in fluvoxamine-refractory obsessive-compulsive disorder [16].
• Nine of 17 patients with obsessive-compulsive disorder responded when neuroleptic was added to fluvoxamine with or without lithium [17].

Biological context of fluvoxamine

• OBJECTIVE: The purpose of this study was to investigate the pharmacokinetics of fluvoxamine in the human brain by using fluorine-19 magnetic resonance spectroscopy (19F MRS) and to assess the relationships among fluvoxamine brain levels, fluvoxamine plasma levels, and clinical efficacy [18].
• Cytochrome P450 1A2 is inhibited by fluvoxamine and is implicated in drug interactions with theophylline, clozapine, and others [19].
• In the group treated with fluvoxamine plus pindolol all the genotypes acted like l/l treated with fluvoxamine alone [20].
• RESULTS: Elimination of fluvoxamine in the brain and plasma was optimally described by first-order kinetics; the mean elimination half-lives were 58 hours and 26 hours, respectively [21].
• The biotransformation of all the drugs except paroxetine and fluvoxamine results in the formation of pharmacologically active metabolites [22].

Anatomical context of fluvoxamine

• We measured ALLO content in four cisternal-lumbar fractions of cerebrospinal fluid (CSF) before and 8-10 weeks after treatment with fluoxetine or fluvoxamine in 15 patients with unipolar major depression [23].
• High-speed in vivo electrochemical recordings were used to assess the ability of the SSRI fluvoxamine to modulate the clearance of locally applied serotonin in the CA3 region of hippocampus in drug- or vehicle-treated rats [24].
• CONCLUSIONS: After improvement of OCD with either fluvoxamine or behavioral therapy, hyperactivation of the frontal lobe related to a symptom-provocative state decreases, and posterior brain activity related to action-monitoring function increases [25].
• A comparison of the effects of imipramine and fluvoxamine on the thyroid axis [26].
• In a human liver microsome preparation, fluvoxamine showed a concentration-dependent inhibition of clozapine N-demethylation [27].

Associations of fluvoxamine with other chemical compounds

• This polymorphism has been shown to influence the antidepressant response to fluvoxamine and paroxetine [28].
• CONCLUSIONS: Imipramine with subsequent lithium addition is superior to a similar strategy with fluvoxamine for treatment of severely depressed inpatients [29].
• One hundred and two inpatients with major depression with psychotic features were randomly assigned to treatment with a fixed dose of fluvoxamine and either placebo or pindolol for 6 weeks [20].
• OBJECTIVE: This study used fluorine-19 magnetic resonance spectroscopy (19F MRS) to characterize the elimination of fluvoxamine from the human brain after abrupt drug discontinuation [21].
• Fluoxetine, sertraline, and fluvoxamine are believed to inhibit cytochrome P450 2C because of observed interactions with phenytoin, diazepam, and other drugs metabolized by these enzymes [19].

Gene context of fluvoxamine

• For CYP1A2, CYP2D6, and CYP3A, fluvoxamine therapy changed the phenotyping measures by a median of -44.4%, 123.5%, and -34.4%, respectively [30].
• Fluvoxamine (FX), at a concentration of 20 microM, decreased NDV production by 46% consistent with the capacity of FX to inhibit CYP3A, 2C9, and 2C19 [31].
• Fluvoxamine is a substantial inhibitor of CYP1A2 and CYP2C19, and a moderate inhibitor of CYP3A3/4 [32].
• Thus, assuming comparable molar concentrations at the site of inhibition, fluvoxamine can be expected to have the highest probability of interfering with the metabolism of CYP2C9 substrates [33].
• 3. Norfluoxetine, sertraline and fluvoxamine inhibited CYP1A1 (7-ethoxyresorufin O-deethylase) in microsomes from human placenta (IC50 values 29 microM, 35 microM and 80 microM, respectively) [34].

Analytical, diagnostic and therapeutic context of fluvoxamine

• Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Preliminary findings [14].
• METHOD: During phase I, patients participated in a double-blind study of the effects of imipramine versus fluvoxamine, with final evaluation of response 4 weeks after patients attained the target plasma level [29].
• Brain fluvoxamine concentration in the children was lower, consistent with a lower dose/body mass drug prescription; when brain concentration was adjusted for dose/mass, age effects were no longer significant [15].
• RESULTS: Compared with placebo, fluvoxamine was associated with a significantly greater rate of reduction in the frequency of binges, rate of reduction in CGI severity scores, rate of increase in CGI improvement scores, level of response for patients who completed the 9-week study, and rate of reduction in body mass index [2].
• METHODS: The serum concentration of fluvoxamine was determined by high-performance liquid chromatography for 48 hours after oral administration of a single dose of 50 mg fluvoxamine to 12 smokers (> or = 10 cigarettes per day) and 12 nonsmokers [35].

References