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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a double-blind, placebo-controlled study of 72 patients with bulimia nervosa treated successfully with inpatient psychotherapy, the efficacy of fluvoxamine in maintaining improvement was tested. Fluvoxamine and placebo, respectively, were given over a period of about 15 weeks (2-3 weeks inpatient titration phase, 12 weeks outpatient relapse-prevention [maintenance] phase). The variables assessed concerned bulimic behavior and other aspects of eating disorders, global status, depression, anxieties, obsessive-compulsive behavior, and other aspects of psychopathology. Because the dropout rate was relatively high (N = 27 [33%]) and because it was considerably higher in the fluvoxamine group (19 out of 37 subjects), analyses were performed on the intent-to-treat sample (ideally including all 72 subjects). Results of the completer sample analyses (including only those subjects who finished the study) are briefly presented for comparison. In both the intent-to-treat and the completer analyses, the following scales showed fluvoxamine to have a significant effect in reducing the return of bulimic behavior: (1) self-ratings: Eating Disorder Inventory (EDI)-bulimia, urges to binge in previous week and the number of actual binges in the previous week; (2) expert ratings: Psychiatric Status Rating Scales for Bulimia nervosa, Structured Interview for Anorexia and Bulimia nervosa (SIAB)-"total score," SIAB-subscale "fasting," and SIAB-subscale "vomiting." Two further variables (EDI-total score and SIAB-subscale "bulimia") showed the superior relapse prevention effects of fluvoxamine compared with placebo for the completer sample, while they did not reach significance for group-by-time interactions in the intent-to-treat sample. During a final, short (4-week) off-medication phase, no effect of the discontinuation of medication was observed.
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PMID:Fluvoxamine in prevention of relapse in bulimia nervosa: effects on eating-specific psychopathology. 883 13

This 7- to 8-week, multicenter, randomized, double-blind, placebo-controlled study was performed to determine the dose-effect relationship and minimum effective dose for fluvoxamine maleate in a titrated fixed-dose study of major depressive disorder. Gradual titration over 2 weeks to fixed maintenance doses was employed to minimize dropout due to initial side effects. The study enrolled 600 outpatients, male and female, age 18-65, meeting DSM-III-R criteria for major depressive disorder. A 13-item subscore of the standard 21-Item Hamilton Depression Scale was used to minimize the possible contribution of known side effects from serotonin reuptake inhibitors to the overall HAM-D score. Secondary efficacy assessments included the HAM-D retardation factor, HAM-D depressed mood item, CGI-severity of illness item, and SCL depression factor. Fluvoxamine (50-150 mg/day) was therapeutically effective and well tolerated during 6 weeks of therapy. Based on the HAM-D depressed mood item, efficacy was dose dependent. The minimum effective dose was 50 mg/day. Fluvoxamine maleate shows dose-related effectiveness in the acute treatment of major depressive disorder.
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PMID:The oral dose-effect relationship for fluvoxamine: a fixed-dose comparison against placebo in depressed outpatients. 889 32

The recently introduced antidepressants, the selective serotonin reuptake inhibitors (SSRIs) [citalopram, fluoxetine, fluvoxamine, paroxetine and sertraline], are known for their clinical efficacy, good tolerability and relative safety. They differ from each other in chemical structure, metabolism and pharmacokinetic properties. Therapeutic drug monitoring of these compounds is not widely used, as the plasma concentration ranges within which clinical response with minimal adverse effects appears to be optimal are not clearly defined. Almost all recent assays developed for the quantitative determination of SSRIs and their metabolites in blood are based either on the separation of SSRIs by high performance liquid chromatography (HPLC) or gas chromatography (GC). Citalopram and fluoxetine have been introduced as racemic compounds. There are some differences in the pharmacological profile, metabolism and pharmacokinetics between the enantiomers of the parent compounds and their demethylated metabolites. Stereoselective chromatographic methods for their analysis in blood are now available. With regard to the SSRIs presently available, no clearcut plasma concentration-clinical effectiveness relationship in patients with depression has been shown, nor any threshold which defines toxic concentrations. This may be explained by their low toxicity and use at dosages where serious adverse effects do not appear. SSRIs vary widely in their qualitative and quantitative interaction with cytochrome P450 (CYP) isozymes in the liver. CYP2D6 is inhibited by SSRIs, in order of decreasing potency paroxetine, norfluoxetine, fluoxetine, sertraline, citalopram and fluvoxamine. This may have clinical consequences with some but not all SSRIs, when they are taken with tricyclic antidepressants. Except for citalopram and paroxetine, little is known about the enzymes which control the biotransformation of the SSRIs. There have been many reports on marked pharmacokinetic interactions between fluoxetine and tricyclic antidepressants. Fluoxetine has a stronger effect on their hydroxylation than on their demethylation. Interactions observed between fluoxetine and alprazolam, midazolam and carbamazepine seem to occur on the level of CYP3A. Fluvoxamine strongly inhibits the N-demethylation of some tricyclic antidepressants of the tertiary amine type and of clozapine. This may lead to adverse effects but augmentation with fluvoxamine can also improve response in very rapid metabolisers, as it increases the bioavailability of the comedication. Fluvoxamine inhibits with decreasing potency, CYP1A2, CYP2C19, CYP2D6 and CYP1A1, but it is also an inhibitor of CYP3A. Fluoxetine and fluvoxamine have shown to increase methadone plasma concentrations in dependent patients. Some authors warn about a combination of monoamine oxidase (MAO) inhibitors with SSRIs, as this could lead to a serotonergic syndrome. Studies with healthy volunteers suggest, however, that a combination of moclobemide and SSRIs, such as fluvoxamine, should not present serious risks in promoting a serotonin syndrome. A combination of moclobemide and fluvoxamine has successfully been used in refractory depression, but more studies are needed, including plasma-concentration monitoring, before this combined treatment can be recommended. Paroxetine is a substrate of CYP2D6, but other enzyme(s) could also be involved. Its pharmacokinetics are linear in poor metabolisers of sparteine, and non-linear in extensive metabolisers. Due to its potent CYP2D6 inhibiting properties, comedication with this SSRI can lead to an increase of tricyclic antidepressants in plasma, as shown with amitriptyline and trimipramine. CYP3A has been claimed to be involved in the biotransformation of sertraline to norsertraline. Clinical investigations (with desipramine) confirmed in vitro findings that CYP2D6 inhibition by sertraline is only moderate. (ABSTRACT TRUNCATED)
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PMID:Pharmacokinetic-pharmacodynamic relationship of the selective serotonin reuptake inhibitors. 896 57

Fluvoxamine, a serotonin selective reuptake inhibitor, has been available as an antiobsessional agent in the United States since 1995. However, it has been utilized as an effective antidepressant for many years in various European countries. The controlled trials of fluvoxamine in the pharmacotherapy of depression are reviewed. The drug compares well with a variety of other antidepressants. It appears safe and well tolerated in daily doses of 50 to 300 mg. The most common adverse events are gastrointestinal complaints, particularly nausea. Initiating pharmacotherapy at lower doses and increasing over the period of 1 to 2 weeks minimizes this discomfort.
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PMID:Fluvoxamine: a review of the controlled trials in depression. 918 23

The efficacy of fluvoxamine in maintaining improvement of general psychopathology (depression, obsessive-compulsive symptoms, anxieties, interpersonal trust, and body perception) was tested in a double-blind placebo-controlled study of 72 patients with bulimia nervosa who were being treated successfully with inpatient behavioral psychotherapy. Over a period of about 15 weeks (2-3 weeks inpatient titration phase, 12 weeks outpatient relapse-prevention phase), fluvoxamine or placebo were given. The relapse-prevention design was used to avoid potential confounding effects of other concomitant treatments. Assessments concerning general psychopathology were made on the basis of expert ratings (CGI, HDRS) and self ratings (HSCL, Eating Disorders Inventory (EDI)-subscales "ineffectiveness," "perfectionism," "maturity fears," "interpersonal distrust," and "interoceptive awareness"). Fluvoxamine had significant effects in preventing relapse as measured on the basis of the Clinical Global Impression (CGI) scale "severity of illness", and a positive trend for relapse preventing effects was observed for the HSCL "general symptomatic index". Further, a relapse preventing effect was observed for the HSCL subscale "obsessive-compulsive symptoms", but not for the EDI subscale "perfectionism". Various dependent variables measuring depression showed no significant relapse-preventing effects of fluvoxamine, but only positive trends. Fluvoxamine had no relapse preventing effects according to our results for dependent variables assessing anxieties, interpersonal trust, and body perception. During a final short (4-week) off-medication phase, no statistically significant effects of discontinuation of medication, but some trends in the expected directions, were observed.
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PMID:Effects of fluvoxamine on depression, anxiety, and other areas of general psychopathology in bulimia nervosa. 921 69

Knowing the negative effect of depression on lymphocyte number and activity in humans, we investigated the effect of antidepressant therapy on various lymphocyte subgroups. Cancer patients receiving treatment for at least 6 months were asked to take the antidepressant, fluvoxamine, for 28 days. Before and at the end of the study, physical and psychiatric examinations were performed, and the severity of depression was assessed by the Hamilton Scale for Depression (HAM-D). In addition, a sample of blood was withdrawn from the patients to quantify the following parameters: total leukocyte and lymphocyte counts, T4, T8, and Natural Killer (NK) cells, and lymphocyte response to the mitogens phytohemagglutinin (PHA) and pokeweed (PWM). Ten adult patients completed the study. Five of the 10 responded favorably to fluvoxamine treatment. Mean improvement was 50% from the score on day one. There was a significant correlation between the change in the HAM-D score of the "responders" and the change in NK cell counts (p = 0.02). The mean increment in NK cell number was 53%. In 4 of the 5 "non-responders", NK cell number dropped by 65% (mean). No correlation between the change in HAM-D score and any other immunological parameters was detected. Fluvoxamine increases NK cell counts in cancer patients, probably by its antidepressant effect.
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PMID:The antidepressant fluvoxamine increases natural killer cell counts in cancer patients. 943 7

The syndrome of mixed anxiety and depression (MAD) has been described and is familiar to both general psychiatrists and nonpsychiatrists. It was included in the DSM-IV appendix as a syndrome proposed for further study. Fluvoxamine, a selective serotonin reuptake inhibitor (SSRI) approved for the treatment of obsessive-compulsive disorder, was studied for its effectiveness in treating anxiety and depression simultaneously during an 8-week, open-label trial of patients with MAD. Thirteen patients were included in the final, intent-to-treat, analysis. Fluvoxamine showed moderately strong effectiveness in improving anxiety and depression with a greater effect on the depressive component. Nausea, insomnia, delayed ejaculation, and nervousness were the most common side effects reported, with no serious adverse events occurring. Future double-blind placebo-controlled studies will give more conclusive results.
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PMID:An open-label pilot study of fluvoxamine for mixed anxiety-depression. 964 Oct 5

Depression with psychotic features has been shown to respond to selective serotonin reuptake inhibitors (SSRIs). The serotonin transporter (5-HTT) is a prime target for SSRIs. A functional polymorphism within the promoter region of the 5-HTT gene, leading to different transcriptional efficiency, was recently reported. We tested the hypothesis that allelic variation of the 5-HTT promoter could be related to the antidepressant response to fluvoxamine and/or augmentation with pindolol (a serotonin autoreceptors antagonist) which has been suggested as an augmentation therapy for nonresponders. 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. Depression severity was assessed once a week using the Hamilton Depression Rating Scale. Allelic variation in each subject was determined using a PCR-based method. Data were analyzed with a three-way repeated measures analysis of variance. Both homozygotes for the long variant (l/l) of the 5-HTT promoter and heterozygotes (l/s) showed a better response to fluvoxamine than homozygotes for the short variant (s/s). In the group treated with fluvoxamine plus pindolol all the genotypes acted like l/l treated with fluvoxamine alone. Fluvoxamine efficacy in delusional depression seems to be related to allelic variation within the promoter of the 5-HTT gene. Even though other factors may be implicated, genotyping at 5-HTT promoter may represent a promising tool to individualize the pharmacological treatment of depression.
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PMID:Polymorphism within the promoter of the serotonin transporter gene and antidepressant efficacy of fluvoxamine. 1082 34

An 80-year-old woman presented with an embolic stroke secondary to atrial fibrillation and mitral stenosis. She was initially on intravenous heparin and was subsequently maintained on oral warfarin. She was also given digoxin for atrial fibrillation and colchicine for gouty arthritis as well as fluvoxamine in her fourth week in hospital, to treat her depression. However, her INR (international normalised ratio) became markedly elevated within a week. Fluvoxamine and warfarin were stopped immediately. When warfarin was reintroduced 6 days later, her INR value increased again. The coagulation profile only became stable after 2 weeks of cessation of fluvoxamine. Low dose fluvoxamine can interact significantly with warfarin in the elderly and the effect may persist for up to 2 weeks of stopping the antidepressant.
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PMID:Interaction of fluvoxamine with warfarin in an elderly woman. 1056 Feb 76

Fluvoxamine (Depromel), a selective serotonin reuptake inhibitor (SSRI), was launched in May 1999 in Japan with more than 10 years' delay from the marketing in Europe and the United States. Fluvoxamine has been approved in about 80 countries as the indication to "depression" since 1983. As the indication to obsessive-compulsive disorder (OCD), fluvoxamine was first approved in the United States in 1994 and then in about 30 countries. Efficacy of the drug on "depression and depressed state" was found to be comparable to traditional tricyclic antidepressants (TCAs) by the clinical studies in Japan. Indication to OCD was first approved for fluvoxamine in Japan. The antidepressant and the anti-OCD action are considered the result of the serotonin reuptake inhibition at the serotonergic neurons. Fluvoxamine has little affinity for muscarinic, adrenergic alpha 1- and histamine H1-receptors, which TCAs have. Therefore, fluvoxamine possesses less side effects such as dry mouse, disuria, dizziness, orthostatic hypotension and drowsiness, etc.; and it is useful for elderly patients and long-term treatments for depression and OCD.
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PMID:[Pharmacological and clinical aspects of fluvoxamine (Depromel), the first selective serotonin reuptake inhibitor approved for clinical use employed in Japan]. 1087 78


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