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

Although it is well established that the diagnosis and treatment of depression in the elderly are major health care problems, the relative efficacy of antidepressant treatment in the elderly compared with younger adults has not been definitively established. In this study, we analyzed antidepressant response in 528 nondemented consecutive inpatients affected by a major depressive episode. The sample was divided based on a cut-off of 60 years (< or = 60 n = 354; mean age 46.6 +/- 10.4 years; > 60 n = 174; mean age 66.1 +/- 4.2 years); all the patients were treated with fluvoxamine for at least 6 weeks and they were assessed weekly by using the Hamilton Rating Scale for Depression. Fluvoxamine proved to be effective in our elderly sample, even if antidepressant response was lower in the elderly compared with that of younger subjects (chi2 = 6.27, P = 0.01). Moreover, when compared with younger subjects, the older ones showed significantly slower reduction of depressive symptoms (P = 0.0006). This difference between the 2 age groups was evident since the 2nd week of treatment, and it appeared to be independent of other clinical variables.
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PMID:Comparison of response to fluvoxamine in nondemented elderly compared to younger patients affected by major depression. 1462 82

In the present study, we investigated the effects of fluvoxamine, a selective serotonin reuptake inhibitor, on brain tetrahydrobiopterin (BH4) levels. We directly measured levels of BH4 by Tani and Ohno's direct method as well as the serotonin (5-HT) turnover ratio, i.e. 5-hydroxyindoleacetic acid (5-HIAA)/5-HT, after sub-acute s.c. injection of fluvoxamine in the hippocampus of mice. Our animal model incorporated two risk factors of depression, social isolation and acute environmental change. Male ddY mice (6W) were housed in isolation (1 per cage; 35 days), injected with fluvoxamine (20 or 40 mg/kg; days 29-35), and exposed to novelty stress (20 min; day 35). In the stress session, behavioral parameters, i.e. total distance and rearing behavior, were measured. Isolation housing increased both behaviors. Fluvoxamine attenuated rearing behavior, but did not influence total distance. Isolation housing increased BH4 levels. Novelty stress increased BH4 levels in group housing, although it did not change them in isolation housing. Fluvoxamine suppressed BH4 levels. In isolation housing, fluvoxamine increased 5-HT turnover ratios, while it decreased them in group housing. In conclusion, fluvoxamine, housing condition, and novelty stress regulated BH4 levels. Fluvoxamine may have changed behavior and 5-HT turnover by suppressing BH4 levels as well as by inhibiting 5-HT reuptake.
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PMID:Fluvoxamine, a selective serotonin reuptake inhibitor, suppresses tetrahydrobiopterin in the mouse hippocampus. 1497 89

BACKGROUND: There is emerging evidence that postpartum women are at risk for the development or worsening of obsessive-compulsive disorder. The purpose of this study was to provide data regarding the demographics, phenomenology, associated psychiatric comorbidity, family history, and response to open treatment with fluvoxamine in subjects with postpartum-onset obsessive-compulsive disorder. METHOD: Seven consecutive subjects were recruited from an outpatient obstetrical practice and by advertisement. Subjects completed the Structured Clinical Interview for DSM-IV, the Yale-Brown Obsessive Compulsive Scale, and a semistructured interview for family history, demographic data, and clinical features. Three of the 7 subjects participated in a 12-week, open-label trial of fluvoxamine treatment of postpartum-onset DSM-IV obsessive-compulsive disorder. RESULTS: The women described a mean age at onset of 28 years, and 4 subjects had a chronic course. Six subjects reported onset after the birth of their first child, and the mean time to onset was 3.7 weeks postpartum. All subjects experienced both obsessions and compulsions and reported aggressive obsessions that involved their children. None of the subjects acted on their obsessions to harm the children, but 5 reported dysfunctional mother-child behavior. All 7 subjects met criteria for at least 1 comorbid psychiatric disorder, with a mood disorder the most common. Family histories were notable for high rates of mood disorders and psychoactive substance use disorders in first-degree relatives. Two of the 3 subjects who entered the open-label trial of fluvoxamine experienced a positive response, defined as a 30% or greater decrease in the total score of the Yale-Brown Obsessive Compulsive Scale. CONCLUSION: Obsessive-compulsive disorder may present in the postpartum period and become chronic. Symptoms of the disorder may adversely affect the mother-child relationship, and it is important to assess for obsessions and compulsions in postpartum women who present with anxiety and/or depression. Fluvoxamine may be effective in reducing the symptoms of postpartum-onset obsessive-compulsive disorder. Controlled studies are needed to confirm these findings.
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PMID:A Case Series of Women With Postpartum-Onset Obsessive-Compulsive Disorder. 1501 82

Case 1: female, age 76. Fluvoxamine (50 mg/day) initiated a reduction of pain on the 14th day of administration and completely ameliorated pain as well as depression. Case 2: female, age 76. Fluvoxamine (25 mg/day) was administered with tandospirone (15 mg/day) which augments the effect of an SSRI. This combination regimen induced a reduction of PHN-pain on the 10th day and as the analgesic effect attained nearly 50%, there occurred a reflaming of pain on the 35th day. Increasing fluvoxamine to 50 mg/day reameliorated pain on the 49th day, and a further increase to 75 mg/day finally eliminated pain and depression at the end of the 3rd month. The long latency of fluvoxamine action, its shortening by tandospirone and the parallel changes of PHN and depression are all indicative of that the same mechanism, namely renormalization of the dysfunctioned central serotonergic transmission would be underlying both the anti-PHN and antidepressant actions. It would be concluded that fluvoxamine alleviates PHN by restoration of the descending serotonergic inhibition of primary afferent activity that carries pain impulses.
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PMID:[Postherpetic neuralgia alleviated by an SSRI fluvoxamine: two cases of PHN accompanied with depression were treated with fluvoxamine]. 1516 15

Selective serotonin [5-hydroxytryptamine (5-HT)] reuptake inhibitors (SSRIs) and the 5-HT noradrenaline reuptake inhibitor, venlafaxine, are mainstays in treatment for depression. The highly specific actions of SSRIs of enhancing serotonergic neurotransmission appears to explain their benefit, while lack of direct actions on other neurotransmitter systems is responsible for their superior safety profile compared with tricyclic antidepressants. Although SSRIs (and venlafaxine) have similar adverse effects, certain differences are emerging. Fluvoxamine may have fewer effects on sexual dysfunction and sleep pattern. SSRIs have a cardiovascular safety profile superior to that of tricyclic antidepressants for patients with cardiovascular disease; fluvoxamine is safe in patients with cardiovascular disease and in the elderly. A discontinuation syndrome may develop upon abrupt SSRI cessation. SSRIs are more tolerable than tricyclic antidepressants in overdose, and there is no conclusive evidence to suggest that they are associated with an increased risk of suicide. Although the literature suggests that there are no clinically significant differences in efficacy amongst SSRIs, treatment decisions need to be based on considerations such as patient acceptability, response history and toxicity.
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PMID:Tolerability and safety of fluvoxamine and other antidepressants. 1662 Mar 64

There is an association between depression and chronic pain, and some antidepressants exert antinociceptive effects in humans and laboratory animals. We examined the effects of fluvoxamine, a selective serotonin reuptake inhibitor, on mechanical allodynia and its mechanism of action in the mouse chronic pain model, which was prepared by partially ligating the sciatic nerve. The antiallodynic effect was measured using the von Frey test. Fluvoxamine produced antiallodynic effects following both systemic and intrathecal administration. In 5-hydroxytryptamine (5-HT)-depleted mice, prepared by intracerebroventricular injection of 5,7-dihyroxytryptamine, the fluvoxamine-induced antiallodynic effect was significantly attenuated. The antiallodynic effects of systemic fluvoxamine were also reduced by both systemic and intrathecal administration of ketanserin, a 5-HT2A/2C receptor antagonist. In addition, fluvoxamine also induced antinociceptive effect in the acute paw pressure test, and this effect was antagonized by the 5-HT3 receptor antagonist granisetron. These results indicate that fluvoxamine exerts its antiallodynic effects on neuropathic pain via descending 5-HT fibers and spinal 5-HT2A or 5-HT2C receptors, and the antinociception on acute mechanical pain via 5-HT3 receptors.
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PMID:Fluvoxamine, a selective serotonin reuptake inhibitor, exerts its antiallodynic effects on neuropathic pain in mice via 5-HT2A/2C receptors. 1684 19

A prospective, open-label clinical trial was conducted for two aims: first, to evaluate the role of fluvoxamine, one of selective serotonin reuptake inhibitors, in the treatment of dizziness for the first time and to investigate its effective mechanisms. Second, to test the hypothesis that dizziness in patients without abnormal neuro-otologic findings would be induced by psychiatric disorders rather than by unnoticed neuro-otologic diseases. Nineteen patients with neuro-otologic diseases (Group I) and 22 patients in whom standard vestibular tests revealed no abnormal findings (Group II) were treated by fluvoxamine (200 mg/day) for eight weeks. Subjective handicaps due to dizziness using a questionnaire, anxiety and depressive symptoms measured with the Hospital Anxiety and Depression Scale (HADS), and stress hormones (vasopressin and cortisol) were examined before and 8 weeks after treatment. Overall, fluvoxamine decreased subjective handicaps of both Groups I and II. Fluvoxamine decreased HADS of only patients whose subjective handicaps were reduced (=responders) in both groups, suggesting that fluvoxamine was effective for dizziness via psychiatric action rather than a recovery of vestibular function through serotonergic activation. In non-responders of Group II, pre-treatment HADS was higher than in Group I non-responders and it was not decreased by the treatment, suggesting that dizziness of Group II non-responders was due to severe psychiatric disorders rather than unnoticed neuro-otologic diseases. Anxiety and depression components of HADS showed a good correlation at both pre- and post-treatment periods. No post-therapeutic decrease was observed in either vasopressin or cortisol even in responders, suggesting that dizziness was not the sole cause of stress in chronic dizziness patients. In conclusion, patients with or without physical neuro-otologic deficits who report chronic dizziness accompanied by anxiety and depression (as measured by HADS) showed improvements across a full range of subjective handicaps and psychological distress, while patients with physical neuro-otologic defects and minimal anxiety or depression did not benefit. The main causes of dizziness in patients without physical neuro-otologic findings were psychiatric disorders.
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PMID:Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients with or without neuro-otologic diseases. 1821 99

Although catatonia has been identified in individuals with autism spectrum disorders, little is known about this relationship. Studies on previous case reports dealing with the relationship between catatonia and autism spectrum disorders are reviewed, then the case of a 28-yr.-old Japanese woman with high-functioning autism spectrum disorder who exhibited mood disorder and catatonia is described. Her mood disorder was apparently induced by a crisis of her "inner world," constituted as a way of coping with a sense of alienation, related to her impaired development in reciprocal social interaction. Environmental change, a precipitating factor, induced alternation between catatonia and depression. Fluvoxamine ameliorated both features. The catatonia identified in this patient is considered to be symptom derived from depression. Given the limitation of this single case, such a conclusion is necessarily tentative. Closer investigation into cases in which patients with high-functioning autism spectrum disorders describe their own psychological experiences should be pursued.
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PMID:Catatonia in high-functioning autism spectrum disorders: case report and review of literature. 1823 55

Selective serotonin reuptake inhibitors (SSRIs) are first line drugs for treating not only depressive disorder but also anxiety disorder. Fluvoxamine, a SSRI, is mainly metabolized by cytochrome P450 (CYP) 2D6 and 1A2. However, paroxetine, an another SSRI is potent inhibitor for CYP 2D6. We report a case with depression whose plasma fluvoxamine level rapidly increased after the addition of paroxetine while switching from fluvoxamine to paroxetine. The case indicates that emerging adverse effects via the pharmacokinetic interaction of these drugs when switching patients from fluvoxamine to paroxetine can occur.
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PMID:A case with occurring adverse effects when cross-over titration from fluvoxamine to paroxetine associated with increasing the plasma fluvoxamine level in major depressive disorder. 1860 33

Fluvoxamine is a selective serotonin reuptake inhibitor widely used in the treatment of depression and other psychiatric diseases. The aim of this study was to assess the clinical impact of cigarette smoking on plasma fluvoxamine concentration in Japanese patients, and evaluate whether the cytochrome P450 (CYP) 1A2 and CYP2D6 genotypes have effects on that concentration. Thirty-two Japanese patients receiving fluvoxamine were enrolled. They were maintained on the same daily dose of fluvoxamine (mean + or - S.D., 109.4 + or - 66.2 mg/d) for at least 4 weeks to obtain the steady-state plasma concentration. The steady-state plasma concentration-to-dose (C/D) ratio of fluvoxamine in patients who smoked (n = 6, 11.8 + or - 6.5 ng/ml/dose) was significantly lower than that in non-smoker patients (n = 26, 22.8 + or - 11.2 ng/ml/dose). There was no significant difference for the C/D ratio of fluvoxamine in patients with CYP1A2 -3860G/G, -3860G/A, and -3860A/A between non-smokers and smokers. Among non-smoker patients, the C/D ratios of fluvoxamine in those with one and two mutated alleles of CYP2D6 were 1.6- and 1.4-fold higher, respectively, than those with no mutated alleles, though the differences among those three genotype groups were not significant. Furthermore, stepwise multiple regression analysis revealed that cigarette smoking and daily dose had significant positive correlations with the plasma concentration of fluvoxamine. Our findings suggest that cigarette smoking has a significant impact on the steady-state plasma concentration of fluvoxamine in Japanese patients.
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PMID:Effects of cigarette smoking and cytochrome P450 2D6 genotype on fluvoxamine concentration in plasma of Japanese patients. 2011 54


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