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A patient unable to maintain an effective methadone blood level despite a dose of 200 mg per day was administered fluvoxamine with subsequent increase in her methadone blood level and reduction of opiate withdrawal symptoms.
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Melatonin, the predominant product of the pineal gland, is involved in the maintenance of diurnal rhythms. Nocturnal blood concentrations of melatonin have been shown to be enhanced by fluvoxamine, but not by other serotonin reuptake inhibitors. Because fluvoxamine is an inhibitor of several cytochrome P450 (CYP) enzymes, the authors studied the biotransformation of melatonin and the effects of fluvoxamine on the metabolism of melatonin in vitro using human liver microsomes and recombinant human CYP isoenzymes. Melatonin was found to be almost exclusively metabolized by CYP1A2 to 6-hydroxymelatonin and N-acetylserotonin with a minimal contribution of CYP2C19. Both reactions were potently inhibited by fluvoxamine, with a Ki of 0.02 microM for the formation of 6-hydroxymelatonin and 0.05 microM for the formation of N-acetylserotonin. Other than fluvoxamine, fluoxetine, paroxetine, citalopram, imipramine, and desipramine were also tested at 2 and 20 microM. Among the other antidepressants, only paroxetine was able to affect the metabolism of melatonin at supratherapeutic concentrations of 20 microM, which did not reach by far the magnitude of the inhibitory potency of fluvoxamine. The authors concluded that fluvoxamine is a potent inhibitor of melatonin degradation. Because this inhibitory action is also found in vivo, fluvoxamine might be used as an enhancer of melatonin, which might offer new therapeutic possibilities of fluvoxamine.
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We evaluated the efficacy of buspirone in the augmentation of antidepressant response to the serotonin reuptake inhibitors.
It had been suggested that the antidepressant venlafaxine, which inhibits reuptake of both serotonin and (at higher doses) noradrenaline, may result in better outcomes than treatment with selective serotonin reuptake inhibitors (SSRIs).
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Patients taking an SSRI together with ASA or dual antiplatelet therapy following acute myocardial infarction were at increased risk of bleeding.
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Imipramine with subsequent lithium addition is superior to a similar strategy with fluvoxamine for treatment of severely depressed inpatients. Both strategies were well tolerated.
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Our patient's depressive symptoms were reduced and maintained below remission as a result of treatment with 100 mg/day of fluvoxamine. In addition, it is likely that an additional dose of fluvoxamine (50 mg/day) improved his psychotic-like prodromal symptoms directly, independent of its antidepressive effects.
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A total of 2,243 cases of incident diabetes mellitus and 8,963 matched comparison subjects were identified. Compared with no use of antidepressants during the past 2 years, recent long-term use (>24 months) of antidepressants in moderate to high daily doses was associated with an increased risk of diabetes (incidence rate ratio=1.84, 95% CI=1.35-2.52). The magnitude of the risk was similar for long-term use of moderate to high daily doses of tricyclic antidepressants (incidence rate ratio=1.77, 95% CI=1.21-2.59) and selective serotonin reuptake inhibitors (incidence rate ratio=2.06, 95% CI=1.20-3.52). Treatment for shorter periods or with lower daily doses was not associated with an increased risk.
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Body dysmorphic disorder (BDD), a preoccupation with an imagined or slight defect in appearance, has been described for more than a century and reported around the world. However, this distressing and impairing disorder often goes undiagnosed, even though available data suggest that it is relatively common. Virtually any body part can be the focus of concern, with preoccupations most often involving the hair, nose, or skin. Most patients engage in excessive and repetitive behaviors such as mirror checking, skin picking, and reassurance seeking. Insight is generally poor, and many patients are frankly delusional. Most patients experience significant impairment in functioning, and suicide attempts are relatively common. Although the majority of patients with BDD seek often costly nonpsychiatric treatment-most often, surgical or dermatologic-such treatment usually appears to be unsuccessful. In contrast, preliminary data from open studies suggest that the serotonin reuptake inhibitors are often, and perhaps preferentially, effective for BDD. Augmentation, combination, and switching strategies may be useful in treatment-resistant cases. Preliminary data suggest that cognitive-behavioral strategies using exposure and response prevention may also be effective. Investigation of all aspects of this understudied disorder, including controlled treatment trials, is greatly needed.
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Our data support the assumption that elevation in cholesterol level is not a specific feature of panic disorder (as most assumed), but more generally associated with anxiety disorders. Increased cholesterol levels in patients with anxiety disorders and OCD may be of clinical relevance.
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The results suggest that BT should be combined with fluvoxamine when obsessions dominate the clinical picture and when a secondary depression is present.
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In vivo chronoamperometric recordings were used to determine if the majority of serotonin transporters (SERTs) in the dorsal raphe nucleus (DRN) are functionally active. This was achieved by comparing the clearance of exogenously applied serotonin (5-HT) from the extracellular fluid (ECF) of the DRN to that in the CA3 region of the hippocampus, an area with lower SERT density. Serotonin was pressure ejected into these regions in anesthetized rats and reproducible electrochemical signals measured by carbon fiber microelectrodes were recorded. Consistent with SERT density as measured by [3H]cyanoimipramine binding in these brain regions (DRN>CA3), clearance of 5-HT was significantly faster in DRN compared to that in the CA3 region. The selective serotonin reuptake inhibitor, fluvoxamine, prolonged 5-HT clearance in both CA3 and DRN. It is known that the norepinephrine transporter (NET) contributes to clearance of 5-HT in the dentate gyrus (DG) but not in CA3. Given that the DRN receives noradrenergic innervation, it was also determined if the NET contributes to 5-HT clearance in the DRN. Destruction of the NET with the neurotoxin 6-hydroxydopamine failed to alter 5-HT clearance parameters in the DRN. These data support the hypothesis that serotonin transporters are functionally active in the DRN, that serotonin clearance is mediated primarily by the SERT in the DRN and that the faster clearance of 5-HT from this region is related to its greater density of functional SERTs.