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One hundred patients with GAD, diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision criteria, were enrolled and their main demographic and clinical features collected. Patients were then treated with selective serotonin reuptake inhibitors or venlafaxine for 8 weeks in open-label conditions. Treatment response and other clinical variables were analyzed after dividing the sample into two groups according to DUI (DUI 12 months).
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The effects of long-term administrations of a low (10 mg/kg/day) and a high (40 mg/kg/day) dose of the dual 5-HT and NE reuptake inhibitor venlafaxine (delivered s.c. by osmotic minipumps for 21 days) were assessed on the electrically-evoked release of tritium from hippocampal slices preloaded with either [(3)H]5-HT or [(3)H]NE, 48 h after the removal of the minipump. The high, but not the low, dose regimen of venlafaxine enhanced the electrically-evoked release of [(3)H]5-HT while treatment with the high dose of venlafaxine failed to alter the electrically-evoked release of [(3)H]NE. The inhibitory effect of the 5-HT(1B) agonist CP 93,129 on the electrically evoked release of [(3)H]5-HT was unaltered by the low dose regimen of venlafaxine while it was attenuated in rats treated with the high dose of venlafaxine, indicative of a functional desensitization of the terminal 5-HT(1B) autoreceptor. Unexpectedly, neither regimen of venlafaxine altered the inhibitory effect of UK 14,304 on the electrically evoked release of both [(3)H]5-HT and [(3)H]NE, indicating that neither the alpha(2)-adrenergic auto- nor heteroreceptors were desensitized. Finally, the functions of the 5-HT and NE reuptake process were assessed. None of the treatment regimens altered the basal uptake of [(3)H]5-HT from hippocampal or mesencephalic slices nor that of [(3)H]NE from hippocampal slices. Finally, the enhancing effect of 1 microM of paroxetine in the perfusion medium on the electrical release of [(3)H]5-HT was unaltered in hippocampal slices prepared from rats that had been treated for 21 days with 40 mg/kg/day of venlafaxine. Taken together, these results indicate that, in terms of alteration of the sensitivity of the terminal 5-HT(1B) autoreceptor, alpha(2)-adrenergic auto-and heteroreceptors, the effects of long-term administration of venlafaxine are no different than those observed with classical SSRI's.
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Data were obtained from 9 individual health plans with more than 1.1 million covered lives affiliated with a national managed-care organisation.
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Choosing an antidepressant for a medically ill patient is a common clinical problem. There is an increased prevalence of depression among patients with many medical illnesses. The clinician must be familiar with the recent additions to the antidepressant armamentarium, including the synaptic pharmacology and pharmacokinetics of the available agents. The factors usually used to guide antidepressant selection must be augmented by a careful evaluation of the patient's medical illness and therapeutic regimen. Special attention must be paid to the potential for drug-illness and drug-drug interactions. The author has used the example of four illnesses commonly associated with depression--stroke, cancer, Parkinson's disease, and dementia--to illustrate how these considerations affect the choice of an antidepressant.
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The reduction of prefrontal theta QEEG cordance value after first week of treatment might be helpful in the prediction of response to venlafaxine.
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Metabonomic approach is helpful to further understanding the pathophysiology of depression and assisting in clinical diagnosis of depression and is also a valuable tool for studying the essence of Chinese medicine's syndrome theory and therapeutic effect mechanism of TCM.
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To evaluate the efficacy, safety, and tolerability of flexible-dose venlafaxine ER compared with placebo in the short-term treatment of generalized social anxiety disorder and, secondarily, to compare paroxetine with venlafaxine ER and paroxetine with placebo.
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We report a case of hyponatremia probably caused by venlafaxine. Awareness of this potential problem would be helpful to clinicians and should be considered in the differential diagnosis of hyponatremia.
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Hepatic injury has been reported following duloxetine use. This study further examines the hepatic safety of duloxetine in a large US health insurance database.
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A CT scan documented signs of cortical atrophy in our patient's brain but excluded vascular brain injury, while clinical evaluation and anamnesis excluded a relationship between hallucinations and cortical atrophy. Genetic and pharmacologic factors may be involved in venlafaxine-induced adverse effects. Venlafaxine is metabolized primarily by CYP2D6 and is a substrate of P-glycoprotein. Propafenone, a known substrate and inhibitor of both CYP2D6 and P-glycoprotein, could therefore be involved in venlafaxine-induced hallucinations through the increase of venlafaxine plasma concentrations.
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These results, together with those of previously reported studies, suggest that venlafaxine has antidepressant efficacy comparable to that provided by available antidepressants.