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PubMed1998

A meta-analysis of the effects of venlafaxine on anxiety associated with depression.

Venlafaxine is the first member of a novel class of antidepressants that inhibits the reuptake of both serotonin and norepinephrine. Clinical trials of venlafaxine have demonstrated its efficacy and safety in the treatment of patients diagnosed with major depression. Because patients who have depression also often have anxiety, recent investigations have focused on determining whether venlafaxine can relieve symptoms of anxiety in depressed patients. We performed a pooled analysis of six short-term trials of venlafaxine, retrospectively measuring anxiety in anxious depressed patients using the Hamilton Rating Scale for Depression (HAM-D), Anxiety/Somatization factor and Anxiety Psychic item scores. Three studies were placebo-controlled, and three were placebo- and active-drug-controlled; active controls were imipramine in two trials and trazodone in the third trial. Patients were categorized as having anxiety accompanying depression if baseline HAM-D Anxiety Psychic item scores were 2 or greater. Anxious depressed patients treated with venlafaxine showed greater improvement than those treated with placebo beginning at week 3, according to the HAM-D Anxiety/Somatization factor score, and beginning at week 1, according to the Anxiety Psychic item score. Both effects were maintained at week 6 of treatment (and at week 12 in the one study of longer duration). Finally, treatment with venlafaxine resulted in a highly significant (p < or = 0.001) improvement in depression scores in patients who were anxious at baseline, compared with placebo-treated patients. The results of this analysis demonstrate that venlafaxine is more effective than placebo in reducing symptoms of anxiety in depressed patients and suggest that venlafaxine may afford a monotherapy option for treating patients who have a comorbid diagnosis of depression with anxiety.

Adult↗
PubMed1998

Venlafaxine's effects on healthy volunteers' driving, psychomotor, and vigilance performance during 15-day fixed and incremental dosing regimens.

Effects of venlafaxine, an antidepressant acting by selective serotonin and norepinephrine reuptake inhibition with a potency ratio of 5:1, were assessed in a standardized, actual driving test, a battery of psychomotor tests (Critical Flicker/Fusion Frequency, Critical Tracking, Divided Attention), and a 45-minute vigilance test (Mackworth Clock). Thirty-seven healthy volunteers, 22 of whom completed the study, received venlafaxine in fixed (37.5 mg twice a day) and incremental (37.5-75 mg twice a day) doses as well as mianserin (10-20 mg three times a day) and placebo according to a 4-period (15 days each), double-blind, crossover design. Testing occurred on days 1 and 7 and after dose increments, on days 8 and 15. Plasma concentrations of venlafaxine and its active metabolite were measured on test days for confirming compliance. Venlafaxine had no significant effect on the primary driving parameter (standard deviation of lateral position) and failed to impair psychomotor performance. Mianserin profoundly and consistently impaired driving and psychomotor performance. However, both drugs significantly impaired vigilance performance. Maximal effects occurred on day 1 with mianserin and similarly on day 7 with venlafaxine in both series. The increment in venlafaxine's dose on day 8 did not increase this effect. The drug's selectively impairing effect on vigilance is shared by other "serotonergic" anxiolytics and antidepressants, suggesting that interference with 5-HT transmission reduces arousal in particularly monotonous tasks or environments. This study concludes that venlafaxine does not generally affect driving ability and should be safe for use by patients who drive.

Adult↗
PubMed1998

Efficacy and safety of venlafaxine in the treatment of bipolar II major depressive episode.

As many as 45% of patients with major depression also meet diagnostic criteria for bipolar (BP) II disorder. Although the use of a concurrent mood-stabilizing drug has been suggested in treating BP II depression, antidepressant monotherapy has received less attention. The efficacy and safety of venlafaxine were examined in 17 BP II (mean+/-SD; age, 41+/-14 years) versus 31 unipolar (UP) (45+/-14 years) patients with major depression. Minimum pretreatment Hamilton Rating Scale for Depression (HAM-D21) score was > or = 20. After a 1-week placebo lead-in, patients were randomly assigned to receive double-blind treatment with once- versus twice-daily venlafaxine dosing starting at 37.5 mg daily and increasing up to 225 mg daily. Patients were evaluated weekly for efficacy using the HAM-D21, the Montgomery-Asberg Depression Rating Scale (MADRS), and the Clinical Global Impression (CGI) Scale. We observed a similar overall efficacy in BP and UP patients by 6 weeks of treatment (p = not significant). However, we also observed a more rapid reduction of HAM-D21 (p < 0.03) and MADRS (p < 0.02) scores by week 2 of treatment in BP patients who completed the entire trial. No episodes of venlafaxine-induced "manic switch" were observed in either patient group. In conclusion, our preliminary findings suggest that short-term, 6-week venlafaxine treatment may be a safe and effective antidepressant monotherapy for BP II major depression.

Adult↗
PubMed1999

Venlafaxine in treatment-resistant major depression: a Canadian multicenter, open-label trial.

This was an 8-week, multicenter, open-label study of the efficacy and tolerability of venlafaxine in patients with treatment-resistant depression conducted in Canada. Inpatients or outpatients aged 18 to 70 years with major depression were eligible if they had a 21-item Hamilton Rating Scale for Depression (HAM-D-21) score of 2 > or = 18 and a documented history of unsatisfactory improvement after a minimum of 8 weeks of treatment with an adequate dose of an antidepressant. Treatment with venlafaxine was started at 37.5 mg twice daily, and the dose could be titrated upward to a maximum of 375 mg/day during the first 4 weeks on the basis of the investigator's assessment of clinical response and tolerability. Of the 159 patients enrolled, 152 were evaluable for efficacy. The mean daily venlafaxine dose was 260 mg/day. The mean HAM-D-21 score decreased by 52%, and the mean Montgomery-Asberg Depression Rating Scale score decreased by 50% from baseline to day 56. A response (50% improvement from baseline) was achieved by 58% of patients on the HAM-D-21, and a remission (> or = 75% improvement in the HAM-D-21) was observed in 28% at day 56. By day 56, 88% of patients had improved from baseline on the Clinical Global Impression Improvement scale. Only 8% of the patients discontinued for adverse events. The most common adverse events were headache, insomnia, nausea, constipation, diaphoresis, and xerostomia. In conclusion, these results suggest that venlafaxine is effective and well tolerated for the management of patients with treatment-resistant major depression.

Adolescent↗
PubMed2000

Efficacy of venlafaxine and predictors of response in a prospective open-label study of patients with treatment-resistant major depression.

The aim of this study was to replicate the findings of a 1994 study, in which a 30% response rate to venlafaxine was found in patients with treatment-refractory depression, as well as to examine for any predictors of such an outcome. The study was an 8-week, open-label, prospective investigation of venlafaxine in doses up to 300 mg in 312 patients fulfilling criteria for either "absolute" or "relative" treatment resistance. By week 8, 52.6% of the patients had responded, which was defined as a 50% reduction in scores on the Montgomery-Asberg Depression Rating Scale; 49% of those defined with "absolute resistance" demonstrated such an outcome. Forty-five percent of the patients with absolute resistance who had failed to respond to at least one tricyclic antidepressant responded to venlafaxine. Response rates were higher in those with an absence (57.5%) compared with the presence (31.0%) of any comorbid psychiatric disorder (p < 0.001), "marked" (60.3%) compared with "mild or moderate" (51.6%) or "severe" (43.4%) baseline ratings on the patient-rated Clinical Global Impressions Scale (p < 0.05), and "relative" (61%) compared with "absolute" resistance (49%) (p = 0.06). Furthermore, improvement in scores of 20% or 30% at weeks 1 or 2 was associated with higher rates of final response (p < 0.0005). After logistic regression, both comorbid psychiatric illness (p < 0.001) and early improvement (p < 0.0001) remained significant and independent predictors of final response.

Adult↗
PubMed2000

Lithium augmentation of venlafaxine: an open-label trial.

The authors conducted an open-label study of the efficacy and tolerability of venlafaxine and of lithium augmentation in outpatients with depression who were not responding to venlafaxine. Outpatients aged 18 to 70 years were eligible if they had a minimum baseline score of 16 on the 17-item Hamilton Rating Scale for Depression (HAM-D). Patients were started on venlafaxine 37.5 mg twice daily for 1 week. For weeks 2 through 4, the dose of venlafaxine was increased to 75 mg twice daily, and for weeks 5 through 7, the dose was further increased to 75 mg three times daily. At the end of the 7-week treatment period, patients with a <50% decrease in their HAM-D scores from baseline were given lithium carbonate 600 mg once daily. The dose of lithium carbonate was adjusted to maintain plasma levels in the range of 0.6 to 1.0 mmol/mL. Efficacy was assessed with the 17-item HAM-D, Montgomery-Asberg Depression Rating Scale, and the Clinical Global Impressions Scale. Data were analyzed on an intent-to-treat basis. At the end of the 7-week treatment period, 35% of patients showed a > or = 50% decrease in their HAM-D scores from baseline. Lithium augmentation was initiated in 23 patients. The results showed that the addition of lithium was well-tolerated and led to a further decrease in the HAM-D scores, with eight patients responding and two of them presenting a remission. The addition of lithium to venlafaxine was found to be a well-tolerated strategy in treatment-resistant patients.

Adult↗
PubMed2001

Diphenhydramine alters the disposition of venlafaxine through inhibition of CYP2D6 activity in humans.

CYP2D6 is the major enzyme involved in the metabolism of venlafaxine. Subjects with a low CYP2D6 activity have increased plasma concentrations of venlafaxine that may predispose them to cardiovascular side effects. In vitro and in vivo studies showed that diphenhydramine, a nonprescription antihistamine, can inhibit CYP2D6 activity. Therefore, the authors investigated in this study a potential drug interaction between diphenhydramine and venlafaxine. Fifteen male volunteers, nine with the extensive metabolizer (EM) and six with the poor metabolizer (PM) phenotype of CYP2D6, received venlafaxine hydrochloride 18.75 mg orally every 12 hours for 48 hours on two occasions (1 week apart): once alone and once during the concomitant administration of diphenhydramine hydrochloride (50 mg every 12 hours). Blood and urine samples were collected for 12 hours under steady-state conditions. In EMs, diphenhydramine decreased venlafaxine oral clearance from 104+/-60 L/hr to 43+/-23 L/hr (mean +/- SD; p < 0.05) without any effect on renal clearance (4+/-1 L/hr during venlafaxine alone and 4+/-2 L/hr during venlafaxine plus diphenhydramine). In PMs, coadministration of diphenhydramine did not cause significant changes in oral clearance and partial metabolic clearances of venlafaxine to its various metabolites. Diphenhydramine disposition was only slightly affected by genetically determined low CYP2D6 activity or concomitant administration of venlafaxine. In conclusion, diphenhydramine, at therapeutic doses, inhibits CYP2D6-mediated metabolism of venlafaxine in humans. Clinically significant interactions could be encountered during the concomitant administration of diphenhydramine and other antidepressant or antipsychotic drugs that are substrates of CYP2D6.

Adult↗