Disease relevance of C07187

• Preliminary data have suggested that newer antidepressants, such as venlafaxine, can diminish hot flashes [1].
• Venlafaxine in management of hot flashes in survivors of breast cancer: a randomised controlled trial [1].
• Neuroleptic malignant syndrome after venlafaxine [2].
• Frequencies of some side-effects (mouth dryness, decreased appetite, nausea, and constipation) were significantly higher in the venlafaxine 75 mg and 150 mg groups than in the placebo group [1].
• Treatment of chronic fatigue syndrome with venlafaxine [3].

Psychiatry related information on C07187

• Efficacy of venlafaxine extended-release capsules in nondepressed outpatients with generalized anxiety disorder: A 6-month randomized controlled trial [4].
• Venlafaxine in obsessive-compulsive disorder [5].
• Bupropion and venlafaxine responders differ in pretreatment regional cerebral metabolism in unipolar depression [6].
• Venlafaxine did not alter pain experienced during the cold pressor test or increase the pressure pain thresholds [7].
• METHODS: Each of the groups of rats was treated for 14 days with one of the following: an antidepressant drug (desipramine, paroxetine, venlafaxine, or tianeptine); a mood stabilizer (lithium or carbamazepine); or 8 hours' partial sleep deprivation [8].
• Venlafaxine ER is an effective and reasonably well-tolerated treatment for generalized social anxiety disorder in children and adolescents [9].

High impact information on C07187

• OBJECTIVE: To compare the 6-month efficacy and safety of a flexible dosage of venlafaxine XR in outpatients with GAD without associated MDD [4].
• RESULTS: In the entire cohort, fluoxetine use was associated with the lowest risk (RR, 0.52; 95% confidence interval [CI], 0.30-0.93), and venlafaxine hydrochloride use with the highest risk (RR, 1.61; 95% CI, 1.01-2.57), of suicide [10].
• CONCLUSIONS: This preliminary investigation has shown limbic blood flow increase with IPT yet not venlafaxine, while both treatments demonstrated increased basal ganglia blood flow [11].
• RESULTS: Both treatment groups improved substantially, more so with venlafaxine (mean [SD] HAM-D scores at pretreatment: IPT, 22.7 [2.7], and venlafaxine, 22.4 [3.1]; and posttreatment: IPT, 16.2 [7.1], and venlafaxine, 10.9 [8.6]) [11].
• Statistically significant changes in height, weight, blood pressure, pulse, and cholesterol levels were observed in the extended-release venlafaxine group [12].

Chemical compound and disease context of C07187

• A patient developed neuroleptic malignant syndrome after a single dose of venlafaxine with trifluoperazine treatment [2].
• Venlafaxine extended release vs placebo and paroxetine in social anxiety disorder [13].
• Of the patients receiving fluoxetine, 1.7% had sustained hypertension for > or = 3 consecutive clinic visits-a rate significantly lower than that previously reported with venlafaxine (4.8%) (chi2 = 13.3, p < 0.001) and similar to that previously seen with placebo (2.1%) [14].
• The seizure rate and potential for cardiac conduction changes or orthostatic hypotension with venlafaxine were comparable with rates seen with the serotonin selective reuptake inhibitors [15].
• Venlafaxine extended release in posttraumatic stress disorder: a sertraline- and placebo-controlled study [16].

Biological context of C07187

• Higher doses of venlafaxine may also cause elevations in blood pressure, heart rate, and serum cholesterol [17].
• Venlafaxine and breast-feeding [18].
• RESULTS: Among the 150 women who were exposed to venlafaxine during pregnancy, 125 had live births, 18 had spontaneous abortions, and seven had therapeutic abortions; two of the babies had major malformations [19].
• The inability of venlafaxine to reduce SERT or NET binding sites is not due to its dual uptake inhibiting properties [20].
• CONCLUSION: Bupropion had an effect on the pharmacokinetics of venlafaxine but not those of the SSRIs [21].

Anatomical context of C07187

• Amniotic fluid to maternal serum ratios were higher for venlafaxine: 172% (SD=91%) (N=3) [22].
• CONCLUSION: Venlafaxine increases the pain tolerance threshold to electrical sural nerve stimulation and the threshold at which pain increases (pain summation) [7].
• These findings enhance our understanding of the compromise of the hippocampus by stressful assaults, and may be relevant to the action of venlafaxine in the treatment of patients with major depression, a mental disease thought to be related to the mal-adaptation of subjects to environmental stressors [23].
• O- and N-demethylation of venlafaxine in vitro by human liver microsomes and by microsomes from cDNA-transfected cells: effect of metabolic inhibitors and SSRI antidepressants [24].
• The objective of this study was to determine whether venlafaxine relieves thermal hyperalgesia in rats with neuropathic pain due to chronic constriction injury (CCI) of the sciatic nerve [25].

Associations of C07187 with other chemical compounds

• METHOD: Adult outpatients with nonpsychotic major depressive disorder who had not achieved remission or had withdrawn from treatment because of intolerance in three previous prospective medication trials were randomly assigned to receive open-label treatment with either tranylcypromine (N=58) or extended-release venlafaxine plus mirtazapine (N=51) [26].
• METHODS: One hour after subcutaneous injection of venlafaxine, paroxetine, mirtazapine, or doxepin, knockout and wildtype mice were sacrificed, and the drug concentrations in brain, spleen, kidney, liver, and plasma were measured [27].
• Selectively, compared with control subjects bupropion responders (n = 6) also had cerebellar hypermetabolism, whereas venlafaxine responders (n = 7) showed bilateral temporal and basal ganglia hypometabolism [6].
• Apparent total clearance of venlafaxine and O-desmethylvenlafaxine were both significantly decreased by approximately 55% in the subjects receiving dialysis, and terminal disposition half-life was significantly prolonged for both compounds [28].
• RESULTS: Patients (n = 9) receiving venlafaxine showed a significant decrease (42%) in their CSF 5-HIAA concentrations after treatment, but no change in other CSF measures [29].

Gene context of C07187

• Role of CYP2D6 in the stereoselective disposition of venlafaxine in humans [30].
• Weight decreased slightly but significantly in patients treated with venlafaxine (mean weight loss: 0.4 kg), whereas plasma levels of leptin, TNF-alpha, or soluble TNF receptors did not change significantly [31].
• Quetiapine and venlafaxine synergically regulate heme oxygenase-2 protein expression in the hippocampus of stressed rats [32].
• The homozygote for two defective alleles of CYP2C19 showed a higher concentration of venlafaxine within group 1 and group 2 [33].
• Venlafaxine had minimal or no demonstratable inhibition of CYP1A2, CYP3A4, or CYP2C [34].

Analytical, diagnostic and therapeutic context of C07187

• We hypothesized that venlafaxine hydrochloride and interpersonal psychotherapy (IPT) might each alter brain blood flow in some or all of these areas on sequential single photon emission computed tomography (SPECT) scans [11].
• Venlafaxine, a recently available antidepressant that appears to have efficacy in treatment-refractory depression, may cause nausea that requires gradual upward dosage titration [17].
• Pregnancy outcome following gestational exposure to venlafaxine: a multicenter prospective controlled study [19].
• OBJECTIVE: The purpose of this study was to use functional magnetic resonance imaging (fMRI) to probe the neural circuitry associated with reactivity to negative and positive affective stimuli in patients with major depressive disorder before treatment and after 2 and 8 weeks of treatment with venlafaxine [35].
• The odds ratio of having a PLMI greater than 20 was 5.15 for the SSRI group and 5.24 for the venlafaxine group compared with the control group [36].

References