Research and Clinical Trials on Venlafaxine (Effexor, Efexor)

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This list of current clinical research trials on Venlafaxine (Effexor, Efexor) is followed by a short set of abstracts from the most recent research articles published on the drug.

Venlafaxine (Effexor, Efexor) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Venlafaxine (Effexor, Efexor).

 

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Current Research Literature on Venlafaxine (Effexor, Efexor)

Here are abstracts for some of the latest research articles to have appeared on Venlafaxine (Effexor, Efexor):

Effects of fluoxetine and venlafaxine on serum brain derived neurotrophic factor levels in depressed patients.

Prog Neuropsychopharmacol Biol Psychiatry. 2008 Dec 7;
Başterzi AD, Yazici K, Aslan E, Delialioğlu N, Taşdelen B, Tot Acar S, Yazici A
BACKGROUND: Several studies demonstrated that depressed patients had low serum BDNF levels which correlated with the severity of their depression, and antidepressant treatment increases levels of serum BDNF in depressed patients. It was speculated that agents acting on both noradrenergic and serotonergic transporters might have a greater influence on BDNF levels. The aim of our study was to determine effects of venlafaxine vs. fluoxetine on serum BDNF levels in depressive patients. METHODS: Forty-three patients diagnosed as major depressive disorder according to DSM-IV are included in the study. Forty-three patients were randomized to take fluoxetine (22 cases) or venlafaxine (21 cases). Serum levels of BDNF were measured by ELISA at baseline and 6 weeks after the start of treatment. RESULTS: Baseline levels of BDNF were not significantly different between the patient group and the controls. But male patients and the male controls showed statistical differences with respect to baseline BDNF levels. BDNF levels of the patient group did not change with treatment. Yet, the increase of BDNF levels was close to statistically significant in the fluoxetine group, whereas not significant in the venlafaxine group. There were no significant differences in baseline and 6th week BDNF levels between the responders and the non-responders. CONCLUSION: Further studies controlling for a wide variety of confounding variables are needed, which may help to reach a clear conclusion about the potential of BDNF as a biomarker for depression or as a predictor of antidepressant efficacy.

Probable Trimethoprim/Sulfamethoxazole-Induced Higher-Level Gait Disorder and Nocturnal Delirium in an Elderly Man (January).

Ann Pharmacother. 2008 Dec 23;
Dakin LE
OBJECTIVE: To report a case of probable trimethoprim/sulfamethoxazole (TMP/SMX)- induced higher-level gait disorder (HLGD) and nocturnal delirium in an elderly patient on high-dose oral therapy. CASE SUMMARY: An 82-year-old man with a recent history of depression became comatose following an overdose of escitalopram and oxazepam. He was admitted, ventilated for 7 days in the intensive care unit, and treated with piperacillin/tazobactam and cefepime for aspiration pneumonia. Following discharge to a medical ward, respiratory symptoms persisted and imaging confirmed pulmonary abscesses. Stenotrophomonas maltophilia was isolated from sputum and, on day 15, TMP/SMX 800 mg/160 mg 1 tablet every 12 hours was initiated. On day 35, the dose was increased to 800 mg/160 mg 2 tablets every 12 hours. By day 37, the patient was unsteady when attempting to stand. From day 40, he was noted to have features of HLGD with gait ignition failure, poor balance, and frequent falls. His other medications at this time were thiamine 100 mg daily, multivitamin 1 tablet daily, omeprazole 20 mg every 12 hours, and modified- release venlafaxine 150 mg daily. Investigation did not reveal any cause for his acute gait disturbance. TMP/SMX was stopped on day 48 and, by day 51, the patient's gait had returned to normal. DISCUSSION: Neuropsychiatric adverse reactions with TMP/SMX have been infrequently reported. The Naranjo probability scale indicated that TMP/SMX was the probable cause of HLGD in this patient. CONCLUSIONS: At time of writing, this was the first reported case of HLGD associated with TMP/SMX. Clinicians should consider this adverse reaction as a potential cause of HLGD, especially in the elderly and those with malnutrition and hepatic or renal dysfunction.

Venlafaxine induced-myoclonus in a patient with mixed dementia.

Arq Neuropsiquiatr. 2008 Dec; 66(4): 894-5
Dutra LA, Pedroso JL, Felix EP, Barsottini OG

Headache and hormone replacement therapy in the postmenopausal woman.

Curr Treat Options Neurol. 2009 Jan; 11(1): 10-7
Macgregor EA
Headache and migraine are common symptoms of the menopause, often associated with irregular periods, hot flashes, and night sweats. Perimenopausal women should routinely be asked about headache and migraine, so that they can be offered appropriate advice. If attacks are infrequent, it may be sufficient to optimize acute treatment strategies. Lifestyle changes, alone or combined with a nonprescription treatment such as isoflavones, may be considered, although evidence of efficacy is limited. In women with migraine and more severe menopause symptoms, continuous hormone replacement therapy should be considered, using a nonoral route and the lowest dose effective in controlling symptoms. For women who have contraindications to estrogen therapy or do not wish to use it, compounds that inhibit serotonin reuptake, such as venlafaxine, fluoxetine, and paroxetine, have all shown efficacy for the control of hot flashes and prevention of migraine. Gabapentin is another nonhormonal option that has clinical trial evidence of effectiveness in treating hot flashes and reducing the frequency and severity of migraine attacks. Although clonidine is licensed in several countries for migraine prophylaxis and treatment of vasomotor symptoms, any benefit from treatment is often offset by adverse events. There is evidence that hysterectomy can increase the frequency of migraine and menopause symptoms, with added morbidity and risk of mortality. Therapy should regularly be evaluated to assess its ongoing need, as hormonal triggers are self-limiting and abate after menopause.

Venlafaxine extended release for climacteric women with depression or anxiety diagnosis. An open-label study.

Actas Esp Psiquiatr. 2008 Dec 15;
Iglesias C, Pato E, Ocio S, Ortigosa J, Santamarina S, Merino M, Alonso M, Fernández L, Alonso J, Rodríguez L
Introduction. The objective of this observational study was to assess under real clinical practice conditions the effectiveness and safety of venlafaxine extended release in anxiety-depressed and hormone-related symptoms in climacteric women with anxiety or depressive disorders. Methodology. Observational, prospective, open-label, multicenter, 24-week study, carried out in Spain. A sample of 45 outpatients, adult women between 45 and 55 years of age, diagnosed of depressive disorder, generalized anxiety disorder or social anxiety disorder were analyzed. Venlafaxine extended release was administered for 24 weeks at doses according to the investigator's clinical criteria. Results. Of the total of 45 patients who were included in the study, 43 (95.6%) completed it. The patients' age range was of 47 to 55 years old, median of 50 and mean of 50.82. The clinical condition evolution was assessed with the evaluation scales scores: Blatt-Kuppermann Menopausal Index, Hamilton Depression Rating Scale, Hamilton Anxiety Scale and Clinical Global Impression. During the 24-week period, a significant decrease in the different scales scores showed a clinical improvement. Conclusions. The results achieved show that treatment with venlafaxine extended release significantly improved the clinical condition of climacteric patients with anxiety or depressive disorder. If these results are confirmed with placebo-controlled clinical trials, they will support the utility of Venlafaxine extended release in this kind of patients. Key words: Depression. Open-label. Perimenopause. Climacteric. Venlafaxine extended release. Women. Actas Esp Psiquiatr 2009;37(0):00-00.

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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