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, Prim Care Companion. J Clin Psychiatry, 2001;3:22–27. 5. Masand PS, Gupta S. Long-Term side Effects of Newer-Generation Antidepressants: SSRIS, Venlafaxine, Nefazodone, Bupropion, and Mirtazapine. Annals of Clinical Psychiatry, 2002;14:175-182. 6. Harvey AT, Rudolph RL, Preskorn SH. Evidence of the Dual Mechanisms of Action of Venlafaxine, Arch Gen Psychiatry, 2000;57:503-509. 7. Kraus T, Haack M, Schuld A, Hinze-Selch D, Koethe D, Pollmächer T. 8. Body Weight, the Tumor Necrosis Factor System, and Leptin Production during Treatment with Mirtazapine or Venlafaxine

. 1962;10:799-812. doi:10.2466/PR0.10.3.799-812 Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry. 1960;23:56-62. doi:10.1136/jnnp.23.1.56 PMID:14399272. Altamura AC, Pioli R, Vitto M, Mannu P. Venlafaxine in social phobia: a study in selective serotonin reuptake inhibitor non-responders. Int Clin Psychopharmacol. 1999;14(4):239-45. doi:10.1097/00004850-199907000-00006 PMID:10468317. Thase ME, Friedman ES, Howland RH. Venlafaxine and treatment-resistant depression. Depress Anxiety. 2000;12 Suppl 1:55-62. doi:10

: 446-457. Dunn AJ, Wang J and Ando T. (1999). Eff ects of cytokines on cerebral neurotransmission: Comparison with the eff ects of stress. Adv Exp Med Biol 461: 117-127. Eren I, Nazıroğlu M, Demirdaş A, Celik O, Uğuz AC, Altunbaşak A, Ozmen I and Uz E. (2007). Venlafaxine Modulates Depression-Induced Oxidative Stress in Brain and Medulla of Rat. Neurochem Res 32: 497-505. Garate I, Garcia-Bueno B, Madrigal JL, Caso CR, Alou L, Gomez-Lus ML, Mico CA, Leza JC. (2013). Stress-Induced Neuroinfl ammation: Role of the Toll- Like Receptor-4 Pathway. Biol Psychiatry 73: 32

References [1] Bavle A. Venlafaxine induced QTc interval prolongation in a therapeutic dose. Asian J Psychiatr. 2015;16:63-64. [2] Bourke CH, Stowe ZN, Neigh GN et al. Prenatal exposure to escitalopram and/or stress in rats produces limited effects on endocrine, behavioral, or gene expression measures in adult male rats. Neurotoxicol Teratol. 2013;39:100-109. [3] Bögi E, Belovičová K, Csatlósová K et al. Impact of pre-gestational stress on offspring neurobehavioral development and hippocampal functioning. Interdiscip Toxicol. 2018;11(1):75. [4] Capello CF, Bourke

Introduction Venlafaxine is a serotonin-noradrenaline reuptake inhibitor and is highly effective in the treatment of major depressive disorder [ 1 ]. Overdose is associated with numerous life-threatening complications like adrenergic excess. There are numerous case reports of refractory cardiogenic shock and arrhythmias due to ingestion of high amounts of venlafaxine [ 2 , 3 , 4 ]. Two pathomechanisms of cardiac output failure have been suggested in venlafaxine intoxication. The first hypothesis is myocardial stunning by excessive adrenergic stimulation [ 5

REFERENCES Abozguia K, Chudley S, Gammage M. (2006). Dose-dependent Venlafaxine-induced sinus tachycardia. Int J Cardiol 113 : E9–10. Alosaimi FD, Abalhassan M, Alhaddad B, Alzain N, Fallata E, Alhabbad A, Alassiry MZ. (2017). Prevalence of metabolic syndrome and its components among patients with various psychiatric diagnoses and treatments: A cross-sectional study. Gen Hosp Psychiatry 45 : 62–69. Bavle A. (2015). Venlafaxine induced QTc interval prolongation in a therapeutic dose. Asian J Psychiatr 16 : 63–64. Bilora F, Vettore G, Barbata A, Pastorello M

References Bellantuono C, Migliarese G, Maggioni F, Imperadore G. (2007) Anridepressant drugs and breastfeeding. Recent Prog Med 98 : 29-42. Chung TK, Lau TK, Yip AS, Chiu HF, Lee DT. (2001). Antepartum depressive symptomatology is associated with adverse obstetric and neonatal outcomes. Psychosom Med 63 : 830-834. Da-Silva VA, Alterburg SP, Malheiros LR, Thomaz TG, Lindsey CJ. (1999). Postnatal development of rats exposed to fl uoxetine or venlafaxine during the third week of pregnancy. Braz J Med Biol Res 32 : 93-98. DeSantis DT, Schmaltz LW. (1984). The

References [1] Abozguia K, Chudley S., Gammage M. Dose-dependent venlafaxine-induced sinus tachycardia. Int J Cardiol. 2006;113:E9-E10 [2] Hanash JA, Hansen BH, Hansen JF, Nielsen OW, Rasmussen A, Birket-Smith M. Cardiovascular safety of one-year escitalopram therapy in clinically nondepressed patients with acute coronary syndrome: results from the Depression in patients with Coronary Artery Disease (DECARD) trial. J Cardiovasc Pharmacol. 2012;60(4): 397-405. [3] Leonard C.E., Bilker W.B., Newcomb C., Kimmel S.E., Hennessy S. Antidepressants and the risk of


Introduction: With an increasing prevalence of major depressive disorder (MDD) in population there is a particular interest in finding a suitable biomarker for diagnosis and prognosis of the disease. Many studies have shown that MDD is linked to a systemic inflammatory process, so blood elements counts and ratios have been suggested to be promising indicators in the management and effectiveness of the disease therapy. The aim of this retrospective study was to compare absolute and relative white blood cells counts and to search for any changes in their ratios before and after the therapy of the patients.

Methods: Our study included 36 patients who were admitted to hospital with either a new diagnosis or a recurrent episode of MDD and who were treated by a standard protocol. The peripheral blood samples were collected both at admission and at hospital discharge. Absolute white blood cell count and counts of neutrophils, lymphocytes, monocytes, platelets, as well as mean platelet volume, red blood cell distribution width, neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, and monocyte/lymphocyte ratio before and after hospitalization (14–29 days) were evaluated and compared. The test of normality was performed and, accordingly, single t-test or Mann-Whitney U-test was used for data analysis.

Results: There were no significant differences between any blood cell ratios in blood samples before and after stay in hospital and appropriate treatment. Monocyte count was significantly higher in MDD patients after hospital discharge (p=0.007), there was a significantly higher difference in discharged patients suffering from MDD recurrent episode (F.33) compared to newly diagnosed MDD (F.32) patients (p=0.010). In patients treated with venlafaxine (N=23) there was a significant increase in monocyte/lymphocyte ratio observed at the end of hospitalization (p=0.018).

Conclusions: The pharmacotherapy and additive treatment of the patients suffering from MDD led only to mild changes in blood cells counts. As our study included only a small number of patients, and blood cell parameters and ratios were compared after a relatively short duration of treatment, further and more detailed research is needed for final conclusions.


In the previous research at Jessenius Faculty of Medicine in Martin has been studied depression and its treatment from the aspects of the quality of life and functioning of the patients, as well as comparing the efficacy and safety of venlafaxine versus venlafaxine and olanzapine treatment. Last years have been studied the parameters of the autonomic nervous system in the context of depression. Our new work will build on these findings, during the exploration of efficacy and safety of a novel antidepressant vortioxetine in monotherapy and in combination with olanzapine. Since combination of vortixetine and olanzapine is not yet understood, it is unknown whether the effect of the treatment of depressive symptoms and associated problems will be stronger and faster compared to vortioxetine monotherapy.