Venlafaxine: a new class of antidepressant

Hardy, Julia; Argyropoulos, Spilios V.; Nutt, David

doi:10.12968/hosp.2002.63.9.1952

Cited by 8 publications

(3 citation statements)

References 20 publications

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“…-Inhibidores selectivos de la recaptación dual de 5-HT y de NA. La venlafaxina es la primera en esta nueva clase de AD, con menos efectos indeseables y un comienzo rápido de la acción terapéutica, útil en pacientes con depresión refractaria a otros tratamientos, y con mayor tasa de remisión que con los inhibidores de recaptación de 5-HT [15,[24][25][26].…”

Section: Inhibidores Selectivos De La Recaptación De La 5-ht La Na Ounclassified

Avances en la terapéutica molecular de la depresión

Páez¹,

Hernández²,

T³

2003

RevNeurol

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The objective of this study is to survey present and future antidepressant drug therapy based on the progress made in the field of biotechnology. Development. The simplistic and mistaken view that one single system of neurotransmission is altered in depression and that there is, therefore, just one single treatment has changed. Molecular biology and Genetics have enabled us to determine other possible chemical alterations in the brain, beyond the sole participation of the monoaminergic modulation systems, which is the classical hypothesis. In this paper we describe the evidence for the relations between depression and the therapeutic effect the classical antidepressants have on: 1. The peptidergic system of the corticotropin-releasing hormone, cortisol and the functional state of its receptors; 2. Intracellular signalling systems such as cAMP on transcription factors like CREB and neurotrophins; 3. The immune system and cytosines; 4. Glutamate transmission; and 5. The neuropeptidergic system of substance P, neuroactive steroids and the neuroglia. This has allowed other biochemical hypotheses about depression and the possibility of new treatments to be put forward. Conclusions. We are still not certain about the exact cause or the processes that determine mental illnesses such as depression or how improvements are achieved with the antidepressants we currently have available. Nevertheless, biotechnology is expected to be a great help in advancing towards a better understanding of the interrelations between the nervous, immune and endocrine systems, with their intracellular cascades and final outcomes in genetic expression and protein function, in depression. This will enable more efficient, more selective and faster-acting drugs to be developed and, in the future and with the help of psychogenomics, even make it possible to produce tailor-made medication for each patient.

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Section: Inhibidores Selectivos De La Recaptación De La 5-ht La Na Ounclassified

Avances en la terapéutica molecular de la depresión

Páez¹,

Hernández²,

T³

2003

RevNeurol

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“…VEN is a serotonin-norepinephrine reuptake inhibitor (SNRI) prescribed to treat depression [ 1 ]. VEN is also used off label for the treatment of posttraumatic stress disorder (PTSD) [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Palpitations and Asthenia Associated with Venlafaxine in a CYP2D6 Poor Metabolizer and CYP2C19 Intermediate Metabolizer

García

Schuh

Cheema

et al. 2017

Case Reports in Genetics

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Cardiotoxicity has been extensively reported in venlafaxine (VEN) overdoses. Asthenia is also among the common side effects described for this antidepressant. VEN is metabolized mainly by CYP2D6 and to a minor extent by CYP2C19 to the major active metabolite O-desmethylvenlafaxine (ODV). Altered pharmacokinetic parameters in patients with polymorphisms in the CYP2D6 and CYP2C19 genes that result in decreased enzymatic activity have been documented. Here we describe a patient case of VEN associated palpitations and asthenia. The patient takes VEN extended release 150 mg twice daily. Genotyping confirmed the patient is a poor metabolizer for CYP2D6 and an intermediate metabolizer for CYP2C19. We propose that the palpitations and asthenia are related to sustained VEN exposure due to reduced metabolism.

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“…The use of these drugs was further supported by their inhibitory actions on dopamine and norepinephrine metabolism -findings consistent with the hypothesis of decreased catecholamine activity in ADHD (Mohammadi and Akhondzadeh, 2007 as a possible treatment alternative in ADHD. It has no significant affinity for muscarinic, cholinergic, histaminic, or alpha-1-adrenergic receptors and a relative short half-life, and is given in divided doses (Ninan, 2000;Hardy et al, 2002;Gutierrez et al, 2003). Some small open-label studies suggest that venlafaxine may be an effective medication in treating the core symptoms of ADHD in children and adolescents (Mukaddes and Abali, 2004;Findling et al, 2007).…”

Section: Introductionmentioning

confidence: 99%