A survey of prescribing practices in the treatment of depression.
ABSTRACT With the increasing number and type of antidepressants available to clinicians, there is a need to better understand current prescribing practices and to what degree these practices reflect research findings. The purpose of this study was to examine prescribing practices in a sample of psychiatrists attending a psychopharmacology review course and compare these results with empirical evidence.
439 of 800 clinicians asked (55%) responded to a 10-item questionnaire that was given prior to beginning the review course. Items covered three major content areas: first-line preferences in the treatment of depression, antidepressant agents most associated with certain side effects, and first-line preferences in the treatment of certain depressive subtypes.
214 (49%) clinicians indicated a belief that one antidepressant type is more efficacious than others. Of these 214 clinicians, 103 (48%) indicated selective serotonin reuptake inhibitors (SSRIs) as being most efficacious, while 53 (25%) indicated venlafaxine as being most efficacious; 378 (93%) clinicians indicated SSRIs as their first-line treatment preference. Mirtazapine (56%) was endorsed as most likely to be associated with weight gain, fluoxetine (57%) with sexual dysfunction, paroxetine (48%) with a discontinuation syndrome, and fluoxetine (52%) with agitation. For the treatment of anxious, atypical, and melancholic depression, SSRIs were the first choice of treatment (58%, 57%, and 57%), and for depression with prominent insomnia, mirtazapine and nefazadone (31% and 27%) were the first choices of treatment.
Despite the lack of evidence of a significant difference in efficacy between older and newer agents, clinicians perceive the newer agents to be more efficacious than the older drugs [tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs)] even in the melancholic and anxious depressive subtypes. Similarly, although sexual dysfunction and agitation appear to occur at similar rates with all the SSRIs, fluoxetine was perceived to be most likely to cause these side effects. These findings are significant as they highlight the discrepancy between empirical evidence and clinical practices and suggest that other factors influence clinicians' medication choices in the treatment of depression.
SourceAvailable from: Marzyeh Ghassemi[Show abstract] [Hide abstract]
ABSTRACT: Background Recent observational studies have found an increased risk of adverse effects such as hemorrhage, stroke, and increased mortality in patients taking selective serotonin reuptake inhibitors (SSRI's). The impact of prior use of these medications on outcomes in critically ill patients has not been previously examined. We performed a retrospective study to determine if pre-admission use of SSRIs or serotonin norepinephrine reuptake inhibitors (SNRIs) is associated with mortality differences in patients admitted to the intensive care unit.Methods The retrospective study employed a modifiable data mining technique applied to the publicly available MIMIC 2.6 database. 14,709 patient records, consisting of 2,471 in the SSRI/SNRI group and 12,238 controls, were analyzed. The study outcome was in-hospital mortality.ResultsAfter adjustment for age, Simplified Acute Physiology Score, vasopressor use, ventilator use, and combined Elixhauser score, SSRI/SNRI use was associated with significantly increased in-hospital mortality (OR 1.19, 95% CI 1.02 - 1.40, p = 0.026). Among patient subgroups, risk was highest in patients with acute coronary syndrome (OR 1.95, 95% CI 1.21 - 3.13, p = 0.006) and patients admitted to the Cardiac Surgery Recovery Unit (OR 1.51, 95% CI 1.11 - 2.04, p = 0.008). Mortality appeared to vary by specific SSRI with higher mortalities associated with higher levels of serotonin inhibition.Conclusions We found significant increases in hospital stay mortality among those ICU patients on SSRI/SNRIs prior to admission as compared to controls. Mortality was higher in patients receiving those SSRI/SNRI agents that produce greater degrees of serotonin reuptake inhibition. The study serves to demonstrate the potential for the future application of advanced data examination techniques upon detailed (and growing) clinical databases being made available by the digitization of medicine.Chest 12/2013; 145(4). DOI:10.1378/chest.13-1722 · 7.13 Impact Factor
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ABSTRACT: Use of psychostimulants such as methylphenidate (Ritalin) in medical treatments and as cognitive enhancers in the healthy is increasing. Methylphenidate produces some addiction-related gene regulation in animal models. Recent findings show that combining selective serotonin reuptake inhibitor (SSRI) antidepressants such as fluoxetine with methylphenidate potentiates methylphenidate-induced gene regulation. We investigated the endurance of such abnormal gene regulation by assessing an established marker for altered gene regulation after drug treatments – blunting (repression) of immediate-early gene (IEG) inducibility – 14 days after repeated methylphenidate + fluoxetine treatment in adolescent rats. Thus, we measured the effects of a 6-day repeated treatment with methylphenidate (5 mg/kg), fluoxetine (5 mg/kg) or their combination on the inducibility (by cocaine) of neuroplasticity-related IEGs (Zif268, Homer1a) in the striatum, by in situ hybridization histochemistry. Repeated methylphenidate treatment alone produced modest gene blunting, while fluoxetine alone had no effect. In contrast, fluoxetine given in conjunction with methylphenidate produced pronounced potentiation of methylphenidate-induced blunting for both genes. This potentiation was seen in many functional domains of the striatum, but was most robust in the lateral, sensorimotor striatum. These enduring molecular changes were associated with potentiated induction of behavioral stereotypies in an open-field test. For illicit psychostimulants, blunting of gene expression is considered part of the molecular basis of addiction. Our results thus suggest that SSRIs such as fluoxetine may increase the addiction liability of methylphenidate.12/2014; 4:109-116. DOI:10.1016/j.baga.2014.10.001
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ABSTRACT: Depression is a complex, heterogeneous mental disorder. Currently available antidepressants are only effective in about one-third to one-half of all patients. The mechanisms underlying antidepressant response and treatment resistance are poorly understood. Recent clinical evidence implicates the involvement of leptin in treatment response to antidepressants. In this study, we determined the functional role of the leptin receptor (LepRb) in behavioral responses to the selective serotonergic antidepressant fluoxetine and the noradrenergic antidepressant desipramine. While acute and chronic treatment with fluoxetine or desipramine in wild-type mice elicited antidepressant-like effects in the forced swim test, mice null for LepRb (db/db) displayed resistance to treatment with either fluoxetine or desipramine. Fluoxetine stimulated phosphorylation of Akt(Thr308) and GSK-3β(Ser9) in the hippocampus and prefrontal cortex (PFC) of wild-type mice but not in db/db mice. Desipramine failed to induce measurable changes in Akt, GSK-3β or ERK1/2 phosphorylation in the hippocampus and PFC, as well as hypothalamus of either genotype of mice. Deletion of LepRb specifically from hippocampal and cortical neurons resulted in fluoxetine insensitivity in the forced swim test and tail suspension test while leaving the response to desipramine intact. These results suggest that functional LepRb is critically involved in regulating the antidepressant-like behavioral effects of both fluoxetine and desipramine. The antidepressant effects of fluoxetine but not desipramine are dependent on the presence of functional LepRb in the hippocampus and cortex.12/2014; 4:e486. DOI:10.1038/tp.2014.126