Use of Bupropion in Combination with Serotonin Reuptake Inhibitors

Department of Psychiatry, University of California, San Diego, La Jolla, USA.
Biological Psychiatry (Impact Factor: 10.25). 03/2006; 59(3):203-10. DOI: 10.1016/j.biopsych.2005.06.027
Source: PubMed

ABSTRACT Incomplete symptom remission and sexual side effects are common problems for which bupropion often is added to treatment with selective serotonin and serotonin-norepinephrine reuptake inhibitors (SSRIs and SNRIs) for patients with major depressive disorder (MDD). This article reviews the literature on combining bupropion with SSRIs or SNRIs. We used MEDLINE to select studies that included patients diagnosed with MDD treated with any combination of bupropion and an SSRI or SNRI, either to enhance antidepressant response or to ameliorate antidepressant-associated sexual dysfunction. Bibliographies of located articles were searched for additional studies. Controlled and open-label studies support the effectiveness of bupropion in reversing antidepressant-associated sexual dysfunction, whereas open trials suggest that combination treatment with bupropion and an SSRI or SNRI is effective for the treatment of MDD in patients refractory to the SSRI, SNRI, or bupropion alone. The available data suggest that, although not an approved indication, the combination of bupropion and either an SSRI or an SNRI is generally well tolerated, can boost antidepressant response, and can reduce SSRI or SNRI-associated sexual side effects. Additional randomized controlled studies are needed to answer important questions, such as those regarding optimal dose and duration of treatment.

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    • "The current study was an acute experiment, but in light of the Kennedy Study, chronic dosing and further study in animal models are warranted. Certainly clinical studies support the co-administration of SSRIs and SNRIs with bupropion in patients despite our lack of understanding of the neurochemistry involved (Kennedy et al. 2002; for review see Zisook et al. 2006). The current study would suggest that an unanticipated beneficial additive or synergistic action on multiple neurotransmitter systems may, in part, explain such clinical benefit. "
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    ABSTRACT: Venlafaxine is recognised as an effective treatment for depression and is known to inhibit the reuptake of serotonin (5-HT) and noradrenaline (NA). Another antidepressant, bupropion, acts to inhibit dopamine (DA) and NA reuptake and is commonly co-administered with other antidepressants to improve the efficacy of the antidepressant effect. The present study was designed to investigate the acute effect of combining the 2 drugs on extracellular levels of 5-HT, DA, and NA in rat frontal cortex using brain microdialysis, with the drugs being administered by intraperitoneal injection (i.p). Bupropion (10 mg/kg body mass, i.p.) alone had no effect on extracellular 5-HT levels, whereas venlafaxine (10 mg/kg, i.p.) alone significantly elevated extracellular 5-HT over basal values. As expected, bupropion alone elevated extracellular dopamine above basal values at 40 min post-drug administration, and this effect lasted for a further 2 h. Venlafaxine alone did not statistically elevate extracellular dopamine. The co-administration of venlafaxine with bupropion resulted in a dramatic increase in extracellular dopamine, and this effect was significantly greater than that seen with bupropion alone. In the frontal cortex, NA was elevated by bupropion alone and venlafaxine alone, relative to the control animals. The combination of bupropion and venlafaxine resulted in a marked elevation of NA.
    Canadian Journal of Physiology and Pharmacology 04/2012; 90(6):803-9. DOI:10.1139/y2012-045 · 1.55 Impact Factor
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    • "Bupropion is an antidepressant with properties of norepinephrine- and dopamine-reuptake inhibition instead of serotonergic action. The combination of bupropion and an SSRI or SNRI is widely used as an option that has a triple reuptake inhibitor-like action, and bupropion also seems to reverse certain adverse effects associated with serotonergic agents and to enhance the efficacy of initial antidepressants.41,42 On the other hand, in this study when the initial antidepressants were newer dual-action and other antidepressants including TCAs, other (50%) and newer dual-action antidepressants (44.5%), respectively, were frequently chosen as the concomitant antidepressant. "
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    ABSTRACT: This study aimed to investigate antidepressant prescribing patterns, including initial choice, switching and combining, and concomitant use of non-antidepressant agents, for depressive disorders in naturalistic clinical care settings in Korea. Patients with depressive disorder were recruited from both outpatient and inpatient settings in 18 hospitals from all over Korea. Treatment was performed in naturalistic patterns based on each clinician's decision. Data were collected on the prescription of antidepressants and concomitant agents from baseline to 12-week follow-up. Selective serotonin reuptake inhibitors (SSRIs) were the most commonly prescribed initial antidepressant (48.9%), followed by newer dual-action antidepressants (45.8%). When an SSRI was the initial antidepressant, 46.2% of patients whose medication was changed were moved to newer dual-action antidepressants, and 67.4% of combination cases were combined with newer dual-action ones. When a newer dual-action antidepressant was the initial antidepressant, 70.6% of patients whose medication was changed were moved to SSRIs, and other antidepressants including tricyclic antidepressants were most commonly added for combination treatment (50% of combination cases). During the treatment period, 20.6% of antidepressants prescribed were augmented by non-antidepressant agents, and 75.1% were used concomitantly with anxiolytics or hypnotics. The most commonly used concomitant non-antidepressant agent was quetiapine. The selection of antidepressants and the concomitant use of non-antidepressant agents are becoming increasingly diversified, and the results of this study reflect changes in the prescribing pattern in actual Korean practices.
    Psychiatry investigation 09/2011; 8(3):234-44. DOI:10.4306/pi.2011.8.3.234 · 1.15 Impact Factor
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    • "Dopamine release within the mesolimbic system has been implicated as a major mechanism in sexual function (Bitran et al. 1988; Segraves 1989; Hull et al. 1999). Noradrenaline regulates sexual arousal (Lee and Pfaff 2008) and bup ropion, a dopamine and noradrenaline reuptake in hibitor, has been reported to decrease SSRI-induced SD (Zisook et al. 2006; Safarinejad 2010b,c). However, the mechanisms through which SSRIs cause SD remain poorly understood (Segraves 2007; Perlis et al. 2009). "
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    ABSTRACT: Sexual dysfunction (SD) is a frequently reported side-effect of antidepressant treatment, particularly of selective serotonin reuptake inhibitors (SSRIs). In the multicentre clinical and pharmacogenetic GENDEP study (Genome-based Therapeutic Drugs for Depression), the effect of the serotonin transporter gene promoter polymorphism 5-HTTLPR on sexual function was investigated during treatment with escitalopram (SSRI) and nortriptyline (tricyclic antidepressant). A total of 494 subjects with an episode of DSM-IV major depression were randomly assigned to treatment with escitalopram or nortriptyline. Over 12 weeks, depressive symptoms and SD were measured weekly with the Montgomery-Asberg Depression Rating Scale, the Antidepressant Side-Effect Checklist, the UKU Side Effect Rating Scale, and the Sexual Functioning Questionnaire. The incidence of reported SD after 12 weeks of treatment was relatively low, and did not differ significantly between antidepressants (14.9% escitalopram, 19.7% nortriptyline). There was no significant interaction between the 5-HTTLPR and antidepressant on SD. Improvement in depressive symptoms and younger age were both associated with lower SD. The effect of age on SD may have been moderated by the 5-HTTLPR. In GENDEP, rates of reported SD during treatment were lower than those described in previous reports. There was no apparent effect of the 5-HTTLPR on the observed decline in SD.
    The World Journal of Biological Psychiatry 03/2011; 12(7):528-38. DOI:10.3109/15622975.2011.559270 · 4.23 Impact Factor
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