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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The original Expert Consensus Guidelines on the Treatment of Bipolar Disorder were published in 1996. Since that time, a variety of new treatments for bipolar disorder have been reported; however, evidence for these treatments varies widely, with data especially limited regarding comparisons between treatments and how to sequence them. For this reason, a new survey of expert opinion was undertaken to bridge gaps between the research evidence and key clinical decisions. The results of this new survey, which was completed by 58 experts, are presented in The Expert Consensus Guideline Series: Medication Treatment of Bipolar Disorder 2000, which was published in April 2000 as a Postgraduate Medicine Special Report. In this article, the authors describe the methodology used in the survey and summarize the clinical recommendations given in the resulting guidelines. The expert panel reached consensus on many key strategies, including acute and preventive treatment of mania (euphoric, mixed, and dysphoric subtypes), depression, rapid cycling, and approaches to managing treatment resistance and comorbid psychiatric conditions. Use of a mood stabilizer is recommended in all phases of treatment. Divalproex (especially for mixed or dysphoric subtypes) and lithium are the primary mood stabilizers for both acute and preventive treatment of mania. If monotherapy with these agents fails, the next recommended intervention is to combine them. This combination of lithium and divalproex can then serve as the foundation to which other medications are added if needed. Carbamazepine is the leading alternative mood stabilizer for mania. The experts rated the other new anticonvulsants as second-line options (i.e., their use is recommended if lithium, divalproex, and carbamazepine fail or are contraindicated). For milder depression, a mood stabilizer, especially lithium, may be used as monotherapy. Divalproex and lamotrigine are other first-line choices. For more severe depression, the experts recommend combining a standard antidepressant with lithium or divalproex. Bupropion, selective serotonin reuptake inhibitors (SSRIs), and venlafaxine are preferred antidepressants. The antidepressants should usually be tapered 2-6 months after remission. Monotherapy with divalproex is recommended for the initial treatment of either depression or mania in rapid-cycling bipolar disorder. Antipsychotics are recommended for use in combination with the above regimens for mania or depression with psychosis, and as potential adjuncts in nonpsychotic episodes. Atypical antipsychotics, especially olanzapine and risperidone, were generally preferred over conventional antipsychotics. The guidelines also include recommendations concerning the use of electroconvulsive therapy (ECT), clozapine, thyroid hormone, stimulants, and various novel agents for patients with treatment-refractory bipolar illness. The experts reached high levels of consensus on key steps in treating bipolar disorder despite obvious gaps in high-quality data. To evaluate many of the treatment options in this survey, the experts had to extrapolate beyond controlled data; however, their recommendations are generally conservative. Experts give their strongest support to initial strategies and medications for which high-quality research data or longstanding patterns of clinical usage exist. Within the limits of expert opinion and with the understanding that new research data may take precedence, these guidelines provide clear pathways for addressing common clinical questions and can be used to inform clinicians and educate patients about the relative merits of a variety of interventions.
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PMID:Medication treatment of bipolar disorder 2000: a summary of the expert consensus guidelines. 1599 Apr 85

Nicotine addiction leads to withdrawal symptoms in many persons who quit smoking. In addition to craving, the most commonly experienced symptoms are: depression; difficulty sleeping; irritability, frustration, or anger; anxiety; difficulty concentrating; restlessness; decreased heart rate; and increased appetite or weight gain. The severity of withdrawal symptoms are variable, and often lead to relapse. By altering the course of withdrawal symptoms it is possible to improve the chances of the quit attempt and reduce the risk of relapse. There is strong evidence that dopamine is the primary neurotransmitter in the reward pathway in addiction. The use of nicotine replacement therapies and Zyban (sustained release bupropion hydrochloride), both of which are suspected of exploiting dopamine's role in addiction, enhance the likelihood of long-term smoking cessation. Anecdotal reports of oxygen's capacity to reduce both the desire for nicotine and withdrawal symptoms suggest that this may be a therapeutic possibility for those who do not experience success with more traditional cessation approaches. Oxygen may have a favorable effect on nicotine withdrawal, as it appears to alter the balance of central neurotransmitters such as dopamine.
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PMID:Oxygen as a therapy for reducing nicotine withdrawal symptoms. 1600 32

We report a reanalysis of data from a prior study describing the event history of quitting smoking aided by bupropion, using recurrent-event models to determine the effect of the drug on occurrence of lapses and recoveries from lapse (resumption of abstinence). Data were collected on 1,070 subjects across two similar double-blind randomized clinical trials of bupropion versus placebo and fitted with separate Cox regression models for lapse and recovery. Analyses were split using discrete time-varying covariates between the treatment (weeks 1-10) and follow-up phases (end of treatment to 12 months). Bupropion was associated with slower lapse during treatment for both sexes, and being female was associated with faster lapse across both phases. Drug did not affect time to recovery for males but was associated with faster recovery among females, allowing women to recover as quickly as men. High levels of nicotine dependence did not affect time to lapse but were associated with slower recovery from lapse across treatment and follow-up phases. During the treatment phase, higher levels of baseline depression symptoms had no effect on time to lapse but were associated with slower recovery from lapse. Results highlight the asymmetry in factors preventing lapse versus promoting recovery. Specifically, dependence, depression symptoms, and a sex x drug interaction were found to affect recovery but not lapse. Further research disentangling lapse and recovery events from summary abstinence measures is needed to help us develop interventions that take advantage of bupropion at its best and that compensate where it is weak.
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PMID:Recurrent event analysis of lapse and recovery in a smoking cessation clinical trial using bupropion. 1603 83

Restless legs syndrome (RLS) is a common disorder for which agents that enhance dopaminergic activity, including dopamine agonists and levodopa, are the treatment of choice. However, long-term use of dopaminergic drugs can cause unwanted effects such as rebound, tolerance, and augmentation. Bupropion, an inhibitor of dopamine and noradrenalin reuptake, is an antidepressant that modulates dopaminergic systems. The authors report that a low dose of bupropion rapidly and completely ameliorated RLS symptoms in 3 depressed patients within a few days of the initiation of treatment. To their knowledge, this is the first report to show that bupropion may be an effective alternative for treating RLS. Consequently, bupropion may be useful for the treatment of patients with both depression and RLS.
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PMID:Bupropion may improve restless legs syndrome: a report of three cases. 1634 Mar 89

In a wide range of human diseases of inflammatory nature like Crohn's disease, pathology is mediated in part by pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF) or interferon-gamma. We show here that a commonly used generic antidepressant bupropion, in wide use worldwide to treat depression in humans for a decade now, profoundly lowers levels of TNF, interferon-gamma, and interleukin-1 beta in vivo, in a mouse lipopolysaccharide (LPS) induced inflammation model. Mice challenged with an otherwise lethal dose of LPS were protected by bupropion and levels of the anti-inflammatory cytokine interleukin-10 were increased. Previous data in rodents and humans indicate antidepressant effects of bupropion are mediated by its weak reuptake inhibition of norepinephrine and dopamine. Concordant with this, TNF suppression by bupropion in our mouse LPS model was largely abrogated by beta-adrenergic or dopamine D1 receptor antagonists but not by a D2 antagonist. TNF synthesis is controlled by an inverse relationship with intracellular cyclic adenosine monophosphate (cAMP) and stimulation of either beta-adrenoreceptors or D1 dopaminergic receptors result in increased cAMP but stimulation of D2 receptors lowers cAMP. We conclude that bupropion may suppress TNF synthesis by mediating increased signaling at beta-adrenoreceptors and D1 receptors, resulting in increased cAMP that inhibits TNF synthesis. Bupropion is well tolerated also in non-psychiatric populations and has less risk with long term use than current anti-inflammatory, immunosuppressive or TNF suppressive treatments such as prednisone, azathioprine, infliximab, or methotrexate. New anti-inflammatory treatments are needed. We believe a new chapter in antiinflammatory, TNF lowering treatment of disease has been opened. Bupropion's use for this in humans should be explored.
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PMID:A new chapter opens in anti-inflammatory treatments: the antidepressant bupropion lowers production of tumor necrosis factor-alpha and interferon-gamma in mice. 1664 75

Bupropion is commonly used in the treatment of nicotine dependence and depression, and in most people, does not cause sexual dysfunction, weight gain, or sedation. Given its attractive side effect profile, the efficacy of other newer antidepressants against hot flashes and anecdotal observations of resolution of hot flashes in some patients taking bupropion for nicotine dependence, it was decided to explore its clinical activity as a hot flash remedy in a pilot study. Between January 1999 and October 2004, 21 patients (7 men and 14 women) were enrolled in the study. Self-completed daily hot flash diaries were used to document the frequency and severity of hot flashes at baseline (week 1) and during the treatment period (weeks 2 through 5). Participants received bupropion 150 mg every morning for the first 3 days and then 150 mg twice per day for a total of 4 weeks. One woman did not provide any hot flash information and was excluded from the analysis. Five women could not complete the study because of side effects. The study did not show a reduction in hot flash frequency and/or severity significantly higher than what would be expected with a placebo. Even though the sample size was small, these results are consistent with bupropion's mechanism of action (norepinephrine reuptake inhibition without serotonergic effects) and what it is now hypothesized about the pathophysiology of hot flashes (increased noradrenergic activity and decreased serotonergic activity). These data suggest that bupropion should not be further investigated as a remedy for hot flashes.
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PMID:Pilot evaluation of bupropion for the treatment of hot flashes. 1675 68

Bupropion has been used to treat psychic depression and as a therapy for smoking cessation, the latter mainly in association with nicotine. However, there have been no detailed studies of the hemodynamic effects of the association of bupropion with nicotine during replacement therapy. In this study, we evaluated the effects of such an association on the cardiovascular parameters in anesthetized dogs. Bupropion, either alone or together with nicotine, had no significant effect on the cardiac index (CI; 4.7 +/- 0.2 vs 4.3 +/- 0.1 and 3.5 +/- 0.3 vs 3.4 +/- 0.3 L x min(-1) x m(2), respectively; mean +/- SEM) and mean arterial pressure (MAP; 134 +/- 5.0 vs 145 +/- 11.0 and 118 +/- 5.0 vs 133 +/- 10.5 mmHg, respectively). There was a slight but significant increase in the systemic vascular resistance index (SVRI; 2,165 +/- 93 vs 2,645 +/- 126 and 2,335 +/- 100 vs 2,737 +/- 200 dyn x cm(-5)m(-2), respectively). However, there was a significant increase in the mean pulmonary artery pressure (MPAP; 20 +/- 0.8 vs 25 +/- 1.6 and 18 +/- 1.3 vs 25 +/- 1.6 mmHg, respectively; p < 0.05) and pulmonary vascular resistance index (IRVP; 194 +/- 11 vs 272 +/- 21 and 206 +/- 32 vs 307 +/- 42 dyn x cm-5m(-2), respectively; p < 0.05). These results show that bupropion alone or in association with nicotine does not markedly affect most hemodynamic parameters of the systemic circulation, although the significant increase in MPAP and IRVP can elevate the pulmonary pressure.
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PMID:Hemodynamic effects of a combination of bupropion and nicotine in anesthetized dogs. 1684 83

Bupropion was initially developed and licensed for the treatment of major depressive disorder in the United States in 1989. It was licensed as a pharmacotherapy for smoking cessation in the United States in 1997 and in the United Kingdom in 2000, and for the prevention of seasonal major depressive episodes in patients with seasonal affective disorder in the United States in 2006. Its main mechanism of action is believed to be via dopamine and noradrenalin reuptake inhibition. In addition to proven clinical efficacy for the treatment of major depression, the prevention of depressive episodes in patients with seasonal affective disorder, and as an aid to smoking cessation treatment, bupropion has demonstrated efficacy for attenuation of symptoms of attention deficit hyperactivity disorder, and more recently it has shown anti-inflammatory action against proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), which may be implicated in a number of inflammatory diseases such as Crohn's disease. The twice-daily sustained-release formulation has been extensively evaluated for smoking cessation and has shown continuous smoking abstinence rates at one year of the order of 20% across many clinical groups including healthy smokers, and smokers with cardiovascular disease, chronic obstructive airways disease, depression and schizophrenia. Bupropion is well tolerated with side effects including insomnia, headache, dry mouth, dizziness and nausea. Bupropion is a cytochrome p450 2D6 inhibitor and care must be taken when coprescribing with drugs cleared by this enzyme and when coprescribing with drugs that lower seizure threshold. Despite the clinical effectiveness and cost-effectiveness of bupropion as an aid to smoking cessation, its uptake for this indication remains low when compared with nicotine replacement therapy.
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PMID:Bupropion. 1713 26

Bupropion is a norepinephrine and dopamine uptake inhibitor that has been available for several years for the treatment of depression and aiding smokers to quit. Although bupropion is not approved for treating obesity, three randomized clinical trials have shown some degree of efficacy for this drug in promoting weight loss in obese patients. The present drug profile provides a review of the pharmacology of bupropion, clinical evidence of efficacy with regard to weight reduction, tolerability and risks, and the current and future role of this drug in the management of obesity.
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PMID:Bupropion for weight reduction. 1718 92

Evidence suggests that improving adherence and persistence to antidepressant therapy could enhance clinical and economic outcomes in depression. This study was conducted to assess the impact of dosing frequency (once daily with bupropion XL vs twice daily with bupropion SR) on adherence to bupropion therapy in a nationally representative prescription database in the United States. Demographics of patients with a prescription for bupropion XL or bupropion SR between October 1, 2005, and October 31, 2005, were similar between the XL group (n=257,049; 69% female) and the SR group (n=12,468; 67% female). Refill adherence over a 1-year period was greater with bupropion XL than bupropion SR. The percentage of patients with >or=1 refill over 1 year was 60.1% with bupropion XL compared with 51.3% with bupropion SR (P < 0.0001). The percentage of patients with >or=6 refills over 1 year was 25.3% with bupropion XL compared with 9.5% with bupropion SR. Bupropion XL was associated with significantly greater likelihood of refilling a prescription than bupropion SR as shown by Kaplan-Meier curves (P < 0.0001, log-rank test). The medication possession ratio over a 9-month period was higher for bupropion XL (0.26) than it was for bupropion SR (0.16). Logistic regression analyses show that patients with a prescription for bupropion SR were significantly less likely to fill a future prescription than were patients with a prescription for bupropion XL. These data show that adherence to bupropion therapy in this sample was better with the once-daily XL formulation than with the twice-daily SR formulation across several measures.
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PMID:Better patient persistence with once-daily bupropion compared with twice-daily bupropion. 1730 71


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