Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bupropion, a noradrenaline and dopamine re-uptake inhibitor, has long been indicated for the treatment of depression. Recent studies have demonstrated additional benefits in depression, including: prevention of the recurrence of seasonal affective disorder in depressive subtypes with decreased energy, pleasure and interest; in major depression with concomitant anxiety; in elderly depressed patients; for non-response to initial serotonin re-uptake inhibitor therapy or augmentation of partial efficacy with serotonin re-uptake inhibitors; and in bipolar depression. Efficacy in other conditions has also been shown in studies of attention deficit hyperactivity disorder, nicotine dependence, obesity and hypoactive sexual desire disorder. Thus, bupropion has proven effective across a broad spectrum of depressive conditions, subtypes and comorbidities.
 ...
PMID:Extended-release bupropion: an antidepressant with a broad spectrum of therapeutic activity? 1730 40

Bupropion, an atypical antidepressant commonly used for depression and smoking cessation, is well known to cause seizures in both therapeutic use and overdose, but cardiac effects have been reported as minimal, usually sinus tachycardia. We describe an ingestion of bupropion estimated to be greater than 2 g by a 3-year-old boy that resulted in seizures. The child was decontaminated with whole bowel irrigation (WBI), and he experienced aspiration of polyethylene glycol and electrolyte solution used for the WBI. The patient ultimately developed hypotension and bradycardia requiring cardiopulmonary resuscitation due to the effects of the bupropion combined with the complications of WBI. In contrast to previous literature, which showed few clinical effects aside from seizures from ingestion of bupropion by children, our case highlights the dangers of pediatric bupropion ingestion and highlights risks of WBI.
 ...
PMID:Cardiotoxicity associated with accidental bupropion ingestion in a child. 1800 23

The present study was undertaken to elucidate the alterations in various behavioral and neurochemical basis of antidepressant action of bupropion [(+/-)-alpha-t-butylamino-3-chloropropiophenone], a dopamine reuptake inhibitor and to elucidate the possible mechanism of its action. The involvement of L-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling pathway in the antidepressant action of bupropion was investigated besides its actions on various brain transmitters like norepinephrine, dopamine and homovanillic acid. Bupropion (10, 15, 20 and 40 mg/kg., i.p.) dose dependently inhibited the immobility period in mice in both forced swim test and tail suspension test. ED(50) values of bupropion in reducing the immobility period was found to be 18.5 and 18 mg/kg i.p., in forced swim test and tail suspension test, respectively. Bupropion (10, 20 and 40 mg/kg., i.p.) reversed the reserpine-induced behavioral despair also. When different doses (10, 15, 20 and 40 mg/kg., i.p.) of bupropion were tested for locomotor activity, it (15, 20 and 40 mg/kg., i.p.) increased locomotor activity. At 20 and 40 mg/kg doses the drug showed hypothermia. The neurochemical analysis of brain samples revealed that bupropion dose dependently (10-40 mg/kg., i.p.) increased the brain contents of dopamine and homovanillic acid in the mouse whole brain. The levels of norepinephrine were also increased at 20 mg/kg dose. The antidepressant-like effect of bupropion (20 mg/kg., i.p.) was prevented by pretreatment with L-arginine (750 mg/kg., i.p.) [substrate for nitric oxide synthase (NOS)]. Pretreatment of mice with 7-nitroindazole (25 mg/kg., i.p.) [a specific neuronal nitric oxide synthase (nNOS) inhibitor] produced potentiation of the action of subeffective dose of bupropion (10 mg/kg i.p.). In addition, treatment of mice with methylene blue (10 mg/kg., i.p.) [direct inhibitor of both nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC)] potentiated the effect of bupropion (10 mg/kg., i.p.) in the forced swim test. Furthermore, the reduction in the immobility period elicited by bupropion (20 mg/kg., i.p.) was also inhibited by pretreatment with sildenafil (5 mg/kg., i.p.) [phosphodiesterase 5 inhibitor]. The study indicated that bupropion possesses antidepressant activities in different animal models of depression through its dopaminergic and/or by modulating the L-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling pathway.
 ...
PMID:Involvement of nitric oxide (NO) signaling pathway in the antidepressant action of bupropion, a dopamine reuptake inhibitor. 1750 58

To determine whether age/gender-based differences in efficacy exist between bupropion and the selective serotonin reuptake inhibitors for major depressive disorder, we pooled the findings of 10 double-blind studies comparing bupropion with a selective serotonin reuptake inhibitor. Men (N=943) and women (N=1179) were divided into three age groups (younger than 40, 40-55, older than 55). Improvement in terms of the 17-item Hamilton Depression Rating Scale, as well as the Bech melancholia, anxiety-somatization, and insomnia factors of the Hamilton Depression Rating Scale was compared between the two treatment groups. Of 64 pair-wise comparisons, only one was statistically significant. Specifically, more women treated with a selective serotonin reuptake inhibitor experienced a 50% or greater decrease in Hamilton Depression Rating Scale Anxiety-Somatization scores (58.8 versus 63.8%, P=0.0394). No difference, however, was seen in the degree of resolution of Hamilton Depression Rating Scale Anxiety-Somatization scores (continuous measure) between women treated with bupropion versus a selective serotonin reuptake inhibitor (P=0.114). Bupropion and the selective serotonin reuptake inhibitors, thus, appear to be equally effective in treating depressive symptoms, as well as anxious/somatic symptoms and insomnia in depression. No gender-related or age-related differences were found except that greater improvement was seen in anxious/somatic symptoms of depression among women during selective serotonin reuptake inhibitor treatment. This finding could, however, not be replicated when improvement in anxious/somatic symptoms was defined as a continuous measure.
 ...
PMID:Relative antidepressant efficacy of bupropion and the selective serotonin reuptake inhibitors in major depressive disorder: gender-age interactions. 1751 46

Bupropion was tested for efficacy in increasing weeks of abstinence in methamphetamine-dependent patients, compared to placebo. This was a double-blind placebo-controlled study, with 12 weeks of treatment and a 30-day follow-up. Five outpatient substance abuse treatment clinics located west of the Mississippi participated in the study. One hundred and fifty-one treatment-seekers with DSM-IV diagnosis of methamphetamine dependence were consented and enrolled. Seventy-two participants were randomized to placebo and 79 to sustained-release bupropion 150 mg twice daily. Patients were asked to come to the clinic three times per week for assessments, urine drug screens, and 90-min group psychotherapy. The primary outcome was the change in proportion of participants having a methamphetamine-free week. Secondary outcomes included: urine for quantitative methamphetamine, self-report of methamphetamine use, subgroup analyses of balancing factors and comorbid conditions, addiction severity, craving, risk behaviors for HIV, and use of other substances. The generalized estimating equation regression analysis showed that, overall, the difference between bupropion and placebo groups in the probability of a non-use week over the 12-week treatment period was not statistically significant (p=0.09). Mixed model regression was used to allow adjustment for baseline factors in addition to those measured (site, gender, level of baseline use, and level of symptoms of depression). This subgroup analysis showed that bupropion had a significant effect compared to placebo, among male patients who had a lower level of methamphetamine use at baseline (p<0.0001). Comorbid depression and attention-deficit/hyperactivity disorder did not change the outcome. These data suggest that bupropion, in combination with behavioral group therapy, was effective for increasing the number of weeks of abstinence in participants with low-to-moderate methamphetamine dependence, mainly male patients, regardless of their comorbid condition.
 ...
PMID:Bupropion for the treatment of methamphetamine dependence. 1758 31

Each year, tobacco use causes over 4 million deaths worldwide and billions of dollars are spent on treatment for tobacco-related illness. Bupropion, an atypical antidepressant, improves the rates of successful smoking cessation, however, the mechanisms by which bupropion reduces cigarette smoking and depression are unknown. Here we show that clinical concentrations of bupropion inhibit nicotine's stimulatory effects on brain reward areas. Many drugs of abuse, including nicotine, stimulate dopamine (DA) release in the mesoaccumbens reward system. Nicotinic acetylcholine receptors in the ventral tegmental area (VTA) mediate nicotine's stimulation of DA release, as well as its rewarding effects. Nicotinic receptors are expressed by excitatory and inhibitory neurons that control DA neuron excitability, and by the DA neurons themselves. Bupropion is a broad-spectrum non-competitive nicotinic receptor antagonist. Here we report that pre-treatment of brain slices with a clinically relevant concentration of bupropion dramatically reduces the effects of nicotine on DA neuron excitability. Nicotinic receptors on VTA DA neurons and their synaptic inputs are inhibited by 75 - 95% after bupropion treatment. We also find that bupropion alone reduces GABAergic transmission to DA neurons, thereby diminishing tonic inhibition of these neurons. This increases DA neuron excitability during bupropion treatment in the absence of nicotine, and may contribute to bupropion's antidepressant actions.
 ...
PMID:Bupropion inhibits the cellular effects of nicotine in the ventral tegmental area. 1786 53

Bupropion hydrochloride is currently available in three formulations: immediate-release, sustained-release, and extended-release (ER). Several published reports exist concerning bupropion's history of inducing seizures in both the immediate- and sustained-release formulations. Although the potential of the ER formulation for causing seizures is noted in the drug's prescribing information, there is no previously published report of bupropion ER inducing seizures. In the case reported, a 27-year-old woman who was prescribed bupropion ER as well as clonazepam and lamotrigine (anticonvulsants), hydrocodone bitartrate (for irritable bowel syndrome), and zolipidem tartrate (for depression and associated anxiety and insomnia) experienced a grand mal seizure 6 months after beginning bupropion ER therapy. The patient was taken to the emergency department, where she had a second grand mal seizure 8 hours after the first one. Extended-release bupropion was discontinued, and the patient had not had additional seizures at 8 months follow-up.
 ...
PMID:Extended-release bupropion induced grand mal seizures. 1844 24

Fatigue is a common and highly distressing symptom of cancer associated with reduced quality of life and considerable psychological and functional morbidity. The reported prevalence of cancer-related fatigue ranges from 4% to 91%, depending on the specific cancer population studied and the methods of assessment. Cancer-related fatigue has typically been underreported, underdiagnosed, and undertreated. Fatigue and depression may coexist in cancer patients, and considerable overlap of symptoms occurs. This is partly the reason for the interest in examining the role of psychotropic medications in treating fatigue. Clarifying the relationship between depression and fatigue is necessary to effectively evaluate and treat cancer-related fatigue. Even with International Classification of Diseases criteria, differentiating cancer-related fatigue is difficult. Psychotropic drugs that have been studied for cancer-related fatigue include psychostimulants, wakefulness-promoting agents, and antidepressants. Methylphenidate has been studied most and seems to be effective and well tolerated despite common side effects. Some preliminary data support using modafinil in cancer-related fatigue with less concern about tolerance or dependence. Antidepressant studies have shown mixed results. Paroxetine seems to show benefit for fatigue primarily when it is a symptom of clinical depression. Bupropion, a norepinephrine/dopamine reuptake inhibitor, may have psychostimulant-like effects, and therefore may be more beneficial for treating fatigue. However, studies are currently limited. Randomized, placebo-controlled trials with specific agents are needed to further assess the efficacy and tolerability of psychotropic medications in the treatment of cancer-related fatigue.
 ...
PMID:Update on psychotropic medications for cancer-related fatigue. 1805 30

Bupropion is an antidepressant thought to work through effects on norepinephrine and dopamine. It was first marketed in the USA in 1989 as a thrice-daily immediate-release preparation. This was followed in 1996 by twice-daily sustained-release and, most recently in 2003, by once-daily extended-release preparations. Its clinical efficacy for treating depression is equivalent to that of other antidepressants. In addition, the extended-release preparation has been shown to be effective for treating geriatric depression and depression characterized by reduced energy, pleasure and interest, and for preventing recurrence of seasonal affective disorder. Favorable aspects of its side-effect profile include low likelihood of somnolence, sexual dysfunction and weight gain. This review provides a history of the evolution of bupropion in its three formulations, with an emphasis on the efficacy and tolerability of the extended-release preparation.
 ...
PMID:Bupropion extended-release for depressive disorders. 1845 28

There are 3 first-line medications for smoking cessation i.e. nicotine replacement therapy (NRT), varenicline (a partial nicotine receptor agonist) and slow-release (SR) bupropion. All 3 agents approximately double 1-year quit rates when used for 3 months, although varenicline seems to be a little more efficacious than bupropion SR. An un-blinded study comparing varenicline with nicotine patches are analysed in details and it is concluded that the validity of that study is low regarding the relative efficacy of varenicline versus NRT. Depression and suicidal attempts have been reported with varenicline use but it is probably not induced by varenicline but by the quitting process per se. It is recommended that the first agent to be used in smoking cessation should be NRT as it is the best documented product with mild side effects. It might be optimal to combine the patch with either gum, inhaler, sublingual tablets or nasal spray. In subjects that have failed with NRT, varinicline should be the choice. Bupropion SR is preferred to subjects with depression or smokers who have failed with the previous two agents, due to the many contra-indications and side effects of bupropion SR. With one of the 3 agents combined with follow-up visits with counselling, one can expect a 1-year quit rate around 20-25%.
 ...
PMID:Which drug to be used in smoking cessation? 1861 94


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>