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Case bupropion

The tricyclic antidepressants (TCAs), such as imipramine, can alleviate symptoms of ADHD. Like bupropion, TCAs likely will improve symptoms associated with comorbid anxiety and depression. The mechanism of action of TCAs is in blocking norepinephrine transporters, thus increasing norepinephrine concentrations in the synapse the increase in norepinephrine is believed to alleviate the symptoms of ADHD. TCAs have been demonstrated to be an effective non-stimulant option for ADHD but less effective than stimulants. However, their use in ADHD has declined owing to case reports of sudden death and anticholinergic side effects6,13 (Table 39-3). Further, TCAs may lower seizure threshold and increase the risk of car-diotoxicity, (e.g., arrythmias). Patients starting on TCAs should have a baseline and routine electrocardiograms. [Pg.641]

In cases where the antidepressant response has not been resounding, we prefer switching antidepressants to avoid sexual side effects. The options include bupropion, nefazodone, and mirtazapine, which all effectively treat depression but produce minimal effects on sexual function. Sometimes, if a patient has responded well to one antidepressant but experiences a side effect such as sexual dysfunction, switching within the same class can be a useful approach. [Pg.375]

Cardiac effects Hypertension, in some cases severe, requiring acute treatment, has been reported in patients receiving bupropion alone and in combination with nicotine replacement therapy. Exercise care if bupropion is used in in patients with a recent history of Ml or unstable heart disease. [Pg.1056]

Because bupropion is metabolized in the liver, medications that alter hepatic enzyme metabolism, such as carbamazepine or cimetidine, may effect blood concentrations. Bupropion should not be administered in combination with the MAOIs because of risk of hypertensive crisis. Levo-dopa use in conjunction with bupropion has been associated with confusion, hallucinations, and dyskinesia. Although generally well tolerated, there are case reports documenting that the... [Pg.302]

Inattentiveness, impulsivity, hyperactivity 50% will continue to manifest the disorder into adulthood Stimulants (70% response for uncomplicated ADHD caution in patients with tic disorders) TCAs (70% response, first line for patients with comorbid MD or anxiety disorders, and for patients with ADHD + tics) requires serum levels and cardiovascular monitoring Bupropion Clonidine, guan-facine (first line for patients with ADHD + tics) MAOIs Combined pharmacotherapy for treatment-resistant cases... [Pg.452]

Case reports have suggested that adding stimulant medications or combining a SSRI and a TCA or bupropion may also be effective (APA, 2000), but these combinations need to be done with caution, given the possibility of drug interactions (e.g., SSRIs cytochrome inhibition leading to toxic TCA levels). Additionally, in adults, the combination of antidepressants and psychotherapy (CBT, IPT) for patients with severe or treatment-resistant depression has been found useful (APA, 2000 Keller et al., 2000). [Pg.475]

Bupropion. A brief case report by Emmanuel et al. (1991] describes one patient with depression and social phobia who responded to bupropion, an... [Pg.396]

Tremor and akathisia are less common and can be managed with dose reduction or the addition of a P-blocker such as propranolol (10-40 mg). There are isolated case reports of SSRl-related dystonia and increasing reports of SSRl-related exacerbation of Parkinson s disease (Di Rocco et al. 1998 Linazasoro 2000). The advisability of SSRl use in depressed patients with Parkinson s disease remains to be determined. Bupropion and electroconvulsive therapy (ECT) may be reasonable alternatives for these patients. [Pg.26]

Patients with seizure disorders should not take bupropion. Similarly, an alternative treatment should be considered in the case of patients with a history of significant head trauma, a central nervous system tumor, or an active eating disorder. [Pg.35]

Labbate LA, Pollack MH Treatment of fluoxetine-induced sexual dysfunction with bupropion a case report. Ann Clin Psychiatry 6 13-15, 1994... [Pg.66]

Although the efficacy of tricyclic antidepressants in the treatment of unipolar depression is beyond reproach, the side-effect profile of these agents makes them less desirable as first-line therapeutic agents. Introduction of selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, sertraline, citalopram and fluvoxamine in the past decade has revolutionized the treatment of depression universally. The side-effect profile of SSRIs, such as nausea, diarrhea and sexual dysfunction, is considerably more benign than that of tricyclic drugs. Multiple controlled trials have proven the efficacy of SSRIs vs. placebo (Nemeroff, 1994). Recently, a number of SNRIs (serotonin and noradrenaline reuptake inhibitors) and so-called atypical antidepressants have been marketed that may have additional advantages over SSRIs, such as more rapid onset of action (venlafaxine. mirtazapine) and low sexual side-effect potential ( bupropion, nefazodone). Additionally, it appears that venlafaxine may be more efficacious in cases of treatment-refractory depression (Clerc et al., 1994 Fatemi et al., 1999). Finally, in a recent report (Thase et al., 2001),... [Pg.276]

Fatenri, S.H., Emamian, E.S., Kist, D. Venlafaxine and bupropion combination therapy in a case of treatment-resistant depression. Ann. Phannacother. 33, 701—703, 1999. [Pg.341]

Those who fail to respond to an SSRI may respond to a TCA, and vice versa. Thus, these two broad-spectrum classes can be used in a sequential strategy to adequately treat the majority of cases. However, many physicians try another newer antidepressant (e.g, venlafaxine, bupropion, nefazodone) in such patients because of the safety and tolerability problems associated with TCAs. Of note, the tolerability profile of secondary amine TCAs such as desipramine is as favorable as any of the newer antidepressants and probably better than nefazodone. Nevertheless, the secondary amine TCAs have a therapeutic index as narrow as tertiary amine TCAs (e.g., amitriptyline, imipramine) in terms of lethality in overdoses resulting from cardiotoxicity. [Pg.131]

Thus, the clinician might use TDM with bupropion to guard against the development of unusually high plasma levels of the parent drug or its metabolites. That would be particularly true for the medically compromised or the patient on other drugs that could interfere with the clearance of bupropion. In such a case, the laboratory should assay the parent drug and its three major metabolites—hydroxybupropion, threohydrobupropion, and erythrohydrobupropion. [Pg.141]

As a results of these studies, clinicians have proposed that switching to reboxetine or bupropion might a useful strategy given that these antidepressants share the ability with desipramine and imipramine to block NE uptake. Nevertheless, only one small open label study has been done to test this possibility ( 365). If bupropion is to be used in patients switched from an ineffective trial of fluoxetine, the dose should be kept low for several weeks to allow for the clearance of fluoxetine and norfluoxetine. Case reports indicate that fluoxetine can elevate levels of the active metabolites of bupropion, which, in turn, could mediate an increase risk of adverse effects (366). [Pg.142]

In a review of 37 reported cases, Davidson (426) found that the risk of seizures with bupropion was higher at doses above the recommended maximum (i.e., 450 mg per day). An increased risk of seizures was also noted in eating-disordered patients (i.e., bulimics) on bupropion, leading to its temporary withdrawal from the market. With the immediate release formulation, the seizure risk is four per 1,000 patients when the dose is kept at or below 450 mg per day in those without known risk factors (426, 468). The seizure risk may be as low as one per 1,000 patients with the sustained release formulation when the dose is kept below 450 mg per day and the patient has no preexisting seizure history and is not on any medication that also can lower seizure thresholds or interfere with the metabolism of bupropion. [Pg.151]

Dager S, Heritch A. A case of bupropion-associated delirium. J din Psychiatry 1990 51 307-308. [Pg.163]

FIGURE 7—57. Heroic combo 13 Nefazodone plus NDRI (bupropion). In this case, the serotonergic single boost of nefazodone is added to the NE and DA single boost of bupropion. [Pg.294]

Mercerolle M, Denooz R, Lachatre G et al (2008) A fatal case of bupropion (Zyban) overdose. J Anal Toxicol 32 192-196... [Pg.173]

Stroll et al. (1994), from Harvard s McLean Hospital, compared the blinded charts of 49 consecutive inpatient admissions with antidepressant-induced mania with 49 matched cases of spontaneous mania over a 1-year period, from March 1, 1990, to February 28, 1991. The patients had been exposed to tricyclics (n = 19), fluoxetine (n = 13), monoamine oxidase inhibitors (n = 8), bupropion (n = 6), and mixed antidepressants (n = 3). (It is striking that these doctors were already aware of the risk of Prozac-induced mania approximately 2 years after the January 1988 introduction of Prozac into the market. Meanwhile, too many health care providers remain in denial about this significant risk.)... [Pg.161]

Balit CR, Lynch CN, Isbister GK. Bupropion poisoning a case series. Med J Aust 2003 178 61-3. [Pg.5]

This case suggests that bupropion can rarely cause psychotic symptoms even in people without susceptibility factors, although it is conceivable that this patient might, for example, have had a family history of psychiatric disorder. Amfebutamone is believed to enhance dopaminergic function, and the psychiatric phenomena experienced by the patient, principally paranoid delusions and elevated mood, are consistent with a hypcrdopamincrgic state. [Pg.95]

Oxcarbazepine can also cause hyponatremia, but in this case the hyponatremia appeared to correlate with the prescription of bupropion rather than oxcarbazepine and was also reproduced by amfebutamone re-challenge. This case suggests that amfebutamone can also cause hyponatremia, although it is possible that the presence of oxcarbazepine was necessary for the adverse effect to occur. [Pg.95]

Bagley SC, Yaeger D. Hyponatremia associated with bupropion, a case verified by rechallenge. J Clin Psychopharmacol 2005 1 98-9. [Pg.98]

Shin YW, Erm TM, Choi EJ, Kim SY. A case of prolonged seizure activity after combined use of bupropion and clomipramine. Clin Neuropharmacol 2004 27 192-4. [Pg.98]

Conway CR, Nelson LA. The combined use of bupropion, lithium, and venlafaxine during ECT a case of prolonged seizure activity. J ECT 2001 17(3) 216—8. [Pg.170]

ZOLPIDEM DRUG DEPENDENCE THERAPIES - BUPROPION Cases of agitation hallucinations Uncertain Avoid co-administration... [Pg.273]

Specifications for extended-release products reflect the intended release profile of the product, which in some cases, may be relatively complex. The drug-release specification for Bupropion Hydrochloride Extended-Release Tablets USP requires 25-45% of the nominal content of drug to have dissolved after one hour, 60-85% after four hours and not less than 80% after eight hours. The specifications for Diltiazem Hydrochloride Extended-Release Capsules USP are even more complex, with 13 different tests being prescribed to cover the various products (Table 1). Other products with multiple profiles include Pentoxifylline Extended-release Capsules USP (10 tests). Lithium Carbonate Tablets USP (4 tests) and Indomethacin Extended-release capsules USP (3 tests). [Pg.917]


See other pages where Case bupropion is mentioned: [Pg.173]    [Pg.190]    [Pg.1338]    [Pg.303]    [Pg.536]    [Pg.247]    [Pg.60]    [Pg.63]    [Pg.35]    [Pg.138]    [Pg.155]    [Pg.176]    [Pg.1250]    [Pg.462]    [Pg.71]    [Pg.190]    [Pg.161]    [Pg.172]    [Pg.97]    [Pg.52]    [Pg.174]   
See also in sourсe #XX -- [ Pg.234 , Pg.235 ]




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