State medicaid coverage for tobacco-dependence treatments--United States, 1998 and 2000. Influence of fluoxetine on the ability of bupropion to modulate extracellular dopamine and norepinephrine concentrations in three mesocorticolimbic areas of rats. Rx drugs

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MMWR Morb Mortal Wkly Rep. 2001 Nov 9;50(44):979-82.
State medicaid coverage for tobacco-dependence treatments--United States, 1998 and 2000.

[No authors listed]

The Guide to Community Preventive Services recommends reducing the cost of tobacco-dependence treatments because these interventions increase both the use of treatment by smokers during attempts to stop smoking and the number of smokers who actually stop. The Public Health Service (PHS) Clinical Practice Guideline supports insurance coverage for tobacco-dependence treatment (i.e., individual, group, and telephone counseling, and Food and Drug Administration-approved pharmacotherapy. One of the 2010 national health objectives is to provide coverage in the 50 states and District of Columbia (DC) for nicotine-dependence treatment by Medicaid (objective 27.8b). In 2000, approximately 32 million low-income persons in the United States received their health insurance coverage through the federal-state Medicaid program; approximately 11.5 million (36%) of these persons smoked (CDC, unpublished data, 2000). Medicaid recipients have approximately 50% greater smoking prevalence than the overall U.S. population. To assess the amount and type of coverage for tobacco dependence offered by Medicaid, the Center for Health and Public Policy Studies at the University of California, Berkeley, conducted state surveys in 1998 and 2000. In 1998, 24 states and DC offered some coverage for tobacco-dependence treatment; in 2000, nine started offering some coverage. In 1998 and 2000, one state offered coverage for all the counseling and pharmacotherapy treatments recommended by PHS. These findings indicate that states can reduce smoking prevalence among Medicaid recipients by implementing more extensive Medicaid coverage for treatment of tobacco dependence.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11724152&dopt=Abstract

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Neuropharmacology. 2002 Feb;42(2):181-90.
Influence of fluoxetine on the ability of bupropion to modulate extracellular dopamine and norepinephrine concentrations in three mesocorticolimbic areas of rats.

Li SX, Perry KW, Wong DT.

Neuroscience Research, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA.

The finding that serotonin (5-HT) can modulate dopamine (DA) and norepinephrine (NE) release in the brain has led us to hypothesize that fluoxetine, a selective 5-HT reuptake inhibitor, may influence the ability of bupropion, a preferential DA and NE dual reuptake inhibitor, to modulate extracellular DA and NE concentrations in some brain areas. The present study was designed to evaluate this hypothesis by assessing the effects of fluoxetine on bupropion-induced changes in extracellular monoamine concentrations by means of in vivo microdialysis. Three mesocorticolimbic areas including hypothalamus (Ht), prefrontal cortex (Pfc) and nucleus accumbens (Acb) were selected based on their relevance to depression and antidepressant actions. In the Ht of untreated rats, bupropion dose-dependently (s.c.) increased extracellular DA and NE concentrations either in single injection study or in sequential injection study. Thus, 10 mg/kg of bupropion had no effect on the DA and NE concentrations, while 30 mg/kg of bupropion induced transient but significant increases (about 240% of the baselines), and 100 mg/kg of bupropion induced marked and persistent increases (over 600% of the baselines) in the DA and NE concentrations. In the rats pre-treated with fluoxetine (10 mg/kg, s.c., 90 min interval), the threshold dose of bupropion (10 mg/kg) significantly increased the DA and NE concentrations to more than 350% of the baselines, and 30 mg/kg of bupropion markedly increased the DA and NE concentrations to more than 570% of the baselines in the Ht. The fluoxetine pre-treatment also potentiated the DA increases induced by 10 mg/kg of bupropion in the Pfc (260% for bupropion alone vs 357% for the combination) and in the Acb (224% vs 645%). The bupropion-induced NE increases were potentiated by fluoxetine mainly in the Ht. Bupropion did not significantly affect the extracellular 5-HT concentrations in all the 3 brain areas tested. In summary, the present study demonstrated that bupropion can increase extracellular DA and NE concentrations in several mesocorticolimbic areas, which may have an impact on bupropion's antidepressant actions. Furthermore, fluoxetine can potentiate the bupropion-induced DA and NE increases, which may produce more effective and rapid antidepressant actions.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11804614&dopt=Abstract

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utsouthwestern.edu

OBJECTIVE: To examine the effects of bupropion sustained release (SR) and sertraline on anxiety in outpatients with recurrent DSM-IV-defined major depressive disorder. METHOD: This retrospective analysis was conducted using pooled data from 2 identical, 8-week, acute-phase, double-blind, placebo-controlled, parallel-group studies of bupropion SR (N = 234), sertraline (N = 225), and placebo (N = 233). Symptoms of anxiety and depression were measured using the 14-item Hamilton Rating Scale for Anxiety (HAM-A) and the 21-item Hamilton Rating Scale for Depression (HAM-D-21), respectively. Percentage reduction in baseline HAM-A total score for each treatment week was calculated to determine whether the time to onset of anxiolytic activity differed among antidepressant responders to each agent. Central nervous system (CNS) adverse events were tabulated. RESULTS: Bupropion SR and sertraline were comparably effective, both were superior to placebo in reducing depressive symptoms. and they did not differ in their effect on anxiety symptoms. Antidepressant responders (> 50% reduction in baseline HAM-D-21 score) in both groups showed marked and comparable reductions in HAM-A scores (baseline to exit). There were no differences between bupropion SR and sertraline in the median time (4 weeks) to reach a clinically significant anxiolytic effect (> or = 50% reduction in baseline HAM-A score). CNS adverse events were comparable for bupropion SR and sertraline, except for somnolence, which was more common in sertraline-treated patients. CONCLUSION: Bupropion SR and sertraline had comparable antidepressant and anxiolytic effects and an equally rapid onset of clinically significant anxiolytic activity. There was no difference in the activating effects between the 2 antidepressants. Selection between these 2 agents cannot be based on either anticipation of differential anxiolytic activity or differential CNS side effect profiles.

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