Biomedical subjects

David E Adson

Publications and source records attributed to David E Adson.

7 recordsLinked to original sources

PubMed2006

Effect of bupropion on physiological measures of stress in smokers during nicotine withdrawal.

Studies suggest that among cigarette smokers trying to quit, stress undermines abstinence. Little research has assessed if therapies that increase smoking cessation rates impact physiological measures of stress response. Forty-three subjects completed this repeated-measures study in which a laboratory assessment was completed at baseline and after 17 days of treatment with either placebo (n=15), bupropion sustained release (150 mg twice daily) (n=14) or bupropion with stress reduction counseling (n=14). All subjects quit smoking 3 days prior to the second laboratory assessment. At each laboratory assessment physiological measures of stress (i.e. blood pressure, heart rate, plasma epinephrine, norepinephrine and cortisol concentrations) were measured during rest periods and in response to a speech, a math and a cold pressor task. Among subjects taking placebo, physiological measures of stress were generally lower at rest and during the stressors after smoking cessation. In those taking bupropion these measures were equivalent at the two assessments. Additionally, compared to placebo, those on bupropion had a greater diastolic blood pressure response to the speech stressor and greater systolic blood pressure response to the math stressor during the second laboratory session. This study suggests that bupropion may be maintaining physiological measures of stress during the nicotine withdrawal period.

Adult↗

PubMed2005

Treatment of residual anxiety symptoms with adjunctive aripiprazole in depressed patients taking selective serotonin reuptake inhibitors.

BACKGROUND: Depression and anxiety are common disorders and have substantially overlapping symptom complexes. Not surprisingly, treatment approaches are similar for both conditions with the selective serotonin reuptake inhibitors (SSRIs) as the initial therapy of choice. However, after first line treatments have been deployed, residual symptoms are often problematic. Augmentation strategies to address these difficulties are an area of active investigation. This study assessed aripiprazole as adjunctive therapy to SSRIs for patients with persistent anxiety symptoms complicating a depression or anxiety disorder. METHODS: Ten patients who had been receiving SSRIs for at least 6 weeks, but still had clinically significant anxiety symptoms, were enrolled in an open label, flexibly-dosed study of adjunctive aripiprazole. Clinical status was assessed with the Hamilton Anxiety Rating Scale (HAM-A), Montgomery Asberg Rating Scale (MADRS), and Sheehan Disability Scale (SDS). RESULTS: Eighty percent of the subjects had a greater than 50% reduction of symptoms on these outcome measures by week 2 of therapy, and continued with further decrements in symptoms throughout the course of the study. CONCLUSIONS: The results of this trial provide preliminary evidence that aripiprazole may be an effective adjunctive treatment in individuals on SSRIs with residual symptoms of anxiety or depression. More rigorous double-blind studies are warranted to confirm and elucidate the potential role of aripiprazole in these conditions.

Adult↗

PubMed2005

Inhibition of CYP2D6 activity by bupropion.

The purpose of this study was to assess the effect of bupropion on cytochrome P450 2D6 (CYP2D6) activity. Twenty-one subjects completed this repeated-measures study in which dextromethorphan (30-mg oral dose) was administered to smokers at baseline and after 17 days of treatment with either bupropion sustained-release (150 mg twice daily) or matching placebo. Subjects quit smoking 3 days before the second dextromethorphan administration. To assess CYP2D6 activity, urinary dextromethorphan/dextrorphan metabolic ratios were calculated after an 8-hour urine collection. Thirteen subjects received bupropion, and 8 received placebo. In those receiving active medication, the dextromethorphan/dextrorphan ratio increased significantly at the second assessment relative to the first (0.012 +/- 0.012 vs. 0.418 +/- 0.302; P < 0.0004). No such change was observed in those randomized to placebo (0.009 +/- 0.010 vs. 0.017 +/- 0.015; P = NS). At baseline, all subjects were phenotypically extensive CYP2D6 metabolizers (metabolic ratio <0.3); after treatment, 6 of 13 subjects receiving bupropion, but none of those receiving placebo, had metabolic ratios consistent with poor CYP2D6 metabolizers. Bupropion is therefore a potent inhibitor of CYP2D6 activity, and care should be exercised when initiating or discontinuing bupropion use in patients taking drugs metabolized by CYP2D6.

Adult↗

PubMed2005

Update on drug-induced depression in the elderly.

BACKGROUND: Depression is a common disorder in the elderly. Use of certain medications may be a potentially preventable cause of new-onset depression or worsening of established depression. OBJECTIVE: This paper reviews recent publications evaluating medications commonly used in the elderly as potential causes of depressive symptoms. METHODS: Relevant articles examining the association between medication use and symptoms of depression were identified through searches of MEDLINE (1996-March 2005) and International Pharmaceutical Abstracts (1996-March 2005) using the MeSH heading depression and the subheading chemically induced. Included articles were limited to those that discussed medications commonly used in the elderly and that employed a rigorous study design. RESULTS: A wide variety of medications have been implicated as potential causes of depressive symptoms in numerous reports, although many of these reports relied on data obtained from observational rather than experimental studies. The most extensively studied agents include anti hypertensives, lipid-lowering drugs, and selective estrogen-receptor modulators. The data on antihypertensive agents were contradictory; however, most studies found no association between use of the newer lipid-lowering drugs (statins) or selective estrogen-receptor modulators and the emergence of depressive symptoms. Corticosteroids, although not studied recently, generally have been associated with depressive symptoms in the older literature. CONCLUSIONS: The recent data evaluating whether medications can induce or worsen symptoms of depression are largely contradictory. This reflects a relative lack of controlled studies of this association and the difficulties in determining whether depressive symptoms are caused by a particular medication or by other factors. Nonetheless, when new or worsening symptoms of depression occur, medications should be considered a potential cause and withdrawn as appropriate. Nonpharmacologic and/or pharmacologic treatment is indicated for those whose depressive symptoms do not resolve.

Adrenal Cortex Hormones↗

PubMed2004

Preliminary experience with adjunctive quetiapine in patients receiving selective serotonin reuptake inhibitors.

Treatment of depression and anxiety disorders with selective serotonin reuptake inhibitors (SSRIs) has been shown by numerous studies to be generally effective. Less well understood is how clinically to address the residual anxiety symptoms a significant minority of such patients treated with SSRIs continue to experience. We assessed quetiapine as adjunctive therapy to SSRIs for patients with anxiety symptoms complicating a depressive or anxiety disorder. Patients receiving a stable dosage of an SSRI for at least 6 weeks who also had persistent anxiety symptoms (Hamilton Anxiety scale [HAM-A] > or =16), were enrolled in a 9-week, open-label, variable dose study. Changes in clinical status were assessed with the Hamilton Depression Rating Scale (HAM-D), HAM-A, and State Anxiety Inventory (SAI). Statistically and clinically significant reductions of > or =50% in the HAM-D and HAM-A occurred by the second week of treatment in 10 of the 11 patients. These improvements continued throughout the study along with a significant improvement on the SAI scale. The most frequent side effects reported were mild dry mouth, constipation, and transient drowsiness with dose escalation. The results provide evidence that quetiapine may be an effective adjunctive treatment for recalcitrant anxiety symptoms in individuals treated with SSRIs for either anxiety or depressive disorders. Given the open-label design of the trial, more rigorous studies are clearly indicated.

Dibenzothiazepines↗

PubMed2003

Premature ejaculation associated with citalopram withdrawal.

OBJECTIVE: To report a case of premature ejaculation occurring subsequent to citalopram discontinuation. CASE SUMMARY: A 43-year-old white man being treated for depression with citalopram wished to discontinue treatment. Four or 5 days after stopping citalopram he reported that, during sexual intercourse, his genitals seemed to be extremely sensitive and orgasm was achieved within approximately 1 minute. These symptoms continued over the next 3-4 weeks and remitted after citalopram was restarted. Several subsequent attempts to discontinue citalopram resulted in a return of these symptoms despite using a slow tapering regimen. An objective causality assessment revealed a probable relationship between drug withdrawal and the observed symptoms. DISCUSSION: The ability of selective serotonin-reuptake inhibitors (SSRIs) to delay ejaculation has been well documented; however, discontinuation of these agents generally results in a return to baseline function. Although discontinuation of SSRI therapy has been associated with a number of withdrawal symptoms, this is the first report (MEDLINE, September 2003), to our knowledge, of the emergence of sexual adverse effects in someone with no previous history of these symptoms. CONCLUSIONS: Premature ejaculation is a possible withdrawal effect after SSRI discontinuation. Since patients are usually reluctant to spontaneously report sexual adverse effects, it is important to specifically inquire about them both when starting and stopping treatment with an SSRI.

Adult↗

PubMed2002

A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling.

BACKGROUND: This randomized, double-blind, placebo-controlled study investigated the efficacy and tolerability of paroxetine in the treatment of pathological gambling. METHOD: Patients fulfilling DSM-IV criteria for pathological gambling and scoring > or = 5 on the South Oaks Gambling Screen were enrolled if no other Axis I disorder was present. A 1-week placebo run-in phase was followed by 8 weeks' treatment with paroxetine or placebo. The initial paroxetine dose of 20 mg/day could be increased after week 2 by 10 mg/week to a maximum of 60 mg/day. Changes in clinical status were assessed using the Gambling Symptom Assessment Scale (G-SAS) and the Clinical Global Impressions scale (CGI). Treatment-emergent symptoms were assessed weekly. RESULTS: Forty-five patients were included in an intent-to-treat analysis (N = 23 paroxetine, N = 22 placebo). Statistically significantly greater reductions in the total score of the G-SAS were observed in the paroxetine group compared with the placebo group at weeks 6 through 8 (p = .003, .003, and .042, respectively). Improvement on the CGI was also significantly greater in the paroxetine than in the placebo group at the same timepoints (p = .033, .014, and .025, respectively). A significantly greater proportion of patients in the paroxetine group were responders at weeks 7 and 8 (p = .011 and .010, respectively). CONCLUSION: The results of this trial indicate that paroxetine may be effective in the treatment of pathological gambling. There were no unexpected side effects from this treatment. However, additional studies with larger patient samples and a longer treatment phase are required to establish conclusively the efficacy and safety of paroxetine for this indication.

Disruptive, Impulse Control, and Conduct Disorders↗