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The metabolic fate of [14C]oxaprotiline.HCl in man. II. Isolation and identification of metabolites.

The new antidepressant agent oxaprotiline is extensively metabolized by man. Following an oral 50 mg dose of racemic [14C]oxaprotiline, most of the 14C was excreted in the urine as metabolites (greater than 98% total 14C); only 1% was excreted unchanged. Glucuronidation at the carbinol group of the molecule is the major metabolic pathway (83%). The two diastereoisomeric glucuronides were separated; the more polar O-glucuronide of S(+)-oxaprotiline predominates (44%), suggesting stereoselective disposition of the two enantiomers. Oxidative pathways are minor, and yield desmethyl oxaprotiline (10%) and 3-hydroxy R(-)-oxaprotiline (4%), both of which are conjugated with glucuronic acid. The biotransformation of oxaprotiline in man is less complex than that of other polycyclic antidepressants, which are metabolized mainly by oxidative reactions.

Anthracenes↗

Pharmacotherapy of early-onset depression. Update and new directions.

Although an increased recognition of depressive disorders in youth represents a positive conceptual change over the past decades, there still is a very limited amount of research on useful treatment interventions. The paucity of data is particularly keen for the use of psychotropic drugs. For example, by applying the criteria suggested by the International Psychopharmacology Algorithm Project, there barely are enough first-grade ("Level A," meaning at least two RCTs) data supporting the short-term efficacy of antidepressants (the SSRIs) in the treatment of juvenile depression. And yet, limited data have not translated into limited use in routine clinical practice. In fact, the use of antidepressant medications has increased exponentially over the last decade, a change that is especially conspicuous for individuals less than 18 years of age. The perceived safety of the SSRIs and other novel antidepressants is partly at the root of their increased popularity. Data regarding their safety are likewise quite limited, however, and essentially are nonexistent for longer-term use. Based on the reviewed data, a medication algorithm for the treatment of early-onset depression can be suggested (Fig. 1). The algorithm underscores the need for adequate evaluation and diagnostic assessment, with particular attention to comorbid conditions (such as a bipolar diathesis) that may dictate alternative treatment strategies. In general, psychotherapy is the initial approach to juvenile MDD, with medication use reserved for more severe cases or those not responding to psychotherapy alone. Given that only two types of psychotherapy and two SSRIs have adequate controlled short-term efficacy data, all but the initial steps must be undertaken guided by clinical judgment and an individualized risk-benefit analysis. An algorithm such as this one, based on the very limited efficacy and safety data available, may be viewed as setting priorities for a comprehensive research agenda, more than dictating rigid treatment guidelines. In closing, it can be suggested that future research on the pharmacotherapy of early-onset depressive disorder pay particular attention to the following three aspects: 1. Too many drugs, too few data: Rapid advances in drug development have led to a plethora of available antidepressant agents. It is clear that there are many more agents available than can be adequately studied at present. Because many such agents are mechanistically similar, if not identical, it may be wise to focus research efforts on truly novel agents, particularly those (such as the CRH receptor antagonists, or those affecting neurosteroidogenesis) whose action is based on preclinical and clinical pathophysiologic disease paradigms. 2. Longitudinal follow-up and maintenance studies: Essentially all reviewed treatment studies have been short-term trials. There is a marked paucity of longer-term follow-up data, or of naturalistic and "real-world" effectiveness studies. For example, one of the few studies addressing maintenance pharmacotherapy for early-onset depression has demonstrated surprisingly high recurrence rates, even for those subjects actively on maintenance medication. 3. Long-term safety: Clinicians and parents alike often face difficult decisions regarding the long-term exposure of antidepressant drugs on the developing brain. Although no definitive long-term safety data are likely to become available anytime soon, real risks, such as suicide, and potential sequelae of long-term exposure to the underlying illness itself need all to be part of any decision-making process. Preclinical studies have shown that brain-derived neurotrophic factor (BDNF) levels can be upregulated by antidepressants, and low BDNF factors have been associated with atrophic brain changes in recurrent forms of adult MDD. Although these observations require specific application to juvenile forms of the disorder, they raise the exciting prospect that the natural course of the illne

Adolescent↗

2-(Methyleneaminoxy)methylmorpholine derivatives. Synthesis and antidepressant activity.

The 3-(methyleneaminoxy)methylmorpholines 2 were synthesized as analogues of viloxazine 1, an antidepressant drug, in which the aryloxymethyl group is substituted by a (methyleneaminoxy)methyl moiety (MAOMM). Compounds 2 were tested as potential antidepressant agents by using the test of antagonism to reserpine-induced hypothermy in mice. In addition, their anticholinergic and antihistaminic activity on isolated preparations and their ability to antagonize the toxicity induced by adrenaline in mice were evaluated. "In vivo" and "in vitro" tests showed that some compounds of type 2 possess a pharmacological profile similar to that of viloxazine 1.

Animals↗

Prevalence of depression and its treatment in an elderly population: the Cache County study.

BACKGROUND: Previous estimates of the prevalence of geriatric depression have varied. There are few large population-based studies; most of these focused on individuals younger than 80 years. No US studies have been published since the advent of the newer antidepressant agents. METHODS: In 1995 through 1996, as part of a large population study, we examined the current and lifetime prevalence of depressive disorders in 4,559 nondemented individuals aged 65 to 100 years. This sample represented 90% of the elderly population of Cache County, Utah. Using a modified version of the Diagnostic Interview Schedule, we ascertained past and present DSM-IV major depression, dysthymia, and subclinical depressive disorders. Medication use was determined through a structured interview and a "medicine chest inventory." RESULTS: Point prevalence of major depression was estimated at 4.4% in women and 2.7% in men (P= .003). Other depressive syndromes were surprisingly uncommon (combined point prevalence, 1.6%). Among subjects with current major depression, 35.7% were taking an antidepressant (mostly selective serotonin reuptake inhibitors) and 27.4% a sedative/hypnotic. The current prevalence of major depression did not change appreciably with age. Estimated lifetime prevalence of major depression was 20.4% in women and 9.6% in men (P<.001), decreasing with age. CONCLUSIONS: These estimates for prevalence of major depression are higher than those reported previously in North American studies. Treatment with antidepressants was more common than reported previously, but was still lacking in most individuals with major depression. The prevalence of subsyndromal depressive symptoms was low, possibly because of unusual characteristics of the population.

Age Factors↗

"Cade's disease" and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder.

The diagnosis and treatment of bipolar disorder (BD) has been inconsistent and frequently misunderstood in recent years. To identify the causes of this problem and suggest possible solutions, we undertook a critical review of studies concerning the nosology of BD and the effects of antidepressant agents. Both the underdiagnosis of BD and its frequent misdiagnosis as unipolar major depressive disorder (MDD) appear to be problems in patients with BD. Underdiagnosis results from clinicians' inadequate understanding of manic symptoms, from patients' impaired insight into mania, and especially from failure to involve family members or third parties in the diagnostic process. Some, but by no means all, of the underdiagnosis problem may also result from lack of agreement about the breadth of the bipolar spectrum, beyond classic type I manic-depressive illness (what Ketter has termed "Cade's Disease"). To alleviate confusion about the less classic varieties of bipolar illness, we propose a heuristic definition, "bipolar spectrum disorder." This diagnosis would give greater weight to family history and antidepressant-induced manic symptoms and would apply to non-type I or II bipolar illness, in which depressive symptom, course, and treatment response characteristics are more typical of bipolar than unipolar illness. The role of antidepressants is also controversial. Our review of the evidence leads us to conclude that there should be less emphasis on using antidepressants to treat persons with this illness.

Antidepressive Agents↗

Effects of fish oil on the central nervous system: a new potential antidepressant?

In the last 100 years major depression has increased worldwide. In this study we provided coconut fat (CF, rich in saturated fatty acids) or fish oil (FO, rich in n-3 polyunsaturated fatty acids) to female rats throughout pregnancy and lactation and then to their offspring post-weaning and examined lipid brain profile and the possible effect of FO as antidepressant agent in the offspring in adulthood (F1). Rats were submitted to forced swimming test, elevated plus maze, Morris water maze and open field. Peroxidation rate in the cerebral cortex and hippocampus were measured. Docosahexaenoic acid (DHA) concentration in dam's milk, eicosapentaenoic acid (EPA) and DHA concentration in hippocampus and cerebral cortex from F1 rats FO supplemented increased significantly when compared to control (C) and CF rats. Arachidonic acid/EPA ratio in the cerebral cortex and hippocampus decreased in rats submitted to forced swimming test. Peroxidation rate were not different between the groups. Immobility time in the forced swimming test in FO group was reduced (p < 0.01) when compared to C and CF rats. We conclude that lifelong intake of FO was able to induce an antidepressant effect with EPA and DHA concentration increased in the cerebral cortex and hippocampus.

Animals↗

Mania associated with St. John's wort.

BACKGROUND: St. John's wort, the popular herbal remedy touted as an antidepressant, is generally thought to be benign, with few reported side effects. Given its possible efficacy as an antidepressant, evaluation of its propensity to cause affective switching should be evaluated. METHODS: This report presents two cases of mania temporally associated with the use of St. John's wort (hypericum). RESULTS: As with other antidepressant agents, St. John's wort may precipitate hypomania, mania, or an increased cycling of mood states, particularly in patients with occult bipolar disorder. CONCLUSIONS: Because the majority of people who take this popular over-the-counter preparation do so without formal psychiatric evaluations, risk of hypericum-induced mania may be significant. Physicians should screen patients for a history of hypomania or mania before recommending use of St. John's wort for depression.

Adult↗

Thyrotropin releasing hormone (TRH) as a possible quick-acting but short-lasting antidepressant.

In a double reversal design the potency of thyrotropin releasing hormone (TRH) (500 mug intravenously) as a quick-acting antidepressive agent was evaluated. A first injection did seem to give rise to a very slight short-lasting effect, though this could not be ascertained clearly. There were no visible effects after a second injection. The thyroid stimulating hormone (TSH) response curve after TRH administration in the depressive patients group was blunted in comparison with that in a matched control group of normals.

Adult↗

[Depression in primary health care; international data on prevalence and treatment, among others from The Netherlands].

OBJECTIVE: To establish the prevalence of depression and other psychiatric disorders in the contact population of primary care physicians (PCPs) in several countries. DESIGN: Descriptive. SETTING: World Health Organization (WHO), Geneva, Switzerland. METHOD: The WHO carried out a study in 15 centers in 14 different countries, including the Groningen centre in the Netherlands. This study comprised interviewing 5438 patients with the primary health care version of the 'Composite international diagnostic interview' (CIDI). The PCPs also evaluated their patients' somatic and psychic health. RESULTS: Depression was found to be seen at all centres, according to the CIDI results as well as according to the physicians. Most patients with a depression were treated by the PCPs themselves; only a small proportion were referred. As regards pharmacotherapy, in most centres tranquillizers were prescribed more often than antidepressive agents. Groningen differed from the other centres in that a larger proportion of depressive patients attended the PCPs for a psychological reason for encounter, and in that the patients' somatic health was classified as much better. The Groningen PCPs referred to institutes for mental health care more often than the PCPs in most other centres. CONCLUSION: Depression was diagnosed in all participating countries, both by PCPs and with the aid of the CIDI results.

Antidepressive Agents↗

Antidepressant-related erectile dysfunction: management via avoidance, switching antidepressants, antidotes, and adaptation.

The ideal antidepressant would control depression with no adverse effect on sexual function. Erectile dysfunction and other sexual dysfunction associated with antidepressant medication treatment are problems with many antidepressants and can lead to patient dissatisfaction and decreased compliance with treatment. A computerized MEDLINE search (English language, 1966-2003) was performed using the terms antidepressive agents, erectile dysfunction, and sexual dysfunction. Emphasis was placed on studies with specific sexual function measurements taken before and after treatment and placebo control. Mixed mediator, nonserotonergic antidepressants that block postsynaptic serotonin type 2 receptors (nefazodone, mirtazapine) or that primarily increase dopamine or norepinephrine levels (bupropion) were thought to be good choices for avoiding antidepressant-associated sexual dysfunction or for switching patients in whom antidepressant-associated sexual dysfunction emerged. Comparisons with serotonin reuptake inhibitors (SRIs) have revealed less desire and orgasm dysfunction with nonserotonergic bupropion, less orgasm dysfunction with nefazodone, and superior overall satisfaction with sexual functioning with bupropion or nefazodone. However, most of these studies have design flaws that make evidence-based claims of efficacy difficult to substantiate. Agents proposed for antidote use in antidepressant-associated sexual dysfunction have either not been studied in men or not proved efficacious in randomized placebo-controlled trials. Switching to and augmentation with bupropion or nefazodone have also not clearly shown efficacy in controlled trials and require care and monitoring to avoid SRI discontinuation symptoms and loss of antidepressant efficacy. Few proposed treatment options, apart from avoidance, have proved effective for antidepressant-associated sexual dysfunction, which can have negative consequences on depression management.

Antidepressive Agents↗

Use of placebo control groups in evaluating efficacy of treatment of unipolar major depression.

Double-blind, random-assignment placebo-controlled trials are routinely used in evaluating efficacy of potential antidepressant agents. In recent years concern has risen that placebo response rates in unipolar depression are too high, and this has eroded confidence in both old and new agents. At the same time, the use of placebos has been questioned by patients and their advocates. We review factors that have been commonly explored as associated with placebo response (e.g., length of episode, severity, subtype), as well as issues in methodology (e.g., interrater reliability, statistical artifacts). We discuss possible methods of dealing with the problem of placebo response, emphasizing reconceptualizing effect sizes to design more powerful single trials and a systematic sequence of trials to achieve the right answers.

Antidepressive Agents↗

Paroxetine: an overview of the efficacy and safety of a new selective serotonin reuptake inhibitor in the treatment of depression.

Paroxetine is a novel phenylpiperidine compound that is a potent and selective serotonin reuptake inhibitor. It has little affinity for alpha-adrenergic, dopamine, histamine, and cholinergic receptors. The pharmacokinetic properties of paroxetine are well suited to clinical use. Its bioavailability is not affected by food or antacids; its mean half-life of about 24 hours is consistent with once-a-day dosing; also, it has no pharmacologically active metabolites. In clinical studies involving over 6,700 patients worldwide, the efficacy of paroxetine has been shown consistently to be superior to placebo and comparable to tricyclic antidepressant agents in the treatment of depression. During these trials, paroxetine was used in a broad range of depressed patients, including the moderately to severely depressed, the elderly, and patients whose depressions were accompanied by symptoms of anxiety. In addition, it has been shown to be effective for the prevention of depressive relapse during long-term treatment. Side effects associated with paroxetine tend to be relatively mild, transient, and easily managed. As with other selective serotonin reuptake inhibitors, the most common side effect associated with paroxetine treatment is nausea, although this effect rarely leads to dose reduction or drug discontinuation. Paroxetine should not be coadministered with monoamine oxidase inhibitors or L-tryptophan. Animal data and limited clinical experience suggest that paroxetine is considerably safer in overdose than are tricyclic antidepressant drugs.

Adolescent↗

Serotonin syndrome and rhabdomyolysis in venlafaxine poisoning: a case report.

Newer, more selective, antidepressant agents are increasingly being used as first-line treatment. However, clinical experience in patients after a deliberate overdose is limited. We present a case of venlafaxine intoxication complicated by a late rise in creatine kinase, seizures and serotonin syndrome. Rhabdomyolysis prolonged the hospital stay in our patient but had no other serious consequences. Physicians should be aware of this late phenomenon in patients with venlafaxine poisoning.

Adult↗

The novel antidepressant, tianeptine, reduces stress-evoked stimulation of the hypothalamo-pituitary-adrenal axis.

The possible effect of tianeptine, a novel antidepressant agent, on the neuroendocrine response to stress was investigated in adult male rats. Tube restraint stress for 30 min induced a marked increase of plasma ACTH and corticosterone. A single i.p. injection of tianeptine (10 mg/kg), 120 min before stress caused a significant decrease of ACTH and corticosterone levels. In order to investigate the kinetics of the effect of tianeptine, the drug was injected at various times (from 15 min to 12 h) before restraint stress. The inhibitory effect of tianeptine on stress-induced elevations of plasma ACTH and corticosterone occurred from 1 to 3 h after the injection. Administration of increasing doses of tianeptine revealed that only the highest doses (10 and 20 mg/kg) had a significant effect on stress-evoked stimulation of ACTH and corticosterone secretion. These results show that the antidepressant, tianeptine, reduces the activation of the hypothalamo-pituitary-adrenal (HPA) axis induced by restraint stress. Since depressed patients generally exhibit an elevated cortisol level, the present data suggest that part of the therapeutic properties of tianeptine could be accounted for by the effect of this antidepressant to modulate the activity of the HPA axis.

Adrenocorticotropic Hormone↗

Comparative effects of trazodone and tricyclic antidepressants on uptake of selected neurotransmitters by isolated rat brain synaptosomes.

The effect of trazodone, a new antidepressant agent, on uptake of serotonin (5-HT), norepinephrine (NE), and dopamine (DA) by crude synaptosome preparations from rat hypothalamus was compared with imipramine, desipramine, and clomipramine. Trazodone was determined to be a very selective inhibitor of the 5-HT uptake mechanism with IC50 values of 5.67 X 10(-7), 3.54 X 10(-5), and 5.25 X 10(-5 M, for 5-HT, NE, and DA uptake, respectively. Clomipramine, the only other selective inhibitor of 5-HT uptake studied, had IC50 values of 7.59 X 10(-9), 1.12 X 10(-7), and 2.51 X 10(-7) M, for 5-HT, NE, and DA, respectively. Although less potent, trazodone was 4 +/- 0.6 times more selective than clomipramine in its ability to inhibit synaptosomal uptake of 5-HT with respect to NE. This selectivity for the 5-HT uptake mechanism is consistent with the clinical antidepressant efficacy of trazodone.

Animals↗

Artefactual inhibition of dopamine uptake by psychotropic drugs on striatal synaptosomal preparation.

On striatal synaptosomal preparations, using a double labelling test, numerous antidepressant drugs demonstrated an inhibitory effect on [3H]DA uptake at the same high concentrations producing a [14C]DA release. This releasing effect was also shared by non-antidepressant agents and was observed on synaptosomes preloaded with [3H]5HT. The imipramine-induced release of DA was not modified by increasing concentration of K+, by decreasing concentration of Na+, by deleting Ca2+ from the incubation medium, or by blocking the catecholamine uptake systems with nomifensine or cocaine. The imipramine effect was reversible and was possibly initiated by a transient physico-chemical modification of the synaptosomal membrane. It was concluded that the DA uptake carrier is probably not involved in the effect of these drugs.

Animals↗

Uptake and disappearance of 4-methyl-alpha-ethylmetatyramine in relation to its releasing action on 5-hydroxytryptamine in the brain.

4-Methyl-alpha-ethylmetatyramine (H75/12) was given intraperitoneally to mice and rats. At various time intervals the animals were killed and the concentration of H75/12 and 5-hydroxytryptamine (5-HT) in the brain and of H75/12 in the heart and, in some cases, in plasma was determined. H75/12 was rapidly taken up by the heart and then disappeared bi- or multiphasically. A maximum concentration of about 6 mug/g was obtained in the brain 30--60 min after the administration of 25 mg/kg. H75/12 disappeared from the brain with a half-life of 1.0 and 1.5 hrs in the mouse and rat, respectively. In the mouse the relative uptake of H75/12 increased with the dose given, i.e. the dose-uptake curve had an upward bending. Significant release of 5-HT in the brain was obtained after a single injection of 25 and 100 mg/kg in the rat and mouse, respectively. The 5-HT release was prevented by tricyclic, antidepressive agents, particularly by chlorimipramine. However, these agents had no certain effect of the uptake of H75/12 in the brain. Moreover, it was not possible to demonstrate a decreased uptake of H75/12 in the rat brain after a chronic, transverse cerebral hemisection, although the monoamine-containing neurones had degenerated as indicated by a complete disappearance of 5-HT. It is concluded that only a minor part of the H75/12 measured is located in monoaminergic neurones. The uptake of H75/12 in the rat brain appeared to be increased in starving animals, possibly indicating decreased metabolism of the drug.

Animals↗