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At least 865 records · Page 48Linked to original sources
PubMed1997

The utilization of antidepressants--a key issue in the prevention of suicide: an analysis of 5281 suicides in Sweden during the period 1992-1994.

Antidepressants detected by the National Department of Forensic Chemistry in 5281 suicides in Sweden during the period 1992-1994 were related to data on usage expressed in person-years of exposure. Antidepressants were detected in 874 subjects (16.5%). In relation to their use, fluvoxamine, citalopram, moclobemide, mianserin and trimipramine were found more often than the reference drug, amitriptyline (i.e. over-risks). Toxic concentrations of antidepressants were detected in 232 subjects (4.4%). Most people committing suicide were not taking antidepressants immediately before their death, even though 40-85% may have been depressed. Undertreatment and therapeutic failure are the main problems with antidepressants, not the risk of using antidepressants in overdose. Comparisons of new antidepressants should focus on efficacy in relation to reference tricyclics. The huge increase in the use of antidepressants in Sweden since 1990-1991 has been paralleled by a significant decrease in suicide rates.

Amitriptyline↗
PubMed1998

Economic comparisons of the pharmacotherapy of depression: an overview.

As many countries find that their health care expenditure is taking up an increasing proportion of their financial resources, economic aspects of care processes have become more important in the choice of optimal strategies. This review of the economic studies of the comparative treatment of depression shows that nearly every aspect of treatment has important economic consequences. Cost-of-illness studies have documented the high burden on society of this disorder, and the associated loss of productivity and work. Comparative cost-effectiveness/utility studies, the majority of which are based on modelling techniques, have consistently shown a better cost-effectiveness ratio of the newer antidepressants over more traditional tricyclic antidepressants (TCAs), when all therapy-related costs are taken into account.

Antidepressive Agents↗
PubMed2003

Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants.

Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Nocturnal enuresis: a placebo controlled trial of two antidepressant drugs.

A multicentre, randomised, double blind treatment trial was set up comparing imipramine (a tricyclic antidepressant with anticholinergic action), mianserin (a quadricyclic antidepressant without anticholinergic activity), and placebo, (a) possibly to identify an effective alternative drug and (b) to elucidate the action of imipramine in enuretic children. Eighty children (65 boys, 15 girls) aged 5-13 years, wet three or more nights a week, were studied. Exclusions were a urinary tract infection or abnormality, other organic illness, or severe emotional disorders. After a four week assessment, 25 children were randomised to eight weeks' treatment with imipramine 25 mg, 26 to mianserin 10 mg and 29 to placebo, followed by four weeks without treatment. Dry nights and a wetness score were recorded throughout. During treatment, imipramine was superior to both placebo and mianserin (p < 0.001) in achieving dry nights and reducing wetness scores. It led to a definite improvement in 72% of children. Mianserin produced a mildly beneficial effect that was not superior to placebo. No side effects were recorded. Mianserin would not be a satisfactory alternative treatment for nocturnal enuresis. The efficacy of imipramine is unlikely to be the result of its antidepressant activity.

Adolescent↗
PubMed2003

Antidepressant induced cholestasis: hepatocellular redistribution of multidrug resistant protein (MRP2).

BACKGROUND: We report two cases of antidepressant induced cholestasis. CASE REPORTS: We describe the first reported case of acute cholestasis due to citalopram (selective serotonin reuptake inhibitor) occurring in a patient who also experienced obstetric cholestasis in association with each of three pregnancies; in a second patient cholestasis developed due to dothiepin (tricyclic antidepressant), and six years later due to paroxetine. In both cases liver biopsies showed features of a "pure" cholestasis with total resolution within 1-6 months after withdrawal of the causative drug. Immunostaining for the canalicular transporter, multidrug resistant protein 2 (MRP2), responsible for biliary secretion of several organic anions including bilirubin glucuronides, showed sustained expression in both biopsies as well as relocalisation with appearance of strong staining of the basolateral membrane of the hepatocyte. This finding has also not been reported previously. CONCLUSIONS: We postulate that intracellular redistribution of MRP2 may reflect an adaptive compensatory mechanism which helps in the elimination of the drug or its cholestatic metabolites from the hepatocyte back to the sinusoidal space and subsequent excretion in urine. Changes seen in these two patients differ from findings previously reported in rats where downregulation of mrp2 occurs in response to experimentally induced cholestasis. We speculate that the rat is more advanced than humans in its ability to downregulate canalicular transporter expression as protection against progressive intrahepatic cholestasis.

Acute Disease↗
PubMed2006

Tranylcypromine versus venlafaxine plus mirtazapine following three failed antidepressant medication trials for depression: a STAR*D report.

OBJECTIVE: The purpose of this study was to compare the effectiveness and tolerability of tranylcypromine and combination treatment with extended-release venlafaxine and mirtazapine in patients with treatment-resistant major depression whose current depressive episode had not responded adequately to treatment in three prior prospective medication trials. METHOD: Adult outpatients with nonpsychotic major depressive disorder who had not achieved remission or had withdrawn from treatment because of intolerance in three previous prospective medication trials were randomly assigned to receive open-label treatment with either tranylcypromine (N=58) or extended-release venlafaxine plus mirtazapine (N=51). The primary outcome measure was whether patients achieved remission, which was defined as a score < or =7 at exit on the 17-item Hamilton Depression Rating Scale (HAM-D). The HAM-D was administered by telephone by raters to whom treatment was masked. RESULTS: Remission rates were not significantly different between the two treatment groups (6.9% for the tranylcypromine group and 13.7% for the venlafaxine plus mirtazapine group). The mean daily dose at exit for tranylcypromine was 36.9 mg (SD=18.5); for venlafaxine, 210.3 mg (SD=95.2); and for mirtazapine, 35.7 mg (SD=17.6). Tranylcypromine was associated with significantly less symptom reduction and greater attrition due to intolerance. CONCLUSIONS: Remission rates were modest for both the tranylcypromine group and the extended-release venlafaxine plus mirtazapine group, and the rates were not statistically different between groups. The lower side effect burden, lack of dietary restrictions, and ease of use of venlafaxine and mirtazapine suggest that this combination may be preferred over tranylcypromine for patients with highly treatment-resistant depression who have not benefited adequately from several prior treatments.

Adult↗
PubMed2003

Mortality and poststroke depression: a placebo-controlled trial of antidepressants.

OBJECTIVE: Poststroke depression has been shown to increase mortality for more than 5 years after the stroke. The authors assessed whether antidepressant treatment would reduce poststroke mortality over 9 years of follow-up. METHOD: A total of 104 patients were randomly assigned to receive a 12-week double-blind course of nortriptyline, fluoxetine, or placebo early in the recovery period after a stroke. Mortality data were obtained for all 104 patients 9 years after initiation of the study. Demographic and clinical measurements were collected at 3, 6, 9, 12, 18, and 24 months after the stroke. Survival data were analyzed by using the Kaplan-Meier method. RESULTS: Of the 104 patients, 50 (48.1%) had died by the time of the 9-year follow-up. Of 53 patients who were given full-dose antidepressants, 36 (67.9%) were alive at follow-up, compared with only 10 (35.7%) of 28 placebo-treated patients, a significant difference. Logistic regression analysis showed that the beneficial effect of antidepressants remained significant both in patients who were depressed and in those who were nondepressed at enrollment, after the effects of other factors associated with mortality (i.e., age, coexisting diabetes mellitus, and chronic relapsing depression) were controlled. There were no intergroup differences in severity of stroke, impairment in cognitive functioning and activities of daily living impairment, and other medications received. CONCLUSIONS: Treatment with fluoxetine or nortriptyline for 12 weeks during the first 6 months poststroke significantly increased the survival of both depressed and nondepressed patients. This finding suggests that the pathophysiological processes determining the increased mortality risk associated with poststroke depression last longer than the depression itself and can be modified by antidepressants.

Adrenergic Uptake Inhibitors↗
PubMed2006

Inhibition of N-methyl-D-aspartate receptor function appears to be one of the common actions for antidepressants.

In order to explore the possible common action mechanisms of three kinds of classical antidepressants, inhibition of drugs on the N-methyl-D-aspartate (NMDA)-Ca(2)-nitric oxide synthase (NOS) signal pathway was observed. With 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and lactic dehydrogenase (LDH) assay, classical antidepressants, desipramine (1, 10 microM), fluoxetine (0.625-10 microM) or moclobemide (2.5, 10 microM) antagonized NMDA 300 M induced-lesion in PC12 cells. Using fura-2/AM (acetoxymethyl ester) labelling assay, desipramine or fluoxetine at doses 1, 5 microM attenuated the intracellular Ca(2) overload induced by NMDA 200 microM for 24 h in PC12 cells. Meanwhile, using confocal microscope, it was also found that desipramine 5 microM, fluoxetine 2.5 microM or moclobemide 10 microM decreased the NMDA 20 microM induced intracellular Ca(2) overload in primarily cultured rat hippocampal neurons. Furthermore, desipramine (1, 5 microM), fluoxetine (1, 5 microM) or moclobemide (2.5, 10 microM) significantly inhibited NOS activity in NMDA (300 microM) treated PC12 cells for 4h. In summary, we suggest that inhibition on the function of NMDA-Ca(2) -NOS signal pathway appears to be one of the common actions for antidepressants despite their remarkably different structures, which is expected to have great implication for the evaluation and screening in vitro of new antidepressants.

Animals↗
PubMed1998

The serotonin transporter: a primary target for antidepressant drugs.

The serotoninergic system is known to modulate mood, emotion, sleep and appetite and thus is implicated in the control of numerous behavioural and physiological functions. Decreased serotoninergic neurotransmission has been proposed to play a key role in the aetiology of depression. The concentration of synaptic serotonin is controlled directly by its reuptake into the pre-synaptic terminal and, thus, drugs blocking serotonin transport have been successfully used for the treatment of depression. In addition to tricyclic antidepressants (TCAs; e.g. imipramine) which also block noradrenaline reuptake, highly specific serotonin reuptake inhibitors (SSRIs) such as fluoxetine and paroxetine have been developed, which are increasingly prescribed for depressed patients. The mode of action of these antidepressant drugs on their direct target, the serotonin transport protein, and possible regulatory mechanisms with respect to long-term alleviation of depression, although having been investigated both neurobiologically and clinically over the last years, are not yet understood. The cloning of the cDNA encoding the serotonin transporter has allowed a more precise characterization of this protein at the molecular level. This will show how antidepressants act at this target, thereby affecting the biochemical, pharmacological and electrophysiological properties of the serotoninergic system and give an introduction of how they might exert their therapeutic effect. This review gives an overview of the recent developments in this field, discusses mechanisms of antidepressant action on this target, and also possible interactions with other components of serotoninergic neurotransmission.

Antidepressive Agents↗
PubMed1998

Repeated administration of fluoxetine, desipramine and tranylcypromine increases dopamine D2-like but not D1-like receptor function in the rat.

We tested the effect of repeated treatment (twice daily for 14 days) of rats with the antidepressant drugs fluoxetine, desipramine and tranylcypromine, on the behavioural response to the non-selective dopamine (DA) receptor agonist, apomorphine, the D1-like receptor agonists, SKF 38393 and SKF 81297 and the D2-like receptor agonists, RU 24213 and quinpirole. Agonist-induced behaviour was monitored by automated activity meters and direct observation using a checklist scoring method. Fluoxetine, desipramine and tranylcypromine enhanced (albeit to a varying degree) the behavioural responses to apomorphine (0.75 mg/kg, s.c.), quinpirole (0.25 mg/kg, s.c.) and RU 24213 (0.75 mg/kg, s.c.). In contrast, fluoxetine, desipramine and tranylcypromine did not increase the behavioural responses to SKF 38393 (7.5 mg/kg, s.c.) and SKF 81297 (0.5 mg/kg, s.c.). Finally, fluoxetine, despiramine and tranylcypromine did not modify the behavioural responses to the concomitant administration of SKF 38393 (7.5 mg/kg, s.c.) and quinpirole (0.25 mg/kg, s.c.). Our data suggest that repeated administration of fluoxetine, desipramine and tranylcypromine increases central DA D2-like but not D1-like receptor function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2003

Chronic treatment with antidepressants decreases intraoperative core hypothermia.

UNLABELLED: We investigated temperature regulation during anesthesia and postoperative shivering in chronically depressed patients given antidepressant drugs. We studied 35 depressed patients and 35 control patients who underwent orthopedic surgery. Tympanic membrane temperatures 60, 75, and 90 min after induction in the depression group were significantly (P < 0.05) higher than those of the control group. There were no significant differences in mean skin temperature between the depression and the control groups. Eight of 35 patients in the depression group and 2 of 35 patients in the control group developed postanesthetic shivering. The incidence of shivering in the depression group was significantly more frequent than that in the control group (P = 0.04). The tympanic membrane temperature of the patients treated with clomipramine tended to be higher than that of the patients treated with maprotiline. In conclusion, intraoperative core hypothermia in chronically depressed patients was decreased. However, the incidence of shivering in depressed patients was significantly more frequent. IMPLICATIONS: Thermoregulation in chronically depressed patients is often altered. The alteration of body temperature is affected by depression itself and by antidepressants. General anesthesia has an influence on thermoregulatory control. However, temperature regulation during anesthesia in chronically depressed patients remains unclear.

Adult↗
PubMed1998

The effect of antidepressants on rat aggressive behavior in the electric footshock and apomorphine-induced aggressiveness paradigms.

The effects of acute antidepressant treatment were studied in the electric footshock and apomorphine-induced aggressiveness paradigms and found to be ineffective in both experimental models. In the apomorphine-induced aggressiveness test, 100 mg/kg L-tryptophan challenge manifested the antiaggressive effect of 10 mg/kg fluoxetine (a selective serotonin reuptake inhibitor) treatment. Thus, concomitant L-tryptophan plus fluoxetine treatment decreased the intensity of aggressive postures and increased the time of latency before first attack. In conclusion, our study demonstrates the involvement of the serotoninergic neurotransmission in the neurobiology of aggressive behavior, but after acute treatment in normal rats, the antidepressants do not elicit antiaggressive effects.

Aggression↗
PubMed2003

Antidepressant-induced hepatotoxicity.

Depression is a chronic, severe and increasingly prevalent illness associated with substantial morbidity, mortality and healthcare costs. Antidepressant drugs, the cornerstone of depression treatment, are not devoid of adverse effects, including hepatotoxicity. To review the risk of liver toxicity related to major antidepressants, the authors have followed structural criteria focusing on the underlying mechanism presumably involved and the role of particular chemical structures. The clinicopathological expression goes from transient increases in liver enzymes to fulminant liver failure. Classical antidepressants such as monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants (TCAs) seem to have the highest potential to induce liver damage compared with the newer drugs such as selective serotonin re-uptake inhibitors (SSRIs). The potential for severe hepatotoxicity associated with nefazodone is stressed. Guidelines for therapy and prevention of antidepressant-induced hepatotoxicity are also discussed.

Antidepressive Agents↗
PubMed2003

Safety of antidepressants in the elderly.

Until the 1980s, the two major classes of antidepressants, the tricyclics and the monoamine oxidase inhibitors (MAOIs), were effective but had severe side effects, requiring monitoring by psychiatrists. The past several years have brought new classes of antidepressants that are safer for the patient to take and far easier for the non-psychiatrist to prescribe. Whilst this is of enormous value, it leaves the physician with the dilemma of which one to prescribe. These new antidepressants cannot safely be used interchangeably. This paper will discuss each of the antidepressants presently available, with particular emphasis on safety in the elderly. Drug interactions, side effects and particular challenges to the older patient will be described. The authors will then advise a general strategy for prescribing antidepressants.

Aged↗
PubMed2003

Safety of antidepressant drugs in the patient with cardiac disease: a review of the literature.

Patients with cardiac disease, specifically ischemic heart disease and heart failure, have a higher frequency of major depressive disorder than patients without cardiac disease. The pathophysiologic reason for this is not completely understood. Previous depression, other debilitating illnesses, and type A personality are risk factors for the development of depression in cardiac patients. Depression has been shown to lower the threshold for ventricular arrhythmias. Therefore, treatment of depression potentially may prolong life in these patients. Antidepressant options that have been evaluated include several of the tricyclic antidepressants, trazodone, bupropion, and several of the selective serotonin reuptake inhibitors. Individual antidepressant drugs vary in their pharmacologic activity and side-effect profiles. Although clinical data are limited, it is important to individualize therapy in order to minimize cardiac adverse effects. Clinicians are encouraged to evaluate patients with cardiac disease for major depressive disorder and to consider antidepressant drug therapy for these patients when appropriate.

Antidepressive Agents↗
PubMed2004

New formulations of existing antidepressants: advantages in the management of depression.

For nearly 50 years, antidepressant drugs have been the first-line treatment for various forms of depression. Despite their widespread use, these medications have significant shortcomings, in particular problems of patient compliance due to adverse effects. The introduction of new formulations of existing antidepressant medications may provide patients with benefits in terms of convenience of use. As a consequence, improvements in compliance may lead to better antidepressant efficiency.An orally disintegrating formulation of mirtazapine (mirtazapine SolTab), a once-weekly formulation of fluoxetine, an enantiomer-specific formulation of citalopram (escitalopram), an extended-release formulation of venlafaxine (venlafaxine XR), a controlled-release formulation of paroxetine (paroxetine CR) and intravenous formulations of some of the newer antidepressants have all been evaluated in limited clinical trials. In this article, a review of the pharmacokinetics and clinical evaluations of these formulations is presented. While there do not appear to be major clinical advantages for the new formulations in terms of antidepressant efficacy, none of them is less efficacious than their older counterpart. Indeed, some of the new formulations are more acceptable to patients (fluoxetine once-weekly, paroxetine CR), others have pharmacokinetic advantages (venlafaxine XR, paroxetine CR), while others may have a faster onset of effect (mirtazapine SolTab, intravenous formulations). Further evaluation of some formulations is still required (mirtazapine SolTab, fluoxetine once-weekly), while others (venlafaxine XR, escitalopram) are finding widespread acceptance in clinical practice.

Animals↗