Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of antidepressants have emerged in the U.S. market in the past two decades. Selective serotonin reuptake inhibitors have become the drugs of choice in the treatment of depression, and they are also effective in the treatment of obsessive-compulsive disorder, panic disorder, and social phobia. New indications for selective serotonin reuptake inhibitors include post-traumatic stress disorder, premenstrual dysphoric disorder, and generalized anxiety disorder. Extended-release venlafaxine has recently been approved by the U.S. Food and Drug Administration for the treatment of generalized anxiety disorder. Mirtazapine, which is unrelated to the selective serotonin reuptake inhibitors, is unique in its action--stimulating the release of norepinephrine and serotonin. The choice of antidepressant drug depends on the agent's pharmacologic profile, secondary actions, and tolerability. Sexual dysfunction related to the use of antidepressants may be addressed by reducing the dosage, switching to another agent, or adding another drug to overcome the sexual side effects. Augmentation with lithium or triiodothyronine may be useful in patients who are partially or totally resistant to antidepressant treatment. Finally, tapering antidepressant medication may help to avoid discontinuation syndrome or antidepressant withdrawal.
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PMID:Antidepressants: update on new agents and indications. 1520 88

We sought to determine whether mirtazapine is safe and well-tolerated as a treatment for essential tremor (ET). We studied mirtazapine in a randomized, double-blind, placebo-controlled, crossover study of 17 ET patients. Patients were started with 15 mg per day of either mirtazapine or placebo for 1 week and the dose was escalated weekly until the targeted dose of 45 mg per day was achieved. This dose was maintained for 2 weeks. Tremor was assessed at baseline and after 14 days of 45 mg of mirtazapine or placebo. There was a minimum washout period of 14 days between the two arms of the study. Tremor assessments included global improvement, Fahn Tolosa Marin Tremor Rating Scale, Beck Depression Inventory and the Parkinson's Disease Questionnaire-39. Patient global improvement ratings indicated that in the placebo condition 12 patients were unchanged and 1 patient was mildly improved. In the mirtazapine condition, 10 patients were unchanged, 2 were moderately improved and 1 was markedly improved. There was no significant improvement with mirtazapine or placebo compared to baseline as measured by the Tremor Rating Scale. Adverse effects were more common in the mirtazapine group and included drowsiness, confusion, dry mouth, weight gain, polyuria, itching, nausea, gait and balance problems, blurred vision, and bad taste. We conclude that the majority of the ET patients do not benefit from mirtazapine. Mirtazapine has significant adverse effects and should be used cautiously in ET patients.
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PMID:Mirtazapine in essential tremor: a double-blind, placebo-controlled pilot study. 1272 74

The nonselective serotonin (5-HT)-2A antagonists ritanserin, mianserin, and cyproheptadine were found efficacious in neuroleptic-induced akathisia (NIA). Mirtazapine is structurally and pharmacologically similar to mianserin, and the authors sought to determine its anti-NIA activity. Twenty-six neuroleptic-treated schizophrenic patients with DSM-IV diagnosis of NIA received add-on mirtazapine (15 mg/day) or placebo for 5 days in a double-blind design. Patients were assessed at baseline and days 3 and 5 with the Barnes Akathisia Scale (BAS), Positive and Negative Symptom Scale, Hamilton Rating Scale for Depression, and Simpson-Angus Scale for parkinsonism. Analysis of covariance with repeated measurements revealed significant group x time effects in favor of the mirtazapine group in both completers (n = 10 in each group) and intent-to-treat analysis (n = 13 in each group) for the BAS global subscale (F [1, 17] = 14.87, p = 0.001, and F [1, 23] = 13.24, p = 0.01, respectively) and objective subscale (F [1, 17] = 8.25, p = 0.011, and F [1, 23] = 7.35, p = 0.012, respectively) and borderline significant superiority for the BAS subjective subscale (F [1, 17] = 4.39, p = 0.051, and F [1, 23] = 4.12, p = 0.054, respectively) and distress subscale (F [1, 17] = 4.21, p = 0.056, and F [1, 23] = 3.80, p = 0.064, respectively). Significantly more mirtazapine-than placebo-treated patients (53.8% [7/13] vs. 7.7% [1/13], respectively; chi2 = 8.3, p = 0.004) met operational response criterion, a reduction of at least two points on the BAS global subscale. Mirtazapine treatment was associated with modest improvement of psychotic and parkinsonian symptoms. Mild sedation was the only side effect. Our study demonstrated that mirtazapine (15 mg/day) is an efficacious and well-tolerated therapeutic option in NIA. Marked 5HT2A/2C antagonistic activity of mirtazapine apparently accounts for its anti-NIA activity. The role of mirtazapine in the treatment of akathisia induced by atypical antipsychotic agents merits further investigation.
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PMID:Efficacy of low-dose mirtazapine in neuroleptic-induced akathisia: a double-blind randomized placebo-controlled pilot study. 1282 92

This multinational, randomized, double-blind study was specifically designed to prospectively compare the onset of antidepressant efficacy of mirtazapine orally disintegrating tablets and sertraline at dosages commonly used in clinical practice. A total of 345 patients with major depressive episode (DSM-IV) received mirtazapine (30-45 mg/d) or sertraline (50-150 mg/d) for 8 weeks. Mirtazapine was administered in the newly developed fast dissolving, orally disintegrating tablet formulation. Assessments were performed at baseline and on days 4, 7, 10, 14, 28, 42, and 56. The primary efficacy variable (mean absolute change from baseline in the Hamilton Depression Rating Scale [HAMD] total score [17 items]) showed that mirtazapine was significantly (P < 0.05) more effective than sertraline at all assessments during the first 2 weeks of the study. After this time, HAMD total scores were similar in both groups. These findings were supported by analysis of the HAMD response rate (ie, > or =50% reduction in HAMD total score from baseline), HAMD remission rate (HAMD total score of < or =7), and the Montgomery-Asberg Depression Rating Scale (MADRS). Both treatments were well tolerated. In addition, mirtazapine had a greater effect than sertraline on sexual functioning. In conclusion, this first prospective onset of action study using the orally disintegrating tablet indicates that mirtazapine has a faster onset of therapeutic effect than sertraline. The orally disintegrating tablet formulation of mirtazapine used in this study is known to enhance the convenience and compliance by the patient.
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PMID:Mirtazapine orally disintegrating tablet versus sertraline: a prospective onset of action study. 1292 Apr 11

Mirtazapine has been shown to acutely inhibit cortisol secretion in healthy subjects. In the present study, the impact of mirtazapine treatment on urinary free cortisol (UFC) excretion was investigated in depression. Twenty patients (six men, 14 women) suffering from major depression according to DSM-IV criteria were treated with mirtazapine for 3 weeks. The patients received 15 mg mirtazapine on day 0; 30 mg mirtazapine on day 1; and 45 mg mirtazapine per day from day 2 to the end of the study (day 21). UFC excretion was measured before treatment (day 1), at the beginning (day 0), after 1 week (day 7) and after 3 weeks (day 21) of treatment with mirtazapine. Urine samples were collected from 08:00 to 08:00 h the following day. On the days of urine sampling, the severity of depressive symptoms was assessed using the 21-item version of the Hamilton Rating Scale for Depression (21-HAMD). There was a significant reduction of UFC excretion during 3-week mirtazapine therapy, which was already obvious after the first day of treatment (day 0). However, there were no significant across-subjects correlations between UFC reduction and decrease in 21-HAMD sum scores. Apparently, the mirtazapine-induced rapid reduction of cortisol secretion in depressed patients is not necessarily correlated with a favorable therapeutic response.
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PMID:Influence of mirtazapine on urinary free cortisol excretion in depressed patients. 1456 37

Depressive and anxiety disorders appear during the transplant process due to psychological stressors, medications and physiological disturbances. Treatment is necessary to prevent impact on patient compliance, morbidity and mortality. Psychotropic medications provide an effective option, although most are only available as oral formulations. Because of this, they are more susceptible to alterations in pharmacokinetic behaviour arising from organ dysfunction in the pretransplant period. Kinetics are also an issue when considering potential drug-drug interactions before and after transplantation. Prior to transplant, organ dysfunction can change the pharmacokinetic behaviour of some psychotropic agents, requiring adjustment of dosage and schedules. Thoracic or abdominal organ failure may reduce drug absorption through disturbances in intestinal motility, perfusion and function. Cirrhotic patients experience increased drug bioavailability due to portosystemic shunting, and thus dosage is adjusted downward. In contrast, dosage needs to be raised when peripheral oedema expands the drug distribution volume for hydrophilic and protein-bound agents. Drug clearance for most psychotropic medications is dependent upon hepatic metabolism, which is often disrupted by endstage organ disease. Selection of drugs or their dosage may need to be adjusted to lower the risk of drug accumulation. Further adjustments in dosage may be called for when renal failure accompanies thoracic or abdominal organ failure, resulting in further impairment of clearance. Studies regarding the treatment of anxiety and depressive disorders in the medically ill are limited in number, but recommendations are possible by review of clinical and pharmacokinetic data. Selective serotonin reuptake inhibitors are well tolerated and efficacious for depression, panic disorder and post-traumatic stress disorder. Adjustments in dosage are required when renal or hepatic impairment is present. Among them, citalopram and escitalopram appear to have the least risk of drug-drug interactions. Paroxetine has demonstrated evidence supporting its use with generalised anxiety disorder. Venlafaxine is an alternative option, beneficial in depression, post-traumatic stress and generalised anxiety disorders. Nefazodone may also be considered, but there is some risk of hepatotoxicity and interactions with immunosuppressant drugs. Mirtazapine still needs to be studied further in anxiety disorders, but can be helpful for depression accompanied by anorexia and insomnia. Bupropion is effective in the treatment of depression, but data are sparse about its use in anxiety disorders. Psychostimulants are a unique approach if rapid onset of antidepressant action is desired. Acute or short-term anxiolysis is obtained with benzodiazepines, and selection of particular agents entails consideration of distribution rate, half-life and metabolic route.
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PMID:Treatment of anxiety and depression in transplant patients: pharmacokinetic considerations. 1508 75

Currently, there are no data available comparing cost-effectiveness of two antidepressants in the primary care setting in the UK. Alongside a randomized, double-blind, 24-week study of mirtazapine and paroxetine, data were prospectively collected on patients' use of hospital and non-hospital services and days off work. Costs were estimated in each treatment arm from National Health Service (NHS) and societal perspectives, and were compared with selected outcome measures (numbers of 17-item Hamilton Rating Scale for Depression (17-HAMD) responders and changes in Quality of Life in Depression Scale scores between baseline and 24-week endpoint) to explore and compare relative cost-effectiveness. Mirtazapine treatment resulted in a statistically significantly greater improvement in quality of life than paroxetine at endpoint (P=0.021). Although the 17-HAMD response rates were higher for the mirtazapine users at endpoint, the difference (7%) was not statistically significant (P=0.31). However, mean total societal costs per patient were 375 pounds less with mirtazapine (1850 pounds) compared to paroxetine (2225 pounds; P=0.32). Mean total NHS costs per patient were also lower (120 pounds) with mirtazapine (1408 pounds) compared to paroxetine (1528 pounds). The advantage for mirtazapine remained present on all variables analysed after performing sensitivity analyses. The results suggest that mirtazapine may be a cost-effective treatment choice compared to paroxetine for depression in a primary care setting.
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PMID:The cost-effectiveness of mirtazapine versus paroxetine in treating people with depression in primary care. 1510 54

This multicenter, open-label study with a duration of 85 days was performed to evaluate the antidepressant efficacy and safety of mirtazapine (dose range, 30-45 mg) in 12-18-year-old adolescents diagnosed with major depression. Twenty-four (24) patients (15 female patients and 9 male patients) meeting the DSM-IV criteria for major depression and the Hamilton Rating Scale for Depression (HAM-D-17) score of 18 at baseline were enrolled in the study. The primary outcome measures were HAM-D-17, Beck Depression Inventory (BDI), and Clinical Global Impression (CGI) scales. Any changes in symptoms of anxiety were measured using the Hamilton Anxiety Rating Scale (HAM-A). The average age of the 23 subjects, who were eligible for analysis, was 16.3 years (standard deviation (SD) 6.11, median 17.3). The mean daily dose of mirtazapine was 32.9 mg. Mirtazapine showed a marked efficacy on all rating scales and was well tolerated. Mirtazapine had a beneficial effect on sleep. A rapid onset of sleep and pattern of action was seen. No dropouts due to adverse events were recorded. The most common treatment-emergent adverse events were tiredness, increased appetite, and dizziness. The results of this study suggest that mirtazapine may be an effective treatment for major depression in adolescents.
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PMID:Mirtazapine in the treatment of adolescents with major depression: an open-label, multicenter pilot study. 1531 15

Mirtazapine has been shown to acutely inhibit cortisol secretion in healthy subjects. In the current study, the impact of mirtazapine treatment on salivary cortisol secretion was investigated in 12 patients with major depression (DSM-IV criteria). Patients were treated with mirtazapine for 3 weeks, receiving 15 mg of mirtazapine on day 0, 30 mg on day 1, and 45 mg per day from day 2 to the end of the study (day 21). Response to mirtazapine treatment was defined by a reduction of at least 50% in the Hamilton Rating Scale for Depression after 3 weeks of therapy. Salivary cortisol concentrations were measured before treatment (day -1), at the beginning of treatment (day 0), after 1 week (day 7), and after 3 weeks (day 21) of treatment with mirtazapine. Saliva samples were collected hourly from 8 am to 8 pm. A significant reduction in cortisol concentrations was already noted after 1 day of mirtazapine treatment which was comparable in responders and in nonresponders. Mirtazapine therefore appears to be an effective in decreasing hypercortisolism in depression. However, the importance of the acute inhibitory effects of mirtazapine on cortisol secretion for its antidepressant efficacy has to be further clarified.
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PMID:Mirtazapine acutely inhibits salivary cortisol concentrations in depressed patients. 1567 28

Lymphocytes from human peripheral blood exhibit a series of markers of neurotransmitters, such as specific receptors and transporters. A reduction of serotonin transporters and an increase of them has been reported after treatment with fluoxetine in depressed patients. The aim of this study was to determine if the administration of an antidepressant with a different mechanism of action, such as mirtazapine, could produce a similar effect. Twenty eight patients (age 41.40+/-2.45) were diagnosed following the criteria for major depression by the Structured Clinical Interview for Disorders of Axis I of the American Psychiatric Association. Severity was measured by Hamilton Scale and by Beck Inventory for Depression, scores of 30.88+/-7.48 and 30.24+/-10.88, respectively, prior to treatment. Samples from control subjects were obtained alternating with patients before and after the administration of the antidepressant: twenty eight and twenty four, respectively (age 38.80+/-2.95). Mirtazapine was given in a dose of 30 mg/day for 6 weeks. Blood lymphocytes were isolated by density gradient from patients and controls before and after treatment. There was a partial response according to clinical evaluation and scores of the Scale and the Inventory. Serotonin transporters were labeled with [3H] paroxetine. Number of sites (B(max)) were 10.86+/-2.60 and 12.58+/-2.71 fmol/10(6) cells for both groups of controls. The depressed patients had a significant reduction of serotonin transporters in their lymphocytes before treatment and an increase after it, with B(max) values of 6.52+/-0.49 and 15.61+/-0.49 fmol/10(6) cells, respectively. There were no significant differences in the affinity for the ligand. Concentrations of serotonin or noradrenaline in lymphocytes were not modified before the treatment, although there was a significant decrease after taking 30 mg/day of the antidepressant for 6 weeks. Mirtazapine, not being a serotonin reuptake inhibitor, did increase the number of transporters in lymphocytes of major depression patients, indicating a complex mechanism, not only directly related to the transporter, but involved in the therapeutic response.
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PMID:Effect of mirtazapine treatment on serotonin transporter in blood peripheral lymphocytes of major depression patients. 1582 22


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