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)

Twenty-seven inpatients participating in a stroke rehabilitation program were randomized to receive either placebo or trazodone hydrochloride (Desyrel) beginning a mean (+/- SEM) of 44 +/- 4 days after stroke. The target dosage was 200 mg/d. Patients with either a clinical diagnosis of depression or abnormal Zung depression scores showed a consistent trend toward greater improvement in Barthel activities of daily living (ADL) scores with trazodone than with placebo. An abnormal dexamethasone suppression test result was associated with significant improvement in the Barthel ADL scores of patients receiving trazodone (38 +/- 6 vs 20 +/- 6 for placebo). Patients with stroke and evidence of depression are therefore likely to benefit from treatment with trazodone.
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PMID:Antidepressant therapy after stroke. A double-blind trial. 372 55

Severe psoriasis is commonly associated with depression and may be its cause. The hazards of treating such patients with lithium are well known (Lazarus & Gilgor, 1979), but other drugs may also destabilize psoriasis. We report a patient in whom the anti-depressant trazodone hydrochloride (Molipaxin, Roussel), a serotonin antagonist, provoked generalized pustular psoriasis (GPP).
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PMID:Generalized pustular psoriasis precipitated by trazodone in the treatment of depression. 379 Apr 38

Early human pharmaco-EEG and subsequent sleep laboratory studies identified trazodone, a 5-HT(2) antagonist and 5-HT reuptake inhibitor (SARI), as an antidepressant with therapeutic effects on its target symptoms depressed mood, anxiety and insomnia. On the occasion of the introduction of a controlled-release (CR) formulation (Trittico 150 mg retard, marketed in Austria by CSC Pharmaceuticals Handels GmbH, Vienna, Austria) in Austria in July 2000, a multi-center, open, clinical post-marketing study on the therapeutic effects, safety and target symptoms of trazodone CR in depression was carried out at 80 offices of Austrian neuropsychiatrists. 549 outpatients (63% females) of all age groups suffering from five different subtypes of depression were enrolled in the study. After a 2-week fixed dose-titration regimen up to 150 mg and a 4-week adjustment period to the optimum dose, 66% of the patients remained on 150 mg, 20% increased the dose and 11% decreased it. Only 3.7% discontinued treatment. Rating by the neuropsychiatrists based on the Clinical Global Impression showed very much to much improvement in 78.3% of the patients, and no change or a deterioration in only 3.6%. In the Hamilton Depression Scale (HAMD) a statistically significant improvement from a baseline score of 21 to a score of 14 after 2 weeks was found, and a normalization to a score of 8 after 6 weeks. Therapeutic effects were similar in the five groups suffering from different subtypes of depression and in patients with and without comedication. Self-rating by the patients based on the Zung Self-Rating Depression Scale (SDS) and Zung Self-Rating Anxiety Scale (SAS) also showed a significant improvement in the 2nd and 6th week of therapy. Evaluation of the target symptoms of trazodone by ranking the most improved symptoms identified insomnia as the most improved psychopathological item in all three scales. While in the observer ratings also suicidal tendencies and weight loss were found much improved, in the self-rated Zung SDS sadness and loss of drive came second and third in the improvement ranking, in the self-rated Zung SAS anxiety and the feeling of falling apart. Tolerability was very good. In the 2nd week only 16.9% and in the 6th week only 7.6% of the patients reported side effects, mostly characterized by tiredness and rarely by nausea and vertigo. The present clinical study is in agreement with previous studies identifying trazodone as a safe and effective antidepressant, specifically regarding its target symptoms insomnia, depression and anxiety. It also confirms our own early predictions based on neurophysiological investigations concerning the mode of action of the drug.
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PMID:Confirmation of the neurophysiologically predicted therapeutic effects of trazodone on its target symptoms depression, anxiety and insomnia by postmarketing clinical studies with a controlled-release formulation in depressed outpatients. 1467 18

Patients with chronic pain often suffer from sleep disturbances, specifically decreased deep sleep, and thus may get into a vicious circle which maintains their pain condition. Utilizing polysomnography and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients with nonorganic insomnia (F51.0) related to somatoform pain disorder (SPD; F45.4) as compared with age- and sex-matched healthy controls of the Siesta normative database. Patients demonstrated a markedly deteriorated Pittsburgh Sleep Quality Index, a decreased Quality of Life Index, slightly increased self-reported anxiety (Zung SAS) and depression scores (Zung SDS), as well as an increased Epworth Sleepiness Scale and International Restless Legs Syndrome Scale score. Subjective sleep and awakening quality was markedly reduced, while somatic complaints were increased. Polysomnographic evaluation by a recently developed automatic sleep classifier (Somnolyzer 24 x 7) based on the rules of Rechtschaffen and Kales demonstrated reduced slow-wave sleep (SWS), the target variable in the present study, a decreased stage shift index, increased SWS latency and stage 4 sleep (S4) latency and an increased frequency of shifts from S2 to wakefulness (W) in patients as compared with controls. Minimal oxygen saturation was found decreased, periodic leg movements (PLMs) were increased. In the morning, patients showed deteriorated well-being, drive, mood and wakefulness. There were no significant noopsychic or psychophysiological differences between patients and controls (except for a reduced numerical memory and a slightly increased morning diastolic blood pressure in patients). Subsequent evaluation of the acute effects of 100 mg of a controlled-release formulation of trazodone (Trittico retard) in the patients demonstrated an increase in the target variable SWS, accompanied by a reduction in the number of awakenings and stage shifts. It normalized the frequency of shifts from S2 to W and reduced the frequency of shifts from W to S1, from S1 to S2, as well as from any stage to S1 and S2. Trazodone, however, also significantly reduced the total sleep period and S2 and increased the latency to S1. Moreover, the drug increased the reduced minimal O(2 )saturation, reduced the arousal index and the PLMs-in-wake index and normalized the increased morning diastolic blood pressure. In conclusion, our study demonstrated that SPD induced significant changes in subjective and objective sleep and awakening quality, which were partially mitigated by trazodone therapy. The data on the target variable SWS support our hypothesis of a key-lock principle in the diagnosis and drug treatment of sleep disorders. Our study provided the first evidence on the usefulness of the Somnolyzer 24 x 7 and the Siesta database in clinical practice.
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PMID:Insomnia in somatoform pain disorder: sleep laboratory studies on differences to controls and acute effects of trazodone, evaluated by the Somnolyzer 24 x 7 and the Siesta database. 1583 86

The pharmacological properties and possible clinical use of trazodon in the treatment of depression are presented. Trazodon is the only antidepressant from the SARI (Serotonin Antagonists and Reuptake Inhibitors) group available in Poland. It has a wide pharmacodynamic profile (being an antagonist of 5-HT2A and 5-HT2C serotoninergic receptors, alpha1 and alpha2 adrenergic receptors as well as H1 histaminergic receptors, and in higher doses it blocks the SERT serotonine transporter) which explains its wide therapeutic spectrum ranging from symptomatic treatment, through the potentialization of other drugs activity, all the way to monotherapy of depressive syndromes. An especially complex action on the serotoninergic system results in the lack of unwanted side-effects during treatment with trazodon (e.g. sexual dysfunction, significant body weight gain), which may be present during the treatment with other drugs (selective serotonin reuptake inhibitors). It is metabolised by the CYP450 isoenzyme: mainly the 2D6 and 3A4. This requires its dose to be adjusted when administered simultaneously with other drugs influencing the activity of those isoenzymes. Trazodon CR is an orally administered controlled release form, which simplifies its dosage and reduces the risk of adverse effects. Usually doses of 75 to 600mg daily are used; in the elderly those doses should be lower. Trazodon turned out to be effective in the treatment of various depressive syndromes, amongst them depression with insomnia, with anxiety and unrest, as well as depression in the elderly. In the recommended dose spectrum, trazodon is well tolerated. Unwanted adverse effects of the drug appear rarely and they are: somnolence, dizziness, gastrointestinal dysfunctions, and dry mouth.
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PMID:[Trazodon--the antidepressant: mechanism of action and its position in the treatment of depression]. 2223 86