Desyrel is a high-quality medication which is taken in treatment of depression. This remedy is acting by increasing the amount of serotonin. It is serotonin modulator.
Other names for this medication:
Desyrel is a high-quality medication which is taken in treatment of depression. This remedy is acting by increasing the amount of serotonin. It is serotonin modulator.
Other names for this medication:
Also known as: Trazodone.
Desyrel is a perfect remedy in struggle against depression.
This remedy is acting by increasing the amount of serotonin.
Desyrel is also known as Trazodone, Molipaxin, Deprax, Trittico, Thombran, Trialodine, Trazorel.
It is serotonin modulator.
Generic name of Desyrel is Trazodone.
Brand names of Desyrel are Desyrel, Desyrel Dividose.
Take Desyrel tablets orally with food.
Do not crush or chew it.
Take Desyrel at the same time every day with water.
Desyrel can be used by 18 year-old patients or over.
If you want to achieve most effective results do not stop taking Desyrel suddenly.
If you overdose Desyrel and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Desyrel overdosage: abnormal heartbeats, difficulty breathing, painful erection that does not go away, vomiting, feeling drowsy, convulsions.
Store at room temperature between 15 and 30 degrees C (59 to 86 degrees F) away from moisture and heat. Protect from light. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Desyrel are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Desyrel if you are allergic to its components.
Do not take Desyrel if you are pregnant, planning to become pregnant, or are breast-feeding.
Do not take it if you are under 18.
Be careful with Desyrel if you suffer from schizophrenia, other psychiatric illness, suicidal thoughts, heart attack, bipolar disorder (manic depression), drug abuse.
Try to avoid machine driving.
Be careful! Taking Desyrel you can become suicidal.
If you are going to have a surgery, be careful with Desyrel.
It can be dangerous to stop Desyrel taking suddenly.
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A fast and sensitive ultra-high performance liquid chromatography tandem mass spectrometry method using a BEH C18 column with a mobile phase consisting of ammonium acetate/acetonitrile was developed and validated according to international guidelines for the simultaneous analysis of 24 ADs in hair. Methanol/acetonitrile/ammonium formate buffer 1 mmol/L (25:25:50, vol/vol/vol) was used to extract the drugs from the hair matrix before a solid-phase extraction using cation exchange cartridges was applied. Hair samples (n = 18) obtained from a US workplace drug testing center were analyzed to demonstrate the method applicability.
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The QT interval measuring depolarisation and repolarisation has, when lengthened, been implicated as a risk factor for the development of torsades de pointes and sudden death, particularly in patients predisposed to these complications due to cardiovascular impairment. Since some of the medications used in psychiatry have been implicated, an extensive review of available literature was made of the major classes, including antipsychotics, antidepressants, lithium, anticonvulsants and benzodiazepines. Further, where no publications were found on a particular medication, the pharmaceutical firms responsible for these items were contacted concerning possibly unpublished data. Results of the survey indicate that there may be difficulty in one of three situations: immediate (in the first minutes to hours after oral or parenteral administration), short-term use of 4 - 12 weeks or long-term use of 6 months. Based on this approach, the greatest concern is directed at the immediate application of haloperidol, droperidol, pimozide and trazodone, the short-term use of thioridazine, pimozide, sertindole, nortriptyline, clomipramine, doxepin and the long-term use of clozapine, olanzapine and carbamazepine. It is of interest that a reduction in QTc is reported with aripiprazole. Among the antidepressants, the tertiary tricyclic antidepressants (imipramine, amitriptyline and doxepin) appear to have a more general impact, while the secondary tricyclic antidepressants (nortriptyline, desipramine) may impact more on children and the elderly. Among other antidepressants, the only reports of torsades de pointes appeared to occur with mirtazapine. It was also of interest to find data showing no effect or reductions in QTc produced by sertraline, citalopram, paroxetine and bupropion in multiple studies. Effects of medications on other heart parameters are also briefly reviewed. In particular, the safety of sertraline in post-MI patients and of bupropion in heart disease patients is highlighted. Little information was available on other classes of medications used in psychiatric disorders. What is available concerning lithium, the anticonvulsants and the benzodiazepines indicates little effect on the QTc, although there may be effects on other cardiovascular parameters.
Cohen-Mansfield Agitation Inventory (CMAI), Hamilton Depression Rating Scale (Ham-D), and delusional thoughts subscale and hallucinations subscale of the Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD).
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Clinically important weight loss and gain occurred at 6 months in 14.8% and 14.4% of the sample, respectively. In unadjusted analyses, an increased likelihood of loss was found for users of SSRIs (Odds Ratio 1.57; CI 1.30, 1.90) and others (OR 1.89; CI 1.18, 3.03), compared with none. In logistic models accounting for potential confounding factors, however, SSRI use showed a modest association with gain (OR 1.31, CI 1.01, 1.70) and a trend toward a similarly modest association with loss (OR 1.28; CI 0.995, 1.64). TCA use was not associated with weight gain. When weight was examined as a continuous variable, all groups demonstrated a broad range of both loss and gain with mean-unadjusted weight changes < 3 pounds. Pairwise comparisons of adjusted differences in weight change at 6 months for SSRIs (mean loss of 1.6 pounds) and TCAs (mean gain of 0.4 pounds) were of marginal importance (P = .046) given the large sample size. No evidence was found for prescribing bias based on prior weight pattern.
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We located 19 head-to-head trials in total: 11 on anxiety, six on insomnia, and four on pain. For the majority of comparisons, the strength of the evidence was moderate or low: evidence is weakened by inconsistency and imprecision. For treating anxiety, insomnia, and pain moderate evidence suggests that the SSRIs do not differ.
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Academic medical center.
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Chronic pain is considered one of the most prevalent causes of costly and disabling medical conditions. This review will define chronic pain and its categories and then will summarize the effectiveness and side effects associated with the use of various antidepressants, including the tricyclics, the selective serotonin reuptake inhibitors, the serotonin norepinephrine reuptake inhibitors, other miscellaneous antidepressants and the atypical antipsychotics in the treatment of chronic pain.
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Platelet 5-hydroxytryptamine uptake was measured in a group of 28 endogenously depressed patients at three points during the day, before, during and after treatment and in 20 controls at the same three times. Uptake rates varied in control subjects in a manner consistent with the presence of a circadian rhythm in uptake. This variation was absent in depressed subjects. Normal variation was restored in those patients showing a clinical response, irrespective of the effects of treatment on the affinity of the uptake system. This restoration was not found in nonresponders or acutely after treatment was commenced. These findings suggest that depression is associated with a disruption of circadian rhythms, that abnormalities of platelet 5-hydroxytryptamine uptake are secondary to such a disruption and that antidepressants may act to correct this disruption.
In this article, a distinction is proposed between safe and less safe antidepressants. The safety of 18 antidepressants is discussed in relation to 3 principal issues: the safety of the drug in the event of an overdose; the seriousness of its side effects; and the existence of dangerous interactions. On the basis of present information, it can be said with reasonable confidence that fluoxetine, fluvoxamine and paroxetine are safe antidepressants, and with some reservation (mainly because of hypnosedation) the same can be said of mianserin and trazodone.
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We recently encountered 3 patients who had developed reversible paroxetine-associated hepatotoxicity. Two of the patients were over 80 years old and their hepatitis was accompanied by hyponatremia. In the third case, hepatitis was associated with multiple organ failure and the co-administration of trazodone. Here, we will discuss the possible role of preexisting risk factors in the development of paroxetine hepatotoxicity and review the relevant literature.
An open pilot trial of combined trazodone and tryptophan for 11 patients with Obsessive-Compulsive Disorder was conducted to test the hypothesis that increasing serotonin activity is therapeutic for this condition. Results were not encouraging; several patients tolerated the combination poorly, but even among patients completing 2 weeks' treatment benefit was marginal.
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Insomnia in patients with heart transplantation and cardiac disease is a common problem. Organic factors, immunodepressant medication (e.g. ciclosporine and steroids) and psychological factors may account for this symptom. The article reviews different hypnotic drugs and their value in the treatment of insomnia. For short-time treatment, medication with benzodiazepine hypnotics may be useful. If the problems of drug dependence and rebound insomnia are taken into consideration, treatment with non-benzodiazepine hypnotics offers more safety and comfort. If insomnia is part of a depressive syndrome, pharmacotherapeutical intervention with antidepressive sedative medication is required. With regard to cardiac disease, treatment with mirtazapine, nefazodone or trazodone should be preferred because of the chinidine-like effect of tricyclic antidepressants (TCA). Sedative neuroleptic medication (e.g. melperone) is commonly given to geriatric patients; nevertheless, patients with chronic insomnia may also benefit from this medication. The risks and benefits of hypnotic drugs are discussed especially in relation to pharmacological interaction (cytochrome system) and cardiac disease.
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We determined the incidence of new antidepressant use defined by the dispensing of antidepressant drug therapy within 90 days of discharge home. We identified independent correlates of antidepressant initiation using multivariate regression.
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We report a case with refractory insomnia. We diagnosed her case as depression with high levels of anxiety, weakness, with diminished ability to think or concentrate and with a sensory-motor disorder. Although this last symptom was very distressing, it did not satisfy the criteria for RLS (Restless Legs Syndrome). After treatment with paroxetine (20 mg) and zolpidem (10 mg), anxiety and mood deflection were attenuated. Nevertheless, a mild depression, an intermittent awakening (fragmentation of the sleep-wake rhythm) and subsyndromal RLS persisted. Her resistant insomnia was treated with benzodiazepine sleeping drugs (triazolam 0.25 mg, lorazepam 2.5 mg, fluorazepam 30 mg) with only partial insomnia remission, antidepressants (trazodone 150 mg RP, mirtazapine 15-30 mg, agomelatine 50 mg) and antipsychotics (levomepromazine 25 mg, zuclopentixol 25 mg) without results. Her intractable insomnia was markedly responsive to pregabalin without side effects. Our hypothesis is that the therapy with pregabalin may be indicated for resistant insomnia associated with subsyndromal RLS, even when the latter does not satisfy fully all the criteria for diagnosis.
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Ovid/MEDLINE databases were searched by using the following key words: "brain injury," "sleep initiation and maintenance disorders," "hypnotics and sedatives," "benzodiazepines," "trazodone," and "neuronal plasticity."
Although the improvement was not statistically significant, treatment with testosterone and trazodone could be used as an adjuvant therapy in nonorganic male sexual dysfunction. The only treatment superior to placebo seemed to be hypnosis. A more effective treatment may be obtained by combining these therapeutic modalities, but this needs further study.
Trazodone significantly increased total sleep time, percentage of stages 3+4, sleep efficiency index, sleep continuity index and decreased percentage of stage 1, number of awakenings, stage shifts compared to the baseline. This improvement was also obtained after 7 days of treatment. The PSQI score was reduced to 5+/-1.6 at the end of the study. HDRS was reduced to 11.5+/-4.5 with trazodone and to 12.2+/-3 with placebo.
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As a part of a program aimed at discovering compounds endowed with alpha(1)-adrenoceptor (AR) blocking properties, in this paper we describe the synthesis and biological characterization of the compounds designed to fully match a three-dimensional pharmacophore model for alpha(1)-AR antagonists previously developed by our research group. Accordingly, the structure of trazodone (1), identified during a database search performed by using the model as a 3D query, was chosen as the starting point for this study and modified following suggestions derived from a literature survey. In particular, the triazolopyridine moiety of trazodone was replaced with different heteroaromatic rings (such as imidazole, benzimidazole, and indole), and a pyridazin-3(2H)-one moiety was inserted into the scaffold of the new compounds to increase the overall length of the molecules and to allow for a complete fit into all the pharmacophore features. Our aim was also to study the influence of the position of both the chloro and the methoxy groups on the piperazine phenyl ring, as well as the effect of the lengthening or shortening of the polymethylene spacer linking the phenylpiperazine moiety to the terminal heterocyclic portion. Compounds obtained by such structural optimization share a 6-(imidazol-1-yl)-, 6-(benzimidazol-1-yl)-, or 6-(indol-1-yl)pyridazin-3(2H)-one as a common structural feature that represents an element of novelty in the SAR of arylpiperazine compounds acting toward alpha(1)-AR. Biological evaluation by radioligand receptor binding assays toward alpha(1)-AR, alpha(2)-AR, and 5-HT(1A) serotoninergic receptors indicated compounds characterized by very good alpha(1)-AR affinity and selectivity. Very interestingly, chemical features (such as the o-methoxyphenylpiperazinyl moiety and an alkyl spacer of three or four methylene units) that generally do not allow for 5-HT(1A)/alpha(1) selectivity led to compounds 2c and 6c with a 5-HT(1A)/alpha(1) ratio of 286 and 281, respectively. Finally, compounds with the best alpha(1)-AR affinity profile (2c, 5f, and 6c) were demonstrated to be alpha(1)-AR antagonists.
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From a safety perspective, several issues require assessment when a decision is made to prescribe a sleep medication, including next-day residual effects, the potential for abuse, tolerance, and dependence. This article aims to provide an update of the safety profile of agents commonly used in the management of insomnia, with an emphasis on newly approved hypnotics.
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Relationships between plasma concentrations of trazodone and m-chlorophenylpiperazine (m-CPP) and the clinical effects were studied in 26 patients (12 males and 14 females) with major depression during three weeks' treatment of 150 mg/d trazodone using an open-study design. Depressive symptoms were evaluated by Montgomery Asberg Depression Rating Scale (MADRS), and subjective side effects were assessed by UKU side effects rating scale (UKU) before treatment and at weekly intervals. Plasma concentrations of trazodone and m-CPP were measured by HPLC. There were significant linear relationships between the steady-state plasma concentration (Css) of trazodone and both the final MADRS score (rs = -0.529, P < 0.01) and the percent improvement at 3 weeks (r = 0.442, P < 0.05). Moreover, the proportion of responders (a final MADRS score of 10 or less) was significantly higher in the group with a trazodone concentration greater than 714 ng/mL (6/8 vs 3/18, P = 0.008). No significant correlation was found between UKU score and the Css for either compound nor between the UKU score and the ratio of m-CPP/trazodone. The current study suggests that a therapeutic response is dependent on the plasma concentration of trazodone but not m-CPP and that a plasma trazodone concentration of about 700 ng/mL may be a threshold for a good therapeutic response.
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Medications utilized in our outpatient clinic for opioid withdrawal were evaluated for quality-assurance purposes. The treatment regimen generally included clonidine, hydroxyzine, trazodone, diphenoxylate/atropine, and sometimes chlordiazepoxide. Patients were also initially given eight 25-mg tablets of quetiapine and instructed to take 1 or 2 tablets every 4 hours as needed for symptoms of withdrawal or craving (with a maximum daily dose of 200 mg). Data were based on patient evaluations from June 2003 to June 2004.
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Antidepressants are commonly prescribed and used in the management of depression, anxiety disorders, and other psychiatric illnesses. Antidepressants used in therapeutic dosing ranges are associated with causing several adverse drug reactions including hepatotoxicity. Paroxetine, fluoxetine, fluvoxamine, citalopram, mirtazapine and venlafaxine are associated with reversible liver injury upon discontinuation of the agent. Patient cases of hepatotoxicity involving the use of nefazodone, trazodone, duloxetine, bupropion, and sertraline are linked to causing death in its users. Due to the idiosyncratic nature of hepatotoxicity, monitoring of liver function tests and immediate discontinuation upon abnormal lab findings or signs and symptoms of liver dysfunction are crucial since most cases of hepatic damage are reversible when detected early. Onset of antidepressant-associated hepatotoxicity varies from 5 days to 3 years. Antidepressant-induced liver injury can occur in the absence of identifiable, underlying risk factors such as cirrhosis and hepatitis infection; only a few cases of hepatic injury involve patients with chronic hepatitis infection. Some of these cases involve possible drug interactions between antidepressants and concomitant agents that increase the risk for liver injury. Understanding druginduced liver injury associated with antidepressants and the importance of safety monitoring is essential to optimize outcomes for antidepressant treatment.
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With the exception of low-dose doxepin (Silenor-Somaxon), trials evaluating the clinical effectiveness of H(1) receptor antagonists show mixed results and are limited by sample size and generalizability. Large, randomized, appropriately controlled trials are lacking, making it difficult to define the safety and efficacy of these agents. In contrast, low-dose doxepin has been shown to provide consistent sleep benefit compared with placebo.
Pharmacological tests based on the reversal of effects induced by reserpine or reserpine-like drugs have been used extensively for the identification of potential antidepressants. The classical tests detect some of the antidepressants in addition to traditional tricyclics and monoamine oxydase inhibitors, but fail to identify other clinically effective antidepressants like mianserin and trazodone. New methods have therefore been developed including models based on reversal of various behavioural stereotypes of drug-induced effects. No single model is perfect, because all either detect drugs known not to be antidepressant (false positives) or, which is worse, fail to detect some clinically effective antidepressants (false negatives). The most reliable models involve reversal by antidepressants of the effects of bulbectomy in rats or selective suppression of REM sleep in cats, out neither is suitable for screening purposes. Neurochemical tests and receptor binding, like all tests for antidepressant activity, are fated to detect me-too drugs. Better and more relevant models must await a deeper understanding of the nature of depression.
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Tricyclic antidepressants (TCAs) are notorious for a number of disadvantages, but particularly for an array of side-effects that leads to poor compliance, and also for a dangerous toxicity in overdose. Lofepramine is a new tricyclic that seems safer. Selective serotonin reuptake inhibitors (SSRIs) are more limited in their actions. Side-effects include nausea and insomnia, but on the whole the side-effect profile is an improvement on the TCAs. A miscellaneous group of novel antidepressants includes mianserin and trazodone (which both produce drowsiness) and viloxazine (which causes nausea). The reversible inhibitors of monoamine oxidase A (RIMAs) are a group of drugs that, by producing inhibition selectively of monoamine oxidase A (MOA-A), still allow metabolism of tyramine by MAO-B. Moclobemide is a RIMA that has proved itself to be very effective in severe depressive illness. It is remarkably safe and has an exceptionally low incidence of side-effects. It may be expected to be associated with a high acceptability in depressed patients.
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Our study showed similar efficiency and safety of trazodone and venlafaxine for depression disorders. Trazodone efficiency in comparison to venlafaxine was faster, especially in 14th study day. It suggests that trazodone characterized by potentially quicker beginning of activity in patients with depression disorders.
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Interferon-Alpha (IFN) has been effective in the treatment of chronic viral infections and cancer albeit the added risk of severe depression. The literature has reported effectiveness in the use of antidepressants for interferon-induced depression. We report a case of severe protracted depression induced by IFN in a patient diagnosed with melanoma who responded rapidly to a course of methylphenidate using the Hamilton Depressive Rating Scale. Methylphenidate appeared to be effective in the treatment of neurovegetative symptoms of major depression induced by IFN. This report provides further clinical evidence that the neurovegetative symptoms of depression might respond better to a norepinephrine uptake inhibitor or psycho-stimulants.
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Prospective, double blind, randomized, placebo-controlled.
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Previous research has revealed that major depression is accompanied by disorders in excitatory amino acids, e.g. glutamate and aspartate, and alterations in serum levels of other amino acids, e.g. serine, glycine and taurine. The aim of the present study was to examine serum levels of aspartate, asparagine, glutamate, glutamine, serine, glycine, threonine, histidine, alanine, taurine and arginine in major depression patients with treatment-resistant depression (TRD). No significant differences in the serum concentrations of any of the above amino acids could be found between patients with and without TRD and normal controls. Non-responders to treatment with antidepressants during a period of 5 weeks were characterized by significantly lower serum levels of aspartate, asparagine, serine, threonine and taurine. A 5-week period of treatment with antidepressants significantly reduced the serum levels of aspartate, glutamate and taurine, and significantly increased the serum concentrations of glutamine. The results suggest that alterations in serum levels of aspartate, asparagine, serine, threonine and taurine may predict the subsequent response to treatment with antidepressants, and that the latter may modulate serum levels of excitatory amino acids and taurine.
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Solifenacin-induced cognitive adverse effects have not been reported frequently, but solifenacin-induced delirium and hallucinations with successful switching to darifenacin, without additional drug, have not been reported in the literature. In this case report, we present an 80-year-old Caucasian male with insomnia and anxiety symptoms and overactive bladder who developed delirium and hallucinations when treated with solifenacin and trazodone. After solifenacin discontinuation and switching to darifenacin, symptoms significantly improved immediately. Such a case has not yet been described in literature; however, an adverse effect associated with solifenacin can occur, as this report clearly demonstrates.
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