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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In all, 25 clinical trials were found. Six of these met the methodologic assessment criteria (adapted from the McMaster guidelines for the evaluation of clinical trials), which included the stipulation of a score of 18 or more on the Hamilton depression rating scale and a 50% reduction in that score as an outcome measure.
Amphetamines and methamphetamines are part of an important class of drugs included in most urine drugs of abuse screening panels, and a common assay to detect these drugs is the Amphetamines II immunoassay (Roche Diagnostics). To demonstrate that meta-chlorophenylpiperazine (m-CPP), a trazodone metabolite, cross-reacts in the Amphetamines II assay, we tested reference standards of m-CPP at various concentrations (200 to 20,000 g/L). We also tested real patient urine samples containing m-CPP (detected and quantified by HPLC) with no detectable amphetamine, methamphetamine, or MDMA (demonstrated by GC MS). In both the m-CPP standards and the patient urine samples, we found a strong association between m-CPP concentration and Amphetamines II immunoreactivity (r = 0.990 for the urine samples). Further, we found that patients taking trazodone can produce urine with sufficient m-CPP to result in false-positive Amphetamines II results. At our institution, false-positive amphetamine results occur not infrequently in patients taking trazodone with at least 8 trazodone-associated false-positive results during a single 26-day period. Laboratories should remain cognizant of this interference when interpreting results of this assay.
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Diagnosis is based on clinical features, characteristic neuropathologic findings of TDP-43 inclusions, and molecular genetic testing of GRN, the only gene in which mutation is known to cause FTD-GRN.
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Drug-induced hepatotoxicity is a major problem in drug development, and oxidative stress is known as one of the causes. Superoxide dismutases (SODs) are important antioxidant enzymes against reactive oxygen species (ROS). Mitochondria are the major source of superoxide production, and SOD2 is mainly localized in mitochondria and, with other SODs, plays an important role in scavenging superoxide. In this study, we established SOD2-knockdown cells. An adenovirus vector with short hairpin RNA against rat SOD2 (AdSOD2-shRNA) was constructed, and infection of AdSOD2-shRNA to rat hepatic BRL3A cells resulted in significant decreases of SOD2 mRNA and protein by 60%, and SOD2 activity by 50% after 3 days infection. We previously constructed an adenovirus expressing cytochrome P450 3A4 (AdCYP3A4). Co-infection of AdSOD2-shRNA and AdCYP3A4 to BRL3A cells was carried out to evaluate the superoxide- and CYP3A4-mediated formation of active metabolites, and mitochondrial toxicity, ROS and superoxide radical production and lipid peroxidation were selected to assess the cell viability. Albendazole, carbamazepine, dapsone, flutamide, isoniazid, nifedipine, sulfamethoxazole, trazodone, troglitazone, and zidovudine demonstrated significant increases of SOD2- and CYP3A4-mediated cytotoxicity. In conclusion, we constructed a highly sensitive cell system to evaluate oxidative stress and CYP3A4 mediated cytotoxicity that could be useful in preclinical drug development.
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Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs.
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Current use of an antidepressant was defined as a supply of the last prescription for an antidepressant that lasted up to the index date or beyond. Recent past use was defined as a supply of the last prescription for an antidepressant that ended 1-29 days before the index date. SSRIs investigated were citalopram, fluoxetine, fluvoxamine, paroxetine, sertraline and venlafaxine. Non-SSRIs investigated were amitriptyline, clomipramine, dosulepin, doxepin, imipramine, lofepramine, nefazodone, trazodone and trimipramine. Other antidepressants included were amoxapine, desipramine, lithium, maprotiline, mianserin, moclobemide, nortriptyline and protriptyline. Adjusted ORs (with 95% CI) for the current use of SSRIs, non-SSRIs, or other antidepressants, compared with non-use of antidepressants, were 0.63 (95% CI 0.43, 0.91; p=0.02), 0.92 (95% CI 0.77, 1.09; p=0.32) and 0.59 (95% CI 0.29, 1.20; p=0.14), respectively. The adjusted OR of recent past use of SSRIs compared with non-use of SSRIs was 1.42 (95% CI 1.02, 1.97; p=0.04).
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There were 9 episodes of priapism in 8 patients; all cases were low flow and the patients were aged 37-71 years. The duration of the prolonged erection ranged from 4 to 72 hours. Of these 9 cases, the etiology was intracavernosal PGE in 7, after trazodone administration in one case, and unknown in one case. Intracavernosal metoxamine was administered in all cases with excellent results, except one case that required a saphenous-cavernosal shunt and another case that was initially treated with adrenalin also with good results.
All 11 patients demonstrated an average improvement of three Rancho Los Amigos levels within an average treatment duration of 10 days. Simultaneously, 9 of 11 patients were discontinued from treatment and prescribed antipsychotic and sedative agents.
Extracellular single-unit recordings were made from noradrenergic locus coeruleus neurons in chloral hydrate-anesthetized male Sprague-Dawley rats. Acute intravenous administration of the antidepressant trazodone produced a mild excitation of firing of these cells (ED25 = 0.128 mg/kg; ED50 = 0.659 mg/kg). These findings, in combination with previous work showing that trazodone inhibits the firing of serotonergic dorsal raphe neurons indicate that trazodone modulates monoaminergic neuronal activity in the brain and suggest a unique electrophysiological profile for this drug among antidepressants.
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All patients perceived significant subjective sleep improvements. Sleep latency significantly shortened (p=0.03), sleep efficiency increased (p=0.004) and the total sleep time was significantly prolonged (p=0.006) after the CBT treatment in both groups. Sleep architecture showed that the combined approach (CBT + trazodone) resulted in a significant increase in slow wave sleep duration compared to treatment by CBT only (p=0.04).
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A total of 134,833 patients who were prescribed long-term warfarin from June 1, 1999-May 31, 2000.
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A 26-year-old man with bipolar disorder, seizures, and mild mental retardation secondary to a traumatic brain injury began treatment with carbamazepine for aggression and seizure control. After three weeks of carbamazepine therapy, the patient arrived at the emergency department (ED) with severe agitation and aggressive behavior. His oral medications included topiramate, carbamazepine, olanzapine, quetiapine, guanfacine, and desmopressin acetate. The patient's medications had been stable for at least six months except for the addition of carbamazepine one month before his arrival at the ED. Upon admission, the patient's vital signs were found to be within normal limits, as were his liver profile results, complete blood count, thyroid-stimulating-hormone level, and serum chemistry panel. His serum carbamazepine concentration was 3.9 microg/mL (reference range, 4-12 microg/mL), and his serum ammonia concentration was 127 microg/dL (reference range, 19-60 microg/dL). Carbamazepine was discontinued upon admission, and the patient was treated with oral lactulose. Since carbamazepine was discontinued and had been prescribed for bipolar disorder, his olanzapine dosage was increased, and trazodone was added at bedtime for insomnia. Of note, the patient had been on carbamazepine therapy one year earlier and had experienced the same adverse event. He had also developed elevated serum ammonia levels while on valproic acid. The patient's serum ammonia level returned to normal by hospital day 4, and he was discharged to his group home.
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Only trials that evaluated migraine headaches in the pediatric population were included. Trials including adolescent and adult populations are briefly listed, but not reviewed. Trials involving non-prescription medication were also included in the evaluation. Due to the limited information, all clinical trials, retrospective reviews, and abstracts evaluated were included in this review.
1. Bilateral olfactory bulb ablation was performed in C57B1/6j mice (C57). Separate groups of bulbectomized mice were treated with either antidepressants (trazodone, 20 mg/kg i.p., or amitriptyline, 20 mg/kg i.p.) or saline daily for 14 consecutive days starting 14 days after surgery. 2. Celloidine-imbedded 10 microns-thick brain sections containing the nucleus raphe dorsalis (NRD) or locus coeruleus (LC) were stained for Nissl, and the number of functional and pyknotic cells was counted out of 500 total cell count for each animal in every experimental group: sham-operated, bulbectomized treated with saline or one of the two antidepressants. 3. Bulbectomy produced a significant 4 times increase in the proportion of pyknotic cells in NRD as compared to sham-operated control. Both antidepressants reversed the effect bringing the number of pyknotic cells to control level. The proportion of pyknotic cells in LC was also slightly increased (61%) in the bulbectomized mice, but only amitriptyline was able to reverse the effect. 4. Widespread degeneration of the neurons in NRD caused by bulbectomy may be involved in the serotonergic component of the bulbectomy syndrome. The ability of antidepressants to diminish bulbectomy-induced loss of NRD neurons may underlie their restorative effect on the behavior and neurochemical characteristics of bulbectomized animals.
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Twenty PD patients with and without depression were randomly assigned to receive trazodone (group 1) or not (group 2). They were evaluated through UPDRS and Hamilton Depression Rating Scale (HAM-D).
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Trazodone appears effective for the treatment of insomnia and nightmares associated with chronic PTSD. However, controlled trials are needed before any definite conclusions can be drawn. The higher than expected occurrence of priapism warrants clinicians asking directly about this side effect.
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A patient with an 18-year history of depression was treated with a combination of trazodone and phenelzine without any major complications and with good efficacy. The use of this medication combination has not been reported previously.
A retrospective analysis of Iowa City Department of Veteran's Affairs prescription records from March 1, 1995, to March 1, 1998, was performed. Antidepressants prescribed only by psychiatrists were included. Concomitant use was defined as trazodone prescribed on the same date or up to 42 days after the fill date of the primary antidepressant.
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Drug interactions represent a potential risk that is often underestimated by physicians. Pharmacovigilance is a useful tool to optimize resources and prevent negative outcomes associated with medication. It is recommended that systematic search is made to enhance surveillance programs for the rational use of medicines in this country.
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To determine the affinities of human penile alpha-adrenoceptors and cloned human alpha-adrenoceptor subtypes for trazodone, an antidepressant with reported beneficial effects in erectile dysfunction. Materials and methods Competition radioligand binding studies were performed with trazodone in human penile tissue and in cell lines stably expressing all cloned human alpha-adrenoceptor subtypes.
We found antidepressant use did not increase the risk of gastric cancer. The lack of an association between antidepressant prescription and elevated gastric cancer incidence was apparent for across selective serotonin-reuptake inhibitors (SSRIs), tricyclic agents (TCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs), reversible inhibitors of monoamine oxidase A (RIMA), trazodone, mirtazapine and bupropion. There were slightly decreased gastric cancer risks of SSRIs use (≧28 DDD group, adjusted OR = 0.87; 95% CI = 0.78-0.96). Sensitive analysis showed SSRIs, TCAs, and SNRIs did not increase gastric cancer risks significantly even in the group with peptic ulcer history.
The objective of this review was to determine the effectiveness, adverse effects and acceptability of folate in the treatment of depression. Electronic databases (Cochrane Controlled Trials Register and the Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register) and reference lists were searched, and authors, experts and pharmaceutical companies contacted to identify randomized controlled trials that compared treatment with folic acid or 5'-methyltetrahydrofolic acid to an alternative treatment, for patients with a diagnosis of depressive disorder. Three randomized trials (247 participants) were included. Two studies assessed the use of folate in addition to other treatment, and found that adding folate reduced Hamilton Depression Rating Scale (HDRS) scores on average by a further 2.65 points [95% confidence interval (CI) 0.38-4.93]. Fewer patients treated with folate experienced a reduction in their HDRS score of less than 50% at 10 weeks (relative risk 0.47, 95% CI 0.24-0.92). The remaining study found no statistically significant difference when folate alone was compared with trazodone. The identified trials did not find evidence of any problems with the acceptability or safety of folate. The limited available evidence suggests folate may have a potential role as a supplement to other treatment for depression. It is currently unclear if this is the case both for people with normal folate levels, and for those with folate deficiency.
Ten patients received first mianserin (30 mg per day) and second trazodone (150 mg per day), while 9 patients received these treatments in the opposite sequence, with at least 2-week intervals between the two phases. Blood was sampled at steady state, 1-3 weeks after initiation of each treatment. Plasma concentrations of mianserin, the separate enantiomers S(+)- and R(-)-mianserin, desmethylmianserin, trazodone and m-CPP were measured by means of high-performance liquid chromatography.
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Oils formed in several cases resulting in preliminary elimination of mesyl and esyl salts and four crystallizing solvents. Crystallinity was observed in 34 of 44 scaled-up trazodone salts. PXRD, DSC, and hygroscopic analyses indicated a number of new salts that were comparable in physicochemical parameters to the marketed HCl salt. Among them, the tosylate salt showed uniqueness for new applications.
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Numerous "second-generation" antidepressants with pharmacological profiles and chemical structures different from those of the tricyclic antidepressants have recently been developed. We examined the actions of four of these compounds (mianserin, maprotiline, trazodone and fluvoxamine) on the responding of pigeons under two different multiple (mult) schedules of grain presentation (a mult fixed-interval (FI) 600-s fixed-ratio (FR) 30-response and a mult FI 200-s FI 200-s in which responding in one component was punished by intermittent presentation of a brief electric shock). The rate of FI 600-s responding was greatly increased by several doses of maprotiline and mianserin, which either did not affect or produced only small increases in the rate of FR 30 responding. Fluvoxamine and trazodone did not produce similar differential effects. Relatively low doses of maprotiline, mianserin and trazodone decreased the FI quarter-lives. Fluvoxamine only decreased the FI quarter-life at a dose that largely eliminated responding. Mianserin produced proportionally greater increases in the rate of punished FI 200-s responding than in the rate of unpunished FI 200-s responding. Selective effects on punished responding were not seen with maprotiline, fluvoxamine and trazodone.
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To investigate whether the outcome of treatment with trazodone CR in primary insomnia differs between patients with and without subthreshold depression.
Trazodone is commonly used in the treatment of insonmia and nightmares in patients with PTSD. There is little evidence in the literature for this practice.
Overall, 8.6% of patients switched antidepressants during the first 90 days of treatment. The highest rates of switching were among patients initiating trazodone (47.4%), tricyclic antidepressants (26.6%), and mirtazapine (17.2%); the lowest switching rates occurred after starting venlafaxine (6.5%) or sertraline (7.4%). Antidepressant switching was significantly related to recent emergency mental health treatment (adjusted odds ratio [AOR]=1.7, 99% confidence interval [CI]=1.3-2.2); treatment of major depressive disorder versus other depressive disorders (AOR=1.4, CI=1.3-1.5), especially severe major depressive episodes (AOR=1.6, CI=1.4-1.9); and inversely related to moderately high versus low initial antidepressant dose (AOR=.7, CI=.6-.8). Several other patient characteristics were significant but less powerful predictors of antidepressant switching.
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