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We report a patient in whom cyproheptadine-induced hepatitis was followed by prolonged cholestasis marked by elevation of serum alkaline phosphatase levels, gammaglutamyltransferase and bile acid levels, and disappearance of small bile ducts. Chlorpromazine and imipramine, which can induce a similar acute hepatitis followed by protracted cholestasis, have a close chemical structure (i.e., a tricyclic ring). We suggest that this structure might be involved in this type of hepatotoxicity.
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Autism is a neurodevelopmental disorder, with a multifactorial etiology, characterized by severe abnormalities in communications, social awareness and skills, and the presence of restrictive and stereotyped patterns of behaviors. It is traditionally considered a "static" encephalopathic disorder without any specific cure and few effective biomedical interventions. There are various factors which are involved in the etiopathogenesis of autism or autism spectrum disorder (ASD) such as impaired immune responses, neuroinflammation, abnormal neurotransmission, oxidative stress, mitochondrial dysfunction, environmental toxins and stressors. The autism is often associated with a number of genetic disorders such as fragile X syndrome, tuberous sclerosis, epilepsy and Down syndrome. The recent approaches to autism treatment included various non-pharmacological and pharmacological therapy such as food supplementation, detoxification, treatment of neuroinflammation, immunologic treatments and psychotropic medications, which are found to be effective in treating various behavioral symptoms of autism. In current practice, there is no curative treatment for autism but the recommended treatment for autism involves educational therapies: speech therapy, sensory integration therapy, auditory therapy. There are classes of different pharmacological agents which are found to be effective in improving behavioral symptoms of ASD such as neurotransmitter reuptake inhibitors (fluoxetine), tricyclic antidepressants (imipramine), anticonvulsants (lamotrigine), atypical antipsychotics (clozapine), acetylcholinesterase inhibitors (rivastigmine), etc. New classes of drugs with novel mechanisms of action should be there so that this disorder will become less prevalent in the future.
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There are at least two theoretical reasons to believe antidepressants might help in smoking cessation. Nicotine withdrawal may produce depressive symptoms or precipitate a major depressive episode and antidepressants may relieve these. Nicotine may have antidepressant effects that maintain smoking, and antidepressants may substitute for this effect. Alternatively, some antidepressants may have a specific effect on neural pathways underlying nicotine addiction, independent of their antidepressant effects.
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The results showed that moclobemide and imipramine are equally effective in reducing psychic and somatic anxiety in depressed patients, independent of the severity of anxiety or how it was defined. The criterion of 50% decrease of anxiety scores (at week 4) was consistently reached by 60-70% of patients in all drug sub-groups. The time course of effects on anxiety symptoms was similar with both drugs. It ran parallel to the regression of depression, with significant improvement of anxiety symptoms by week 2 on all measures. The frequency of benzodiazepine (BDZ) co-administration was not systematically correlated with the severity of anxiety. Moreover, co-prescription of BDZ did not change the outcome of drug treatment, with respect either to anxiety symptoms or global therapeutic efficacy. In placebo groups, significant negative interactions were found between severity of anxiety and the efficacy of treatment, which decreased with increased anxiety. The incidence of adverse events with moclobemide was barely higher than in the placebo group. Insomnia (4.9%) was the only adverse event significantly higher with moclobemide than with other treatments. Drop-out rates in drug groups were similar (27%) and unrelated to the severity of anxiety. In the placebo group, drop-outs were significantly higher than in drug groups (39%), and were positively correlated with the severity of anxiety.
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The charts of 150 inpatients and 51 outpatients treated with a monoamine oxidase inhibitor (MAOI)-tricyclic antidepressant combination were reviewed. The incidence and severity of side effects among the patients on the combined regimen were essentially the same as those seen in the control groups. There were no deaths or strokes resulting from use of this regimen. The most frequent troublesome side effect was orthostatic hypotension. We conclude that the use of a MAOI-tricyclic combination in oral therapeutic doses is safe. However, the efficacy of this combination has not yet been proved, and it may be particularly toxic if taken in an overdose.
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The take up time of a standardized alimentary material is a simple component of hamster hoarding behaviour. This value was modified by administrations of the following compounds: diazepam, chlorpromazine, meprobamate, apomorphine, d-amphetamine, piribedil, fenfluramine, sulpiride, imipramine, phenobarbital, clonidine and morphine. The change consisted of a varying increase in the take up time, dependent upon the substance and dosage. High doses of chlorpromazine, apomorphine and fenfluramine inhibited the take up. A behavioural study connected with alimentary take up was included in the experiment. Some behavioural modifications (increase or decrease in motor activity, myorelaxation, stereotyped exploration, reciprocating movements) demonstrated differences between the studied compounds related to their pharmacological properties. The immediate consumption of food, without take up and hoarding behaviour, observed with meprobamate treatment, was an interesting and unexpected change in hamster behaviour. The measurement of the take up time and analysis of behavioural modifications may be useful in comparing and preliminary screening of new psychopharmacological compounds.
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Paroxetine is a selective serotonin reuptake inhibitor (SSRI), with antidepressant and anxiolytic activity. In 6- to 24-week well designed trials, oral paroxetine 10 to 50 mg/day was significantly more effective than placebo, at least as effective as tricyclic antidepressants (TCAs) and as effective as other SSRIs and other antidepressants in the treatment of major depressive disorder. Relapse or recurrence over 1 year after the initial response was significantly lower with paroxetine 10 to 50 mg/day than with placebo and similar to that with imipramine 50 to 275 mg/day. The efficacy of paroxetine 10 to 40 mg/day was similar to that of TCAs and fluoxetine 20 to 60 mg/day in 6- to 12-week trials in patients aged > or =60 years with major depression. Paroxetine 10 to 40 mg/day improved depressive symptoms to an extent similar to that of TCAs in patients with comorbid illness, and was more effective than placebo in the treatment of dysthymia and minor depression. Paroxetine 20 to 60 mg/day was more effective than placebo after 8 to 12 weeks' treatment of obsessive-compulsive disorder (OCD), panic disorder, social anxiety disorder (social phobia), generalised anxiety disorder (GAD) and post-traumatic stress disorder (PTSD). Improvement was maintained or relapse was prevented for 24 weeks to 1 year in patients with OCD, panic disorder, social anxiety disorder or GAD. The efficacy of paroxetine was similar to that of other SSRIs in patients with OCD and panic disorder and similar to that of imipramine but greater than that of 2'chlordesmethyldiazepam in patients with GAD. Paroxetine is generally well tolerated in adults, elderly individuals and patients with comorbid illness, with a tolerability profile similar to that of other SSRIs. The most common adverse events with paroxetine were nausea, sexual dysfunction, somnolence, asthenia, headache, constipation, dizziness, sweating, tremor and decreased appetite. In conclusion, paroxetine, in common with other SSRIs, is generally better tolerated than TCAs and is a first-line treatment option for major depressive disorder, dysthymia or minor depression. Like other SSRIs, paroxetine is also an appropriate first-line therapy for OCD, panic disorder, social anxiety disorder, GAD and PTSD. Notably, paroxetine is the only SSRI currently approved for the treatment of social anxiety disorder and GAD, which makes it the only drug of its class indicated for all five anxiety disorders in addition to major depressive disorder. Thus, given the high degree of psychiatric comorbidity of depression and anxiety, paroxetine is an important first-line option for the treatment of major depressive disorder, OCD, panic disorder, social anxiety disorder, GAD and PTSD.
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We subjected Wistar rats to the forced swim test (FST) to compare the effects of two doses of imipramine in physically stressed rats (P: unavoidable electric footshocks), emotionally stressed rats (E: odors), or non-stressed rats (C). Stress or control sessions lasted 35 days. Drug treatments began on day 21 and continued for the next 14 days. E rats were placed for 10 min, once per day for 35 days, in a small non-movement-restricting cage impregnated with urine collected from a P rat. E and P rats exhibited opposite changes in locomotion. After 21 days of stress sessions, P rats displayed the longest immobility times in the FST, followed by E rats. In the P group, on day 7 of treatment (day 28 of the study), imipramine (2.5 mg/kg) reduced immobility time to baseline values. In the E group, immobility time decreased only after 14 days of treatment with the low imipramine dose. The high dose of imipramine (5.0 mg/kg) reduced immobility time at day 7 of treatment in all groups. In conclusion, physical and emotional stress similarly increased immobility time in the FST, but emotional stress appears to be more resistant to imipramine treatment.
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Enuresis is a symptom that is frequently encountered in child psychiatric evaluations. Careful assessment is required to identify specific urologic, developmental, psychosocial, and sleep-related etiologies. For most children with enuresis, however, a specific etiology cannot be determined. Treatment then involves supportive approaches, conditioning with a urine alarm, or medications--imipramine or desmopressin acetate. The psychosocial consequences of the symptom must be recognized and addressed with sensitivity during the evaluation and treatment of enuresis.
Myotonic dystrophy or Steinert's disease is an autosomal dominant hereditary disease affecting the entire system. Apart from the myotonic phenomenon it involves muscular atrophy, endocrine disorders, baldness, cardiac arrhythmias, hyperglycaemia, cataracts. Over the years a number of drugs have been tried with results on the myotonia that are still debated. They include quinine, corticosteroids, L-DOPA, potassium-binding resins, procainamide, phenytoin, diphenylhydantoin, N-propylajmaline, dantrolene sodium, carbamazepine, imipramine, baclofen, mexiletine. It is emphasised that only the identification of the biochemical defect involved in the disease will permit any efficient treatment of its symptoms or causes.
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Characteristics of hyperactive children, including speculation in regard to etiology, are reviewed. Drug effects studies and drug treatment of hyperactive behavior are examined, and unresolved issues are discussed. Conclusions indicate that individual differences in hyperative children should form the basis for treatment planning, rather than simply treating groups of children under the rubric "hyperactivity."
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The UDP-glucuronosyltransferases (UGTs) comprise a major excretion pathway for diverse endogenous and exogenous substrates. Relations are reported between polymorphisms of exon 1 of UGT1 and drug side effects or carcinogenesis, but few studies exist of common exon polymorphisms that exert influence throughout UGT1 isoforms. We analysed the polymorphism c.1091C>T, resulting in the amino acid substitution of p.P364L, found on common exon 4. We studied 187 healthy, adult Japanese volunteers. The allele frequency was 0.0053. We investigated the effect of p.P364L on glucuronidation of β-estradiol, acetaminophen, propofol, lamotrigine, imipramine and cyproheptadine in an in vitro expression study. The V(max) values for β-estradiol of p.P364L-UGT1A1, 1A3, 1A7, 1A8 and 1A10 were 36.6%, 82.1%, 26.8%, 29.2% and 22.5%, respectively, of the corresponding wild-type. Glucuronidation activity towards acetaminophen of p.P364L-UGT1A1, 1A6, 1A7, 1A8, 1A9 and 1A10 was 50.3%, 46.4%, 17.2%, 44.1%, 5.0% and 42.8%, respectively, of wild-type. Glucuronidation activity towards propofol of p.P364L-UGT1A7, 1A8, 1A9 and 1A10 was 44.0%, 49.8%, 29.0% and 71.1%, respectively, of wild-type. Substrate inhibition was observed in lamotrigine, cyproheptadine and imipramine glucuronidation by wild-type UGT1A4 but vanished for p.P364L. The presence of p.P364L near the UDP-glucuronic acid binding site could lead to extensive reduction of enzyme activity of many UGT1s. Our results suggest that p.P364L is an important mutation that could give rise to adverse effects of various drugs, or carcinogenesis. It is important to study common exon mutations because these can reduce activity of all UGT1 isoforms.
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Neo-natal rats emit ultrasonic vocalizations (USVs) when isolated from their mothers and littermates. Clinically effective anxiolytics reliably reduce USVs, making this behavior a useful animal model of the anxiolytic potential of novel pharmacological approaches to the treatment of anxiety. Here, we assess the hypothesis that USV duration (total time spent vocalizing) is a more sensitive measure of anxiolytic and antidepressant efficacy than USV number by testing established and putative anxiolytics in this model. Negative geotaxis and righting reflex latency were measured to assess sedating properties. The benzodiazepines, CDP (1-10 mg/kg) and diazepam (0.3-3 mg/kg), the 5HT(1A) partial agonist, buspirone (0.3-3 mg/kg), and the mGluR5 antagonist, MTEP (1-30 mg/kg), reduced USV duration at lower doses and to a greater magnitude than USV number. The benzodiazepines, unlike buspirone and MTEP, produced measurable sedation, but it was dissociable from reductions in USV duration. The SSRI antidepressants, fluoxetine (1-30 mg/kg) and citalopram (0.3-30 mg/kg), reduced USV duration more than number with no measurable effect on sedation. The tricyclic antidepressants, imipramine (1-10 mg/kg) and amitriptyline (1-30 mg/kg), had no effect dissociable from sedation. These data support USV duration as a more sensitive and useful measure than USV number in the isolated rat pup model.
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The relative efficacies of various antiarrhythmic drugs in the treatment of ventricular tachyarrhythmias are not well known. This study examined the effectiveness of imipramine, mexiletine, pirmenol, procainamide, propafenone, quinidine, and sotalol in patients with ventricular tachyarrhythmias who were enrolled in the Electrophysiologic Study versus Electrocardiographic Monitoring trial.
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Adipose tissue kinetics of chlorpromazine and imipramine, two drugs which are more lipophilic than thiopental, were studied in the rat. After single i.v. doses, the time-course of drug distribution was followed in adipose and various other tissues, until their concentrations in adipose tissues declined. Under these conditions the two drugs behaved almost identically. Among the tissues analyzed, the lowest concentrations were found in adipose tissue, with the exception of plasma. At its maximum concentration after about 30 minutes, total adipose tissue contained only 3% of the dose of administered drugs. Adipose/plasma and adipose/lung concentration ratios were 2-5 and 0.05, respectively. After maximum tolerated oral doses of imipramine for 3 weeks, similar steady state concentration ratios (plasma:adipose:brain:lung 1:3:12:96) were observed. In adipose tissue the imipramine/desmethylimipramine ratio was about 1, and the desmethylimipramine steady state levels did not increase with time. Literature data indicate that many basic lipophilic drugs are not stored in adipose tissue. This is now clearly shown for chlorpromazine and imipramine, even under extreme, subchronic conditions in the case of imipramine.
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To determine the possible role of endogenous opioid peptides in the action of imipramine and paroxetine in painful diabetic neuropathy, beta-endorphin concentrations in plasma were measured in 20 patients during a double-blind, placebo-controlled randomized three-way crossover trial. Despite a significant reduction in neuropathy symptoms during both imipramine and paroxetine treatment, the beta-endorphin level was unaltered throughout the study. The plasma concentration of beta-endorphin was not related to plasma drug concentrations. Thus, this study does not provide evidence of a role of endogenous opioid peptides in the mechanism of action of imipramine and paroxetine in painful diabetic neuropathy.
Spontaneously Hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats differ in their emotional responses to stress and antidepressant administration. We have analysed different neurochemical and psychoneuroendocrine responses to repeated pretreatments with fluoxetine, imipramine or desipramine (10 mg/kg p.o. daily for 4 weeks) in SHRs and WKY rats exposed to a daily 2-h restraint episode for the last 5 days of antidepressant administration. Following a 24-h wash-out period, WKY rats displayed higher plasma antidepressant and antidepressant metabolite levels than SHRs. Fluoxetine pretreatment decreased [(3)H]citalopram binding at midbrain serotonin (5-HT) transporters, whereas tricyclic and/or fluoxetine decreased [(3)H]ketanserin binding at cortical 5-HT(2A) receptors, [(3)H]CGP-12177 binding at cortical ss-adrenoceptors, and [(3)H]nisoxetine binding at midbrain noradrenaline (NA) transporters in both strains. None of the antidepressants affected [(3)H]8-hydroxy-2-(di-N-propylamino)tetralin binding at hippocampal 5-HT(1A) receptors. In WKY rats, repeated restraint triggered a desipramine-sensitive 140% increase in hypothalamus [(3)H]nisoxetine binding; moreover, plasma adrenocorticotropin-releasing hormone responses to a 5-min open field test were amplified by prior repeated restraint in both strains, but desipramine prevented such an amplification in WKY rats only. However, neither elevated plus-maze nor open field behaviors of SHRs and WKY rats were affected by desipramine pretreatment. Thus, the SHR and WKY rat strains may prove useful in understanding how genetic differences in noradrenergic responses to repeated stress and desipramine treatment impact on adaptive processes.
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Examination showed blue-gray facial pigmentation. Light microscopy showed perivascular pigment granule deposits in the upper dermis that stained positively with Fontana-Masson stain and negatively with Prussian blue stain. Electron microscopy showed electron-dense bodies within histiocytes without clearly identifiable melanin granules, consistent with drug-induced pigmentation. Six weeks after switching to sertraline the patient reported a slight improvement of her cutaneous pigmentation.
Clitoral priapism is a rare condition that is associated with an extended duration of clitoral erection due to local engorgement of clitoral tissue resulting in pain. Although the pathophysiology is not completely understood, it has been associated with specific classes of medications, diseases that alter clitoral blood flow or others associated with small to large vessel disease. We present a case report of a 26-year-old patient who developed clitoral priapism without a clear medication or disease related etiology. The patient was treated with opiates, imipramine, non-steroidal anti-inflammatory medication, and local ice packs. She recovered uneventfully.
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The predictive influence of atypical features was not accounted for on the basis of depression severity.
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Results summarize a comprehensive survey of psychotropic effects on messenger ribonucleic acid (mRNA) expression evident in published data for 70 genes linked to PD risk.
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The effect of chronic treatment with antidepressant drugs fluoxetine (20 mg/kg) and imipramine (25 mg/kg) on the number of antibody-producing cells and the main T cell subpopulations in ASC mice characterized by genetic predisposition to depression-like states was studied at the peak of the SE-induced immune response (5×10(8)). Fluoxetine produced an immunostimulatory effect manifested in an increase in the relative and absolute number of IgM antibody-producing cells in the spleen and index of immunoreactivity (CD4/CD8). Administration of fl uoxetine to parental mouse strains without depression (CBA and AKR) had no effect (CBA) or reduced the immune response. The CD4/CD8 ratio did not increase under these conditions. Imipramine was ineffective in the correction of immune reactions in a depression-like state.
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Ro 11-2465, a cyanide derivative of imipramine with serotonin uptake inhibitory properties, was investigated in six healthy volunteers for its effect on serotonin concentration in blood platelets. The initial dose was 1 mg daily, the maximum dose of 3 mg being reached on day 3 and maintained for 7 days. A significant decrease in the platelet serotonin concentration was not observed until 3 days after the start of drug administration, after which depletion was rapid. After 5 days of treatment, the reduction was about 80% compared to pre-drug level. Serotonin restoration after drug withdrawal was very slow, and 5 days after discontinuation, it was still 70% below its baseline level.
Several authors have associated the cardiotoxicity of the tricyclic antidepressants with their capacity to potentiate the response to catecholamines. Trazodone is a psychotropic drug with a clinically proven antidepressant activity. It differes from the tricyclic antidepressants under several aspects (chemistry, pharmacology, mode and mechanism of action, etc.), including interactions with catecholamines. Contrary to the tricyclic antidepressants, it does not potentiate the response to catecholamines, but, instead, has an adrenolytic activity. We therefore decided to compare the cardiotoxicity of trazodone and of a tricyclic antidepressant, i.e. imipramine in the rat. The experiments were conducted on anaesthetized Long Evans rats, the drugs being administered by i.v. infusion until cardiac arrest occurred; ECG (lead II) and blood pressure (BP) were recorded at the same time. The primary effect of trazodone was its hypotensive action. ECG changes, consisting of a lengthening of the PR interval, were observed only when there was a marked drop in BP. The primary effect of imipramine, instead, consisted of disturbances in cardiac conduction. It is concluded that trazodone and imipramine produce different cardiovascular effects.
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This study was conducted to demonstrate stable performance using the FCN avoidance procedure, and examine the effects of drugs previously shown to affect impulsive behaviour using a conventional FCN schedule.
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With its chronic administration in a dose of 100 mg/kg lithium carbonate inhibited shaking of the head induced in mice with 5-hydroxytryptophan (5-HTP). This effect did not differ from the action following a single injection of lithium, when the interval between injection of lithium and of 5-HTP was one hour. With the interval lengthened to 24 hours the frequency of shaking diminished only under the effect of chronic administration. At the 5th, 10th and 21st day of a daily administration lithium failed to produce any effect on the hypothermal action of a reserpine-like agent Po 4-1284, but would reduce the protective action of imipramine in a ptosis test. A single injection of lithium made against the background of a chronic injection of water produced an opposite effect, viz. it significantly reduced the protective action of imipramine in hypothermia, but did not affect it with reference to ptosis. Hence, chronic administration of lithium leads to potentiation in its action of the serotonin-negative and central adreno-negative componets and to extenuating the peripheral adreno-negative component.