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To investigate the relationship between 5-HTT occupancy and a wide range of antidepressant dosing protocols.
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The study was designed to investigate, by weekly thyrotropin-releasing hormone tests, possible patterns of thyroid-stimulating hormone (TSH) responses which may indicate therapeutic mechanisms of antidepressant and neuroleptic drugs in patients with depressive and paranoid-hallucinatory syndrome during their process of recovery (3-9 weeks). 65 depressed women and 33 paranoid-hallucinatory women have been studied while on antidepressant (clomipramine) or neuroleptic (haloperidol) treatment, respectively. Four patterns of TSH response were observed. Patients with a pattern of a 'disblunting TSH response' (normalization of an abnormal low response) during drug treatment had a significantly higher chance to recover compared to patients with other TSH response patterns. This finding was independent of psychopathological features and drugs used for treatment. A hypothesis of 'malactivation' as a pathogenetic indicator of various psychotic states is being presented.
The most frequent symptom of taeniasis is the discharge of proglottids (93.7%). Gravid proglottids which do not have uterine pores are damaged when they exit the anus by their movement. Because of this damage most of the eggs contaminate the perianal tract. The cellophane tape technique that is used for getting perineum material is also a convenient technique for diagnosis of taeniasis. A 36 year-old woman was admitted to our parasitology clinic complaining of a watering mouth for one year, of abdominal pain, and of loss of appetite for 6 months, and who had discharged proglottids from time to time. She had been eating raw meat since her childhood and had had treatment for taeniasis fifteen years ago. She has also been under treatment for obsessive and compulsive neurosis and depression for two years and complained of constipation that was the side effect of the drug clomipramine HCL. She was given treatment with niclosamide and purgative treatment. The result of the treatment was incomplete because the patient refused to use the purgative. She was called for follow up controls two weeks and six months after treatment and after six months did not have any evidence of infection in her stools. When she was asked, the patient said that she did not need to use the drugs for the treatment of obsessive and compulsive neurosis and depression any more since her symptoms had decreased. According to various authorities, taeniasis is thought to be the cause of psychiatric symptoms due to its neural and psychological effects. These claims have been confirmed in our case because of her psychiatric symptoms decreased after the taeniasis treatment. Thus, the view that there is a relationship between intestinal parasites and psychiatric disease has been strengthened.
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A review of the efficacy of antidepressant drug treatment in patients with obsessive-compulsive disorder (OCD), using a meta-analytic approach.
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Although pindolol can accelerate the antidepressant action of selective serotonin reuptake inhibitors in previously untreated patients, it does not elicit a rapid clinical response in treatment-resistant patients within a 10-day period.
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The aim of our study was to analyze the effects of two ADs, the tricyclic (TCA) clomipramine and the serotoninergic antidepressant (SSRI) citalopram on the motor cortex excitability in major depressed patients with TMS.
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Patients taking tricyclic antidepressants (TCA) can experience toxicity or severe side effects. As a rapid and less technically demanding alternative to quantitative serum analysis, most laboratories offer qualitative immunoassays to assist in the evaluation of a suspected TCA overdose. However, the relationship between quantitative serum and qualitative urine levels of TCA-related compounds and their metabolites has not been comprehensively studied. Serum high-performance liquid chromatography results were compared to the qualitative urine results using the Syva Rapid Test and the Biosite Triage. Serum concentrations of amitriptyline, desipramine, doxepin, imipramine, and nortriptyline ranging from subtherapeutic to toxic triggered a positive response on both urine immunoassay devices. On the other hand, neither immunoassay uniformly detected clomipramine, even at serum levels greater than the therapeutic range. False positives due to cyclobenzaprine were more common with the Biosite assay. For virtually all positive urine TCA findings, it was not possible to determine whether the positive results corresponded to subtherapeutic, therapeutic, supratherapeutic, or toxic serum concentrations. Because urine immunoassays are the only option for many laboratories analyzing specimens for TCAs (especially in an emergency setting), clinicians must understand the limitations and interpret results in conjunction with clinical findings and/or quantitation of serum levels.
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A new antidepressant, zimelidine, which is a selective inhibitor of 5-HT-uptake, was tested in an open study of 13 patients, in each of whom the principal clinical diagnosis was phobic neurosis. The dose varied from 200 to 300 mg daily. After 6 weeks of treatment, 6 patients dropped out of the study as they were not appreciably improved, but 7 patients definitely improved and completed a treatment course of at least 12 weeks. In these cases it was possible to observe subjective relief of symptoms, improved social function, increased working capacity and a reduced need for anxiolytics. The effect appeared similar to the previously described effects of clomipramine treatment. The incidence of side effects was low and those that occurred were mild. Tolerance was assessed as very good by the great majority of patients. The study suggests that zimelidine has a favourable effect on mild, moderate, and even in some severe phobic conditions. Some comparisons with MAO-inhibitors were made. The results are sufficiently encouraging to suggest a controlled study.
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An evolution in antidepressant development in recent decades has resulted in agents with selective mechanisms of action. Although agents with a single selective mechanism of action were initially thought to have advantages over other antidepressants, investigators now recognize that combined-action antidepressants, such as venlafaxine and clomipramine, may offer additional advantages in terms of increased efficacy and improved tolerability. In fact, a growing body of clinical evidence suggests that compared with the single-action selective serotonin reuptake inhibitors, both venlafaxine and once-daily venlafaxine extended release (venlafaxine XR) have shown an enhanced efficacy that extends over the entire spectrum of major depression and anxiety disorders, an earlier onset of action, less tendency to cause weight gain, and a low risk for potentially serious drug-drug interactions with many commonly used medications. These advantages make venlafaxine XR an important option for the treatment of major depression and anxiety disorders.
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28 patients aged from 31 to 69 years with endogenous depression were studied. All cases were drug-resistant i.e. they did not improve after a treatment with tricyclic antidepressants and in four cases also after electroconvulsive therapy. The group were managed with intravenous infusions of clomipramine or maprotiline followed by oral administration of the drug. Clomipramine was given i.v. at doses 75-300 mg daily for 7 to 16 days and maprotiline at 75-200 mg daily for 6 to 20 days. Remission of depressive symptoms was observed in 43% of cases and the first signs of improvement were observed on tenth day of the treatment. Tolerance to both drugs given parenterally in majority of cases was satisfactory. Half of the group did not show any untoward events. The rest of the group displayed local tissue reactions, both increased and decreased blood pressure, weakness, drowsiness, anxiety, vertigo, hyperpyretic reactions. Four patients had the treatment discontinued because of local tissue reactions or increased blood pressure or hyperpyretic reactions.
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Linear regression analysis showed that having a partner and sensory phenomena preceding compulsions were associated with better response to clomipramine treatment (P = .04 and P = .002, respectively). Tic comorbidity and early onset of symptoms were not associated with poorer response.
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These neuropeptide results coupled with evidence that central administration of corticotropin-releasing hormone, vasopressin, and somatostatin to laboratory animals increases arousal and acquisition of conditioned behaviors whereas central administration of oxytocin has opposite behavioral effects are consistent with a role for these neuropeptides in the pathophysiologic processes and pharmacologic treatment of obsessive-compulsive disorder.
The purpose of the present work was to study the correlations between clinical response and plasma concentrations of clomipramine or desmethylclomipramine, using two different methods of dosage: radio-immunoassay and high pressure liquid chromatography, compared with mass spectrometry method. The results vary according to the method used, suggesting that methodological problems might explain, at least partly, the discrepancies observed in the literature.
Acute administration in the mid-light phase of a number of antidepressant drugs of different pharmacological profiles elevated pineal and plasma melatonin (measured by radioimmunoassay). Following chronic treatment with the tricyclic antidepressant clomipramine, the elevation was significantly reduced. This may be an effect of reduced beta-adrenergic receptor sensitivity after chronic clomipramine administration, analogous to other findings of reduced beta-adrenergic receptor binding and reduced noradrenaline-sensitive adenylate-cyclase response.
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The corpus callosum (CC) is the main white matter tract involved in interhemispheric brain communication. We establish that uptake of [3H]5-hydroxytryptamine (5-HT) in CC is partially inhibited by some antidepressants. Slices of the adult rat CC had a high-affinity uptake of 5-HT. About 80% of this uptake was Na+ dependent, with a Michaelis-Menten constant, Km, of 420 +/- 80 nM and a rate of 5-HT uptake, Vmax, of 9.5 +/- 0.8 pmol/mg protein/min. The 5-HT uptake was reduced approximately 60% at pH 5 compared with that at pH 7. Fluoxetine (Prozac) inhibited only 43% of 5-HT uptake in a concentration-dependent manner, with an affinity constant, Ki, of 44.7 +/- 10.0 nM. We also studied the effects of other monoamine uptake inhibitors, all at 10 microM, and found that zimelidine, imipramine, and clomipramine inhibited 5-HT uptake in the CC by approximately 30-40%. The fluoxetine-insensitive 5-HT uptake was not altered by high concentrations of dopamine plus norepinephrine. The present data show that Na(+)-dependent 5-HT uptake occurs in the CC and optic nerve and that this uptake is partially sensitive to antidepressants and probably mediated by the serotonin transporter, which may be relevant during depression.
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Premature ejaculation (PE) is commonly defined as ejaculation with minimal sexual stimulation before, on or shortly after penetration and before the person wishes it. PE can be either lifelong and present since first sexual experiences (primary), or acquired (secondary), beginning later (Godpodinoff ML. Premature ejaculation: clinical subgroups and etiology. J Sex Marital Ther 1989;15:130-4). Treatments include behavioural and pharmacological interventions.
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The present study was undertaken to examine the drug interactions between 3,4-methylenedioxymethamphetamine (MDMA) and paroxetine or several compounds including the 3,4-methylenedioxybenzyl (piperonyl) group in mice. The time course of radioactivity in the mouse brain after i.v. administration of the tracer amount (approximately 70 ng/kg) of [3H]MDMA was altered significantly by coinjection of carrier MDMA (15 mg/kg) or by pretreatment with paroxetine (10 mg/kg, i.p., 5 min). Furthermore, the radioactivity in the brain 60 min after injection of [3H]MDMA was increased significantly by pretreatment with paroxetine, but not by pretreatment with 6-nitroquipazine, fluoxetine, clomipramine, GBR 12909 or desipramine, indicating that paroxetine-induced alteration of the brain radioactivity was not due to the inhibitory effect of 5-hydroxytryptamine (5-HT) uptake of paroxetine. The radioactivity in the brain 60 min after injection of [3H]MDMA was increased significantly by pretreatment with 3,4-methylenedioxyamphetamine (MDA), MDMA, 1-piperonylpiperazine and N, alpha-dimethylpiperonylamine, but not by pretreatment with piperonylacetone, piperonyl butoxide and piperonyl isobutyrate. HPLC analyses indicated that the alteration of brain radioactivity 60 min after injection of [3H]MDMA was, in part, due to inhibition in the metabolism of [3H]MDMA to radioactive metabolite(s). The present results suggest that a specific mechanism for the 3,4-methylenedioxyphenyl group which rapidly alters the disposition and metabolism of [3H]MDMA may exist in brain and peripheral organs of mice.
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Using the method of willingness to pay (WTP), this study assesses the value of a new antidepressant, moclobemide, relative to that of tricyclic antidepressants (TCAs), which have equivalent efficacy but less favourable adverse effect profiles. From a published meta-analysis of controlled clinical trials, we identified 7 adverse effects, the risk of which differed significantly between moclobemide and TCAs. We obtained risk reduction data and descriptions of adverse effects from interviews with 95 individuals who had mild to moderate depression and who had been taking one or more TCAs in the previous year. Using a visual analogue scale, respondents ranked and rated each adverse effect. Participants were then asked (using the scenario of additional out-of-pocket drug payment) to quantify the maximum amount that they would pay for a new drug that reduced each adverse effect by the specified probability. Blurred vision and tremor were ranked and rated as the most bothersome adverse effects, with dry mouth being the least bothersome. On average, respondents were willing to pay an additional $Can22 per month [95% confidence interval (CI) 16-28] to reduce the risk of blurred vision from 10 to 5%. The lowest WTP value was for reducing the risk of dry mouth from 40 to 15%, at $Can11 per month (95% CI 8-15). Although not measured directly, we derived 2 estimates of WTP for multiple (i.e. all 7) risk reductions. We obtained upper and lower WTP limits of $Can118 and $Can36 per month, respectively, depending upon aggregation assumptions. Compared with the TCAs amitriptyline and imipramine, the net cost of moclobemide is greater, but the overall net benefit (WTP minus cost) is ambiguous given uncertainty about WTP aggregation over adverse effects. However, compared with the TCAs desipramine and clomipramine, the net benefit of moclobemide is unambiguously positive. We conclude that the WTP approach is a potentially valuable tool that requires more development for use in healthcare economic evaluation.
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It is relevant for medical practitioners to be aware of the severe neuropsychiatric side effects of mefloquine as malaria prophylaxis. It requires investigation of the risk factors such as personal or family history of psychiatric disorders.
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This is the first study about SS based on a large pharmacovigilance database and published in English. Our results reveal not only the frequent involvement of antidepressants and tramadol, the importance of DDIs (both pharmacodynamic and pharmacokinetic), but also the significant risk of SS even with a single serotonergic drug used at normal dose.
Orthostatic hypotension, the clinically most important side effect in treatment with tricyclic antidepressants, was investigated in a double-blind study with clomipramine and the selective serotonin reuptake inhibitor citalopram given for 5 weeks. All patients were initially given placebo for 1 week. In the clomipramine group (n = 17) a significant orthostatic drop in the systolic blood pressure was observed during treatment; this remained significant over the whole investigational period. A curvilinear correlation was demonstrated between the orthostatic drop in systolic blood pressure and the plasma levels of clomipramine and desmethylclomipramine. The most pronounced orthostatic reaction was thus seen in 1-2 weeks, at plasma levels of 25-75 micrograms/l (clomipramine). The correlation between the subjective symptoms and the measured orthostatic drop was poor, as was the correlation between the subjective symptoms and the plasma levels of the two active compounds. The change in orthostatic heart rate during clomipramine treatment was insignificant. In the citalopram group (n = 15) no significant changes in orthostatic blood pressure or heart rate were demonstrated during treatment and these patients had no orthostatic complaints.
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p,p'-DDT (100 to 600 mg per kilogram orally) produced spontaneous and stimulus-sensitive myoclonus in mice and rats. Drugs that enhance brain serotonergic activity reduced p,p'-DDT-induced myoclonus, and serotonin antagonists invariably aggravated this syndrome. p,p'-DDT-treated rats had increased concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in seven regional areas, but serotonin was increased only in the midbrain and cerebellum. We postulate that p,p'-DDT-induced myoclonus may be causally related to blockage of serotonin receptors or inhibition of serotonin release into the synapse, resulting in functional deficiency of this neurotransmiter at the receptor site.
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Macro-autophagy is associated with drug resistance in various cancers and can function as an adaptive response to maintain cell survival under metabolic stresses, including androgen deprivation. Androgen deprivation or treatment with androgen receptor (AR) signaling inhibitor (ARSI), Enzalutamide (MDV-3100, ENZA) or bicalutamide induced autophagy in androgen-dependent and in castration-resistant CaP (castration-resistant prostate cancer (CRPC)) cell lines. The autophagic cascade triggered by AR blockage, correlated with the increased light chain 3-II/I ratio and ATG-5 expression. Autophagy was observed in a subpopulation of C4-2B cells that developed insensitivity to ENZA after sustained exposure in culture. Using flow cytometry and clonogenic assays, we showed that inhibiting autophagy with clomipramine (CMI), chloroquine or metformin increased apoptosis and significantly impaired cell viability. This autophagic process was mediated by AMP-dependent protein kinase (AMPK) activation and the suppression of mammalian target of rapamycin (mTOR) through Raptor phosphorylation (Serine 792). Furthermore, small interfering RNA targeting AMPK significantly inhibited autophagy and promoted cell death in CaP cells acutely or chronically exposed to ENZA or androgen deprivation, suggesting that autophagy is an important survival mechanism in CRPC. Lastly, in vivo studies with mice orthotopically implanted with ENZA-resistant cells demonstrated that the combination of ENZA and autophagy modulators, CMI or metformin significantly reduced tumor growth when compared with control groups (P<0.005). In conclusion, autophagy is as an important mechanism of resistance to ARSI in CRPC. Antiandrogen-induced autophagy is mediated through the activation of AMPK pathway and the suppression of mTOR pathway. Blocking autophagy pharmacologically or genetically significantly impairs prostate cancer cell survival in vitro and in vivo, implying the therapeutics potential of autophagy inhibitors in the antiandrogen-resistance setting.
In this study, antidepressants with selectivity for the noradrenaline transporter (reboxetine and desipramine), or the serotonin transporter (fluoxetine and clomipramine) were examined in terms of their ability to promote an anti-inflammatory cytokine phenotype in human blood. In addition, we examined the ability of trimipramine; a tricyclic antidepressant that is devoid of monoamine reuptake inhibitory properties on cytokine production. Lipopolysaccharide (LPS) was used to stimulate monocyte-derived pro-inflammatory (IL-1beta, TNF-alpha, IL-12) and anti-inflammatory (IL-10) cytokines, whilst concanavalin A (Con A) was used to stimulate T-cell (Th(1): IFN-gamma and Th(2/3): IL-10) cytokines. All of the antidepressants suppressed IFN-gamma production in the 10-50 microM concentration range, irrespective of their preference for serotonin or noradrenaline transporters. This suppression of IFN-gamma production was paralleled by reduced T-cell proliferation, therefore we suggest that the ability of antidepressants to suppress IFN-gamma production may be related to their anti-proliferative properties. The fact that trimipramine also suppressed IFN-gamma production and T-cell proliferation indicates that these immunomodulatory actions of antidepressants are most likely unrelated to inhibition of monoamine reuptake. Interestingly, exposure to a lower concentration (1 microM) of the antidepressants tended to increase T-cell-derived IL-10 production, with significant effects elicited by the noradrenaline reuptake inhibitors reboxetine and desipramine. In contrast to the robust actions of antidepressants on T-cell derived cytokine production, they failed to induce any consistent change in LPS-induced monocyte cytokine production. Overall, our results indicate that IFN-gamma producing T-cells (Th(1) cells) are the major target for the immunomodulatory actions of antidepressants, and provide evidence questioning the relationship between the monoaminergic reuptake properties of antidepressants and their immunomodulatory effects. The potential clinical significance of the anti-inflammatory actions of antidepressants is discussed.
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The number of qualified empirical studies is few. These studies have shown clomipramine and serotonin-reuptake inhibitors to be very effective in the therapy of obsessive-compulsive disorders in childhood and adolescence. On the basis of the studies available, no specific recommendation can be made with regard to pharmacological dosage. For clomipramine the effective daily dose probably ranges somewhere between 75-150 mg, for fluoxetin between 20-60 mg, and for fluvoxamine between 100-250 mg. However, it must be kept in mind that in individual cases, improvement sometimes will not be noticeable until after 8 to 10 weeks of treatment have elapsed.
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Recent studies suggest the occurrence of a neurological dysfunction in Obsessive-Compulsive Disorder (OCD). The purpose of the present study was to verify the clinical value of a neurological evaluation in patients with the disease. We submitted 15 patients with OCD (five of whom were under clomipramine) and 15 controls in a detailed neurological examination, including assessment of the neurological soft-signs. Eleven patients (73.3 percent) and four controls (26.7 percent) presented abnormalities on examination. The main findings among the patients were: palmomental reflex (six cases); mirror movements (five cases); agraphestesia and dysdiadochokinesia (three cases). Three out of the four patients who had a normal examination were on clomipramine. Palmomental reflex was the main finding among the controls. These results, although preliminary, stress the interest and usefulness of performing a detailed neurological examination in OCD.
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A double-blind between-patient study is described which was aimed at assessing the efficacy and tolerability of clomipramine (Anafranil, Geigy Pharmacetuicals) in clinically depressed patients with obsessive-compulsive and phobic psychopathological traits. Twenty patients of either sex aged between 18 and 65 years were randomly allocated to treatment with clomipramine (50 mg twice daily) or to treatment with an identical placebo. Patients were assessed at the commencement of the study and at two-weekly intervals over the six-week duration of the trial. By the methods of assessment used, clomipramine proved to be highly statistically significantly superior to placebo.
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The serotonin syndrome, induced by serotoninergic agents, includes confusion, agitation, myoclonus, diaphoresis, tremor and diarrhea. The authors prospectively evaluated all these symptoms in 38 depressed inpatients fullfilling DSM-III-R criteria for major depression. Sixteen (42%) of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously, and 10 patients presented at the same time tremor plus myoclonus, diaphoresis and shivering. Except for 2 patients, symptoms were transient, lasted less than 1 week and disappeared with the pursuit of treatment.
In this open case series, the dose-response relationship of atypical antipsychotic augmentation in the treatment of obsessive compulsive disorder (OCD), and the dose-severity relationship in atypical anti psychotic-induced OC symptoms were examined. Three patients were identified who had either refractory OCD or OC symptoms following administration of atypical antipsychotics such as olanzapine and risperidone.
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The mainstay of the pharmacologic treatment of obsessive-compulsive disorder (OCD) is a 10- to 12-week trial of a potent serotonin reuptake inhibitor (SRI) at an adequate dose. Double-blind, placebo-controlled trials have established the anti-obsessive-compulsive (OC) efficacy of five different SRIs. One of the most thoroughly studied of these SRIs is fluvoxamine, the focus of this article. Fluvoxamine's pharmacologic and pharmacokinetic properties, its efficacy, and guidelines for its clinical use in OCD and related disorders are briefly reviewed. Potential drug-drug interactions are discussed and placed in clinical perspective. The management of common SRI-induced side effects is also addressed. Recent comparative studies suggest that fluvoxamine may be equivalent in efficacy to clomipramine, yet better tolerated. Fluvoxamine shows promise in the treatment of several so-called OC-spectrum disorders, but additional controlled trials are needed.