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The authors report on a female patient with bipolar affective disorder who presented with marked eosinophilia in conjunction with pneumonia five days after a medication change from amitriptyline to desipramine (for intolerable dry mouth). She improved with discontinuance of medications and supportive management, and her eosinophilia normalized. Reinstitution of desipramine was followed by prompt appearance of asymptomatic eosinophilia, which resolved with discontinuation of desipramine. A subsequent depression managed with amitriptyline was followed by no abnormal white blood count findings. Eosinophilia is occasionally encountered in imipramine or desipramine therapy and, although usually asymptomatic, appears to be manageable by switching to amitriptyline or nortriptyline.
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A sensitive radioimmunoassay for amitriptyline and nortriptyline in blood has been developed. The antibodies used in the radioimmunoassay were raised in a sheep against a conjugate of nortriptyline and bovine serum albumin. Using tritiated amitriptyline as the label, the assay is capable of detecting concentrations as low as 2.0 ng/ml in a 50 microliter sample of plasma. Cross-reactivity studies have demonstrated the specificity of the radioimmunoassay for both amitriptyline and nortriptyline, and comparison with gas-liquid chromatography assay has indicated the applicability of the assay to a routine situation. The radioimmunoassay has been used to study the plasma drug levels after single oral administration of amitriptyline to four volunteers. A wide variation in maximum drug concentrations, ranging from 18 to 62 ng/ml, was seen, with the time taken to reach the maxima ranging between 1.5 and 3 hours. A second concentration peak was seen in three of the volunteers, at 4 to 5 hours after ingestion of the drug.
A study on the possible sites of oxidation and epoxidation of nortriptyline was performed using electrochemical and quantum chemical methods; these sites are involved in the biological responses (for example, hepatotoxicity) of nortriptyline and other similar antidepressants. Quantum chemical studies and electrochemical experiments demonstrated that the oxidation and epoxidation sites are located on the apolar region of nortriptyline, which will useful for understanding the molecule's activity. Also, for the determination of the compound in biological fluids or in pharmaceutical formulations, we propose a useful analytical methodology using a graphite-polyurethane composite electrode, which exhibited the best performance when compared with boron-doped diamond or glassy carbon surfaces.
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In the sweet spot: Cocrystal structures of engineered neurotransmitter transporters reveal the binding mode of commonly prescribed antidepressants, providing a basis for a rational drug design for this class of proteins. The picture shows the structure of the dopamine transporter of Drosophila melanogaster in complex with the antidepressant nortriptyline.
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Randomized or quasi-randomized controlled trials evaluating combinations of pharmacotherapy and behavioural support for smoking cessation, compared to a control receiving usual care or brief advice or less intensive behavioural support. We excluded trials recruiting only pregnant women, trials recruiting only adolescents, and trials with less than six months follow-up.
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Patients were grouped as having early-onset (N = 129) or late-onset (N = 58) depression. Early onset was defined as having a first lifetime episode of major depression at age 59 or earlier; late onset was defined as age 60 or later. The two groups of patients were compared with respect to demographic and clinical characteristics, types of treatment given (nortriptyline and interpersonal psychotherapy), and treatment outcomes.
The drug transporter P-glycoprotein (P-gp) influences drug distribution across the blood-brain barrier (BBB) by actively extruding drugs into the neural capillaries. Several psychotropic drugs, including nortriptyline (NT) and risperidone (Risp), are substrates of P-gp. Here we compared the in vitro P-gp interactions of Risp and its major metabolite, 9-OH-Risperidone (OH-Risp), with their distribution over the BBB in P-gp knock-out mice and in rats where P-gp was inhibited. K(m) and V(max) were determined by an in vitro ATPase assay, and V(max)/K(m) ratios of 2.7 and 0.5 were recorded for Risp and OH-Risp, respectively, suggesting that Risp is a better substrate for P-gp than OH-Risp. In Mdr1a (-/-) knock-out mice, the brain-serum ratios of both Risp and OH-Risp were more than ten times those of control mice (14 and 11, respectively). When P-gp was inhibited with cyclosporine A (CsA) in Wistar rats, the effect was an order of magnitude less than that observed for the knock-out mice experiments (1-1.5 times the controls), and co-administration of NT had no effect. In conclusion, both Risp and OH-Risp interact with P-gp in vitro, and P-gp has a profound effect on Risp and OH-Risp distribution over the BBB, as is evident from the knock-out mice experiments. Drug-drug interaction effects in relation to P-gp, however, appear to be more limited.
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Randomised, cluster-randomised or quasi-randomised studies in which participants using active pharmacological treatment for smoking cessation are allocated to an intervention arm or a control arm. Eligible participants were adult (18+) smokers. Eligible interventions comprised any intervention that differed from standard care, and where the intervention content had a clear principal focus on increasing adherence to medications for tobacco dependence. Acceptable comparison groups were those that provided standard care, which depending on setting may comprise minimal support or varying degrees of behavioural support. Included studies used a measure of adherence behaviour that allowed some assessment of the degree of adherence.
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Protein-drug interactions of seven common pharmaceuticals were studied using solid-phase microextraction (SPME). SPME can be used in such investigations on the condition that no analyte depletion occurs. In multi-compartment systems (e.g. a proteinaceous matrix) only the free portion of the analyte is able to partition into the SPME fiber. In addition if no sample depletion occurs, the bound drug-free drug equilibria are not disturbed. In the present study seven pharmaceuticals (quinine, quinidine, naproxen, ciprofloxacin, haloperidol, paclitaxel and nortriptyline) were assayed by SPME. For quantitative purposes SPME was validated first in the absence of proteins. Calibration curves were constructed for each drug by HPLC-fluorescence and HPLC-UV analysis. SPME was combined to HPLC off-line, desorption occurring in HPLC inserts filled with 200 microL methanol. Binding of each drug to human serum albumin was studied independently. Experimental results were in agreement with literature data and ultrafiltration experiments, indicating the feasibility of the method for such bioanalytical purposes.
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To conduct the first randomized study comparing the efficacy of an antidepressant alone versus an antidepressant plus a neuroleptic in the treatment of late-life psychotic depression.
Major depression is a heterogeneous condition, and the search for neural correlates specific to clinically defined subtypes has been inconclusive. Theoretical considerations implicate frontostriatal, particularly subgenual prefrontal cortex (PFC), dysfunction in the pathophysiology of melancholia--a subtype of depression characterized by anhedonia--but no empirical evidence has been found yet for such a link. To test the hypothesis that melancholic, but not nonmelancholic depression, is associated with the subgenual PFC impairment, concurrent measurement of brain electrical (electroencephalogram, EEG) and metabolic (positron emission tomography, PET) activity were obtained in 38 unmedicated subjects with DSM-IV major depressive disorder (20 melancholic, 18 nonmelancholic subjects), and 18 comparison subjects. EEG data were analyzed with a tomographic source localization method that computed the cortical three-dimensional distribution of current density for standard frequency bands, allowing voxelwise correlations between the EEG and PET data. Voxel-based morphometry analyses of structural magnetic resonance imaging (MRI) data were performed to assess potential structural abnormalities in melancholia. Melancholia was associated with reduced activity in the subgenual PFC (Brodmann area 25), manifested by increased inhibitory delta activity (1.5-6.0 Hz) and decreased glucose metabolism, which themselves were inversely correlated. Following antidepressant treatment, depressed subjects with the largest reductions in depression severity showed the lowest post-treatment subgenual PFC delta activity. Analyses of structural MRI revealed no group differences in the subgenual PFC, but in melancholic subjects, a negative correlation between gray matter density and age emerged. Based on preclinical evidence, we suggest that subgenual PFC dysfunction in melancholia may be associated with blunted hedonic response and exaggerated stress responsiveness.
The three symptom dimensions provided sensitive descriptors of differential antidepressant response and enabled identification of drug-specific effects.
Recovery of good subjective sleep quality by early continuation treatment is useful in identifying which remitted elderly depressed patients will remain well with monthly maintenance interpersonal psychotherapy, following discontinuation of antidepressant medication, and which patients may be more vulnerable to recurrence of major depressive episodes in the absence of antidepressant medication.
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Nortriptyline combined with transdermal nicotine resulted in an increased cessation rate with little effect on withdrawal symptoms. This combination may represent an option for smokers in whom standard therapy has failed.
Brief incubation in low concentrations of nortriptyline, amitriptyline, or fluoxetine (all at 10(-5) M) did inhibit priming but not activation of hPMNs. Imipramine (10(-5) M) affected neither priming nor activation. Prolonged incubation in lower concentrations of all antidepressants influenced neither priming nor activation. However, at higher concentrations, all four compounds exerted cytotoxic effects: virtually all hPMNs were killed by amitriptyline and imipramine (both at 10(-3) M) or nortriptyline and fluoxetine (both at 10(-4) M).
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Subjects with DSM-III-R major depression were recruited for a study looking at prediction of antidepressant response. All patients were assessed using the Structured Clinical Interviews for DSM-III-R Axis I and Axis II, as well as rated on the Hamilton Rating Scale for Depression and the Montgomery-Asberg Depression Rating Scale (MADRS). Patients were then randomly assigned to treatment with fluoxetine or nortriptyline and reassessed at 6 weeks. The major outcome measure was percentage reduction in MADRS scores.
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Pre-treatment and posttreatment dexamethasone suppression test (DST) results in physically healthy elderly major depressives without dementia demonstrated an association between treatment and DST normalization. Sixty percent of subjects were nonsuppressors at baseline compared to 17% after intensive treatment. DST results normalized in 75% of initial nonsuppressors; none of the initial suppressors converted to nonsuppression. A strong correlation between clinical improvement and decreases in afternoon cortisol levels was identified. Initial suppression status did not influence this association. There was a nonsignificant trend for very high (> 15 micrograms/dl) afternoon cortisol levels to be associated with delusional depression. The advantage of using continuous rather than categorical measures to assess the relationship between reversal of depression and DST results is discussed.
Amitriptyline and nortriptyline are tricyclic antidepressants which act by enhancing the actions of norepinephrine and serotonin caused by blocking the re-uptake of various neurotransmitters at the neuronal membrane. A micellar liquid chromatographic procedure was developed to determine these drugs in serum samples for use in clinical monitoring.
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Structural brain measures associated with late life depression may not be related to short-term treatment response.
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Opioids effectively treat PHN without impairing cognition. Opioids and TCA act via independent mechanisms and with varied individual effect.
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Extensive work in the field has indicated a state-dependent hyperactivity of the hypothalamic-pituitary-adrenocortical (HYPAC) functions and unresponsiveness to dexamethasone suppression in at least 50% of patients suffering from endogenous depression. In this study, elderly outpatients, 60-85 years of age, suffering from major depressive illness according to research diagnostic criteria (RDC) were studied with the dexamethasone suppression test (DST). Careful diagnostic evaluation included RDC, the Newcastle index, and clinical interviews focusing on "endogenomorphic features." The great majority (83.3%) of patients diagnosed as endogenous depressives were nonsuppressors (abnormal DST) as compared to 16.7% nonsuppressors amongst nonendogenous patients. In addition, DST tended to normalize the clinical recovery. The research and clinical implications of our findings in this population are further discussed.
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In a situation in which a short-term isolated (I) and a group-housed (S) rat were placed together, the influence of various drugs on social behaviour was analysed. It was found that a single intraperitoneal injection of 7.5 mg/kg of the antidepressant drugs clomipramine, nortriptyline and mianserine normalized the increased social interactions of the isolated rat to the level of the group-housed rat, without affecting the social behaviour of that animal. This action of the drugs was not due to changes in locomotor activity. An opiate (morphine), an opiate antagonist (naloxone), a tranquilizer (diazepam), a neuroleptic (haloperidol) and a psychostimulant (amphetamine) did not preferentially influence the social behaviour of the isolated rat. Chronic treatment with the antidepressants did not reduce the increased social interactions of isolated animals. In spite of this it is clear that the increased social behaviour of short-term isolated rats was specifically affected by the antidepressant drugs. This suggests that this behavioural procedure might be useful for predicting antidepressant activity.
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Smokers try to quit only once every 2 to 3 years and most do not use proven treatments. Repeated, brief, diplomatic advice increases quit rates. Such advice should include a clear request to quit, reinforcing personal risks of smoking and their reversibility, offering solutions to barriers to quitting, and offering treatment. All smokers should be encouraged to use both medications and counseling. Scientifically proven, first-line medications are nicotine gum, inhaler, lozenge, and patch plus the nonnicotine medication bupropion. Proven second-line medications are clonidine, nicotine nasal spray, and nortriptyline. These medications are equally effective and safe and the incidence of dependence is very small. The proven psychosocial therapies are behavioral and supportive therapies. These are as effective as medications and are effective via individual counseling, group, and telephone formats. The writing of this article was supported in part by Senior Scientist Award DA-00450 from the National Institute on Drug Abuse.
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Clinicians rated this sample of patients as experiencing mild to moderate impairment in work-related activities, good to fair interpersonal relations, poor level of involvement in recreational activities, and mild impairment of ability to enjoy sexual activity. Patients and clinicians rated global social adjustment as poor.
Cognitive dysfunctions are common in major depressive disorder, but have been difficult to recapitulate in animal models. This study shows that Flinders sensitive line (FSL) rats, a genetic rat model of depression, display a pronounced impairment of emotional memory function in the passive avoidance (PA) task, accompanied by reduced transcription of Arc in prefrontal cortex and hippocampus. At the cellular level, FSL rats have selective reductions in levels of NMDA receptor subunits, serotonin 5-HT(1A) receptors and MEK activity. Treatment with chronic escitalopram, but not with an antidepressant regimen of nortriptyline, restored memory performance and increased Arc transcription in FSL rats. Multiple pharmacological manipulations demonstrated that procognitive effects could also be achieved by either disinhibition of 5-HT(1A)R/MEK/Arc or stimulation of 5-HT₄R/MEK/Arc signaling cascades. Taken together, studies of FSL rats in the PA task revealed reversible deficits in emotional memory processing, providing a potential model with predictive and construct validity for assessments of procognitive actions of antidepressant drug therapies.
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Using human liver microsomes and heterologously expressed human enzymes, we have investigated the involvement of CYPs 1A2, 2C9, 2C19, 2D6 and 3A4 in the N-demethylation of amitriptyline (AMI), with a view to defining likely influences on its clinical pharmacokinetics.
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The modulation of central postsynaptic alpha 2-adrenoceptors mediating mydriasis in the pentobarbitone-anaesthetized rat was studied after the acute and short/long-term administration of antidepressant treatments (drugs, electroshock). The acute administration of cyclic antidepressant drugs (2.5 mg/kg, i.v.) resulted in different mydriatic effects (amitriptyline greater than protriptyline approximately imipramine greater than clomipramine greater than nortriptyline greater than desipramine approximately maprotiline) which were attenuated (17-55%) by idazoxan (1 mg/kg, i.v., 5 min) and reserpine (5 mg/kg, s.c., 18 h) indicating that, besides the well-known anticholinergic properties of some of these drugs, their mydriatic effects are due in part to activation of alpha 2-adrenoceptors (through endogenous noradrenaline). In contrast, the long-term (7-21 days) but not the short-term (1-4 days) administration of cyclic antidepressant drugs (2.5-10 mg/kg, i.p.), MAO inhibitors (1 mg/kg, i.p.), lithium (20 mg/kg, i.p.) and electroshock (150 mA, 63 Hz, 8 ms during 300 ms) resulted in dose- and time-dependent reductions of the dose-pupillary response curve for clonidine (ED50 increased 1.2-2.0-fold; Emax decreased by 9-29%) which indicated desensitization of postsynaptic alpha 2-adrenoceptors. In line with these findings, treatment for 7 days with clonidine (0.1-1 mg/kg, i.p.) or idazoxan (3-10 mg/kg, i.p.) led to an opposite modulation (down- and up-regulation) of the dose-pupillary response curve for clonidine. The main results demonstrate that cyclic antidepressant drugs, through indirect mechanisms which involve endogenous noradrenaline, can modulate the sensitivity of brain postsynaptic alpha 2-adrenoceptors mediating mydriasis in the rat.
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Age, gender, cumulative illness rating scale-geriatric (CIRS-G) score, two measures of psychomotor retardation [the psychomotor retardation item of the Hamilton Rating Scale for Depression (HRSD) as well as performance on the Purdue Pegboard], and performance on the Stroop Color/Word test (a measure of the response inhibition component of executive functioning) were significantly different between those with VD and non-VD.
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In the study, 90 patients (21 male and 69 females) were included, in the age range 19-68 years and suffering from a depressive disorder of at least moderate severity and meeting the research criteria of ICD-10 and DSM-IV for major depression. All patients were given the written consent for the study. The project was accepted by the local ethics committee. Patients were randomized into two groups: one was treated with the serotonergic drug - escitalopram (n=51) with therapeutic doses between 10-20 mg/day. The second group was treated with the noradrenergic drug--nortriptyline (n=39) with a dose range of 75-150 mg/day. The DNA was extracted from blood cells by the salting out method. The genotype for polymorphism of the Val66Met BDNF gene was established by the PCR-RFLP method in the Laboratory of Psychiatric Genetics of the Psychiatric Clinic. Statistical analysis was performed with the Statistica version 7.1 Results. We have not found any association between the Val66Met polymorphism of the BDNF gene with treatment response neither to escitalopram (p = 0.751 for genotypes, p = 0.798 for alleles) nor for nortryptyline (p = 0.607 for genotypes, p = 0.607 for alleles)