Polymorphisms in the serotonin transporter gene (5-HTT) may influence antidepressant response to selective serotonin reuptake inhibitors (SSRIs). The norepinephrine transporter (NET) is the analogous target for norepinephrine reuptake inhibitors (NRIs).
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Antidepressants, in low concentrations, inhibited priming but not activation of hPMNs. However, at concentrations similar to those attained after local injection, and in marked contrast to local anesthetics, antidepressants are profoundly toxic to hPMNs.
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Personality disorders are neither particularly stable nor treatment resistant. In depressed out-patients, personality disorder symptoms in general improve significantly even in patients whose response to their treatment for depressive symptoms is modest or poor.
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The overview is restricted to Cochrane reviews, all of which include randomised trials. Participants are usually adult smokers, but we exclude reviews of smoking cessation for pregnant women and in particular disease groups or specific settings. We cover nicotine replacement therapy (NRT), antidepressants (bupropion and nortriptyline), nicotine receptor partial agonists (varenicline and cytisine), anxiolytics, selective type 1 cannabinoid receptor antagonists (rimonabant), clonidine, lobeline, dianicline, mecamylamine, Nicobrevin, opioid antagonists, nicotine vaccines, and silver acetate. Our outcome for benefit is continuous or prolonged abstinence at least six months from the start of treatment. Our outcome for harms is the incidence of serious adverse events associated with each of the treatments. We searched the Cochrane Database of Systematic Reviews (CDSR) in The Cochrane Library, for any reviews with 'smoking' in the title, abstract or keyword fields. The last search was conducted in November 2012. We assessed methodological quality using a revised version of the AMSTAR scale. For NRT, bupropion and varenicline we conducted network meta-analyses, comparing each with the others and with placebo for benefit, and varenicline and bupropion for risks of serious adverse events.
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Cytisine appears to be effective compared with placebo, and given its (current) relative low cost may be an acceptable smoking cessation treatment for smokers, particularly those in low- and middle-income countries. Cytisine's 'natural' product status may also increase its acceptability and use among certain groups of smokers, such as indigenous people, smokers in countries where the use of natural medicines is widespread (e.g. China, India), and in those people who do not want to use NRT or anti-depressants to help them quit smoking. However it is important to ascertain the effectiveness of cytisine compared with that of existing cessation treatments.
There are marked interindividual differences in Css of tricyclic antidepressants. These are due mainly to corresponding differences in the rate of elimination of the drugs and hence in drug oxidation. Twin, family, and cross-over studies with NT and DMI show that their kinetics (Css, Kel, and Vd) are controlled mainly by genetic factors (in drug-free individuals). Slow hydroxylators are at risk of developing excessive plasma concentrations of NT and DMI when given per se or when formed from the tertiary amines AT and imipramine. Classic antidepressants have fairly well established concentration-effect curves in endogenous depression. Severe toxicity usually occurs at supratherapeutic plasma levels and might be prevented by tailoring the dosage according to the individual's drug hydroxylating capacity. Monitoring drug plasma levels is particularly relevant in slow hydroxylators. There is a strong association between an individual's ability to hydroxylate NT and DMI and his D hydroxylation phenotype. The ratios between D and 4-OH-D in urine after a single oral dose are bimodally distributed in the population (polymorphism), with 3 to 10% being slow hydroxylators and the remainder rapid hydroxylators. Indices of NT-hydroxylation do not sharply distinguish the two phenotypes. The D metabolic index will predict the patient's capacity to hydroxylate NT and DMI and hence Css during therapy. Possibly similar hydroxylases are involved in the 4-hydroxylation of debrisoquine, in the stereospecific E-10-hydroxylation of NT, and in the 2-hydroxylation of DMI. By contrast demethylation of AT (and probably other tertiary tricyclics) does not significantly correlate to debrisoquine hydroxylation. The increasing knowledge of the clinical pharmacokinetics of tricyclic antidepressants is a distinct advantage over that of the new generation of antidepressants, where little is known about concentration-effect relationships and factors governing their rate of metabolism.
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Several studies have attempted to predict the final response or remission based on improvement during the early course of treatment of major depression. There is however a great variation in cut offs used to define early response and in the optimal week to predict final results.
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CYP2D6 genotyping was not cost-effective at current genotyping costs at a €50 000 per QALY threshold, however at test costs below €40, genotyping could be costs-effective.
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To investigate whether combined therapy has advantages over psychotherapy alone.
The evaluable sample was severely ill with a mean 24-item Hamilton Rating Scale for Depression score of 35.2 (+/-6.9). Of 489 patients, 63.6% (311) met DSM-IV criteria for melancholic features. During acute ECT, 62.1% of those with melancholic features remitted, as compared with 78.7% for those without melancholic features (P = 0.002). During medication continuation treatment (continuation pharmacotherapy), relapse rates were higher for those with melancholic features than for those without these features. Conversely, with continuation ECT, the rate of relapse was lower for those with, compared with those without, melancholic features.
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Data extracted from each study included: proportion of participants a) reporting ≥ 30% pain reduction from baseline OR ≥ moderate pain relief OR ≥ moderate global improvement; b) dropping out of the trial due to treatment-emergent adverse effects; c) reporting each specific adverse effect (e.g. sedation, dizziness) of ≥ moderate severity. The primary comparison of interest was between study drug(s) and one or both single-agent comparators. We combined studies if they evaluated the same drug class combination at roughly similar doses and durations of treatment. We used RevMan 5 to analyse data for binary outcomes.
There is evidence that postpartum depression improves with antidepressant drug therapy, estrogen, individual psychotherapy, nurse home visits, and possibly group therapy. Of the more frequently studied antidepressant drugs in breastfeeding women, paroxetine, sertraline, and nortriptyline have not been found to have adverse effects on infants. Fluoxetine, however, should be avoided in breastfeeding women. By administering effective treatment to women with postpartum depression, we can positively impact the lives of mothers, their infants, and other family members.
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This study is a retrospective chart review.
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We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, and EMBASE from inception to 7 January 2015, and the reference lists of retrieved papers and other reviews. We also searched two clinical trials databases for ongoing or unpublished studies.
Chronic obstructive pulmonary disease (COPD) is an increasing global health problem and cause of death. COPD is a chronic inflammatory disease predominantly affecting small airways and lung parenchyma that leads to progressive airway obstruction. However, current therapies fail to prevent either disease progression or mortality. The mainstay of current drug therapy is long-acting bronchodilators. Several once daily inhaled β(2)-agonists and muscarinic antagonists (and combinations) are now in development. No treatments effectively suppress chronic inflammation in COPD lungs. With better understanding of the inflammatory and destructive process in the pathophysiology of COPD, several new therapeutic targets have been identified. Several mediator antagonists or inhibitors tested in COPD have so far been disappointing, but CXCR2 antagonists that block pulmonary neutrophil and monocyte recruitment are more promising. Broad spectrum anti-inflammatory drugs may be more effective, and include inhibitors of the proinflammatory enzymes phosphodiesterase-4, p38 mitogen-activated protein kinase, Janus kinases, NF-κB kinase and PI3 kinase-γ and -δ, but side effects after oral administration are a major limitation so that in future inhaled delivery may be necessary. A new promising approach is reversal of corticosteroid resistance through increasing histone deacetylase-2 (HDAC2) activity. This might be achieved by existing treatments such as theophylline, nortriptyline and macrolides, or more selectively by PI3 kinase-δ inhibitors. Thus although there have been major advances in the development of long-acting bronchodilators for COPD, it has proved difficult to find anti-inflammatory treatments that are safe and effective.
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A total of 228 PN patients were enrolled approximately equally for monotherapy and adjuvant therapy. Adverse effects and discontinuation rates were similar between amitriptyline and nortriptyline interventions. Weight gain was more common with amitriptyline, while nortriptyline use was associated with greater prevalence of dry mouth. Secondary outcome measures were similar in both groups, demonstrating improvement from baseline.
The ability of 'Medicoal', a new effervescent, activated charcoal preparation, to adsorb nortriptyline, has been investigated both in vitro and in vivo. A single dose of the effervescent charcoal 30 min after a dose of 75 mg nortriptyline produced a 60% mean reduction in both peak plasma levels and nortriptyline availability in healthy volunteers. Multiple doses of the effervescent charcoal produced 70% mean reduction in peak nortriptyline levels and availabiltiy. Activated charcoal is recommended for the treatment of tricyclic antidepressant poisoning. In in-vitro tests, a 10 g packet of the effervescent preparation containing 5 g activated charcoal) had an adsorptive capacity of approximately 3000 mg nortriptyline, a dose not usually exceeded in most cases of trycyclic antidepressant overdose.
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Stimulation of beta(2)-AR is necessary for nortriptyline to exert its antiallodynic action against neuropathic pain. These findings provide new insight into the mechanism by which antidepressants alleviate neuropathic pain. Our results also raise the question of a potential incompatibility between beta-blockers that affect beta(2)-AR and antidepressant drugs in patients treated for neuropathic pain.
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The present analysis provides further evidence that the current use of SSRIs is associated with a slightly decreased risk for AMI.
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This protocol describes the first randomised controlled trial of a tricyclic antidepressant in the treatment of OA. The results of the study may have significant implications for the management of this common and painful condition.
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Both treatments were well tolerated. Of the 36 randomly assigned patients, 2 (1 in each group) dropped out due to treatment-related adverse effects. Four additional patients dropped out for administrative reasons. Thirty patients received nortriptyline for at least 4 weeks combined with either perphenazine (N = 14) or placebo (N = 16) for at least 2 weeks (median = 9 weeks). There was no significant difference between the completers in the 2 treatment groups when comparing their scores on the HAM-D, the BPRS, its psychoticism subscale, or any side effects measure. Rates of response (defined as resolution of both depression and psychosis) did not differ significantly in the 2 groups (nortriptyline-plus-perphenazine group, 50% vs. nortriptyline-plus-placebo group, 44%).
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Varenicline (Chantix, Champix) is an orally administered alpha4beta2 nicotinic acetylcholine receptor partial agonist that is indicated as an aid to smoking cessation. Well designed clinical trials indicate that varenicline is an effective aid to smoking cessation. During the last 4 weeks of treatment, carbon monoxide-confirmed continuous abstinence rates were generally significantly higher with varenicline than with placebo, bupropion sustained release (SR) or nicotine replacement therapy. Varenicline also reduced cravings, the reinforcing effects of smoking and some withdrawal symptoms. Another well designed trial demonstrated that extending varenicline therapy by an additional 12 weeks helped maintain abstinence in individuals who had quit smoking. Varenicline was generally well tolerated in clinical trials; nausea, the most commonly occurring adverse event, diminished over time. More data are needed regarding the potential for neuropsychiatric events in varenicline recipients. Some of these events may be associated with nicotine withdrawal, rather than varenicline, although neuropsychiatric events have been observed in individuals who continued to smoke whilst receiving varenicline. In modelled cost-effectiveness analyses based on data from clinical trials in participants receiving smoking cessation therapy, 12 weeks' treatment with varenicline was predicted to be cost effective from a healthcare payer perspective in numerous countries. With regard to the incremental costs per QALY or life-year gained, 12 weeks' treatment with varenicline consistently dominated bupropion SR and nicotine replacement therapy and was dominant over or considered cost effective relative to unaided cessation, regular brief counselling or nortriptyline in analyses based on Markov models. In additional modelled analyses from a healthcare payer perspective, administering varenicline for an additional 12 weeks in participants who had successfully quit smoking was estimated to have acceptable incremental costs per QALY gained relative to varenicline for 12 weeks and to dominate other smoking cessation options. Moreover, in Swedish analyses that also included societal costs for production and consumption, the incremental cost per QALY gained for varenicline versus bupropion SR, and for an additional 12 weeks of varenicline therapy versus varenicline for 12 weeks only, was below commonly accepted thresholds of cost effectiveness. A US decision-analytic model from the perspective of various US health insurance plans demonstrated that, after 2 years, varenicline was predicted to dominate bupropion SR, in terms of the incremental cost per additional smoking cessation. Varenicline was also dominant or cost effective versus nicotine replacement therapy, and cost effective versus unaided cessation. Sensitivity analyses demonstrated that the results of cost-effectiveness studies were generally robust to plausible variations in key parameters. In conclusion, varenicline is an effective aid to smoking cessation. Varenicline was generally well tolerated in clinical trials, although more data are needed regarding the potential for neuropsychiatric events. The costs associated with varenicline are offset by direct savings associated with the reduction in smoking-related diseases. Despite their limitations, available pharmacoeconomic analyses from numerous countries support the use of varenicline for 12 or 24 weeks as a cost-effective treatment relative to other smoking cessation therapies in smokers who wish to quit smoking.
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The percutaneous absorption of amitriptyline, nortriptyline, imipramine, and desipramine as their hydrochloride salts in vivo was demonstrated without use of a vehicle using the hairless (hr-1/hr-1) mouse as an experimental model for human skin. After topical application of 2 mg of each compound in distilled water, followed by rapid evaporation of the water, concentrations were measured in heart, lung, brain, liver, and blood in 1-, 2-, 4-, and 6-hour study groups. Lung consistently demonstrated the highest concentrations for all four compounds while heart and liver had the lowest. Concentrations in heart remained essentially constant for all compounds during the 6-hour study period. The concentrations in solid tissues were much lower than those commonly seen in man after overdose, whereas the concentrations in blood resembled low therapeutic to toxic concentrations in humans. Percutaneous absorption may provide a feasible route of administration for the tricyclic antidepressants which may lead to improved compliance with fewer gastrointestinal side effects.
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Depression is a psychiatric condition that affects about 120 million people worldwide and can interfere with independence and productivity in essentially all aspects of daily life. Depression is also associated with risk of self-harm, and ultimately suicide. Antidepressant medications are widely used to treat symptoms of depression. While there are several classes of antidepressants, therapeutic drug management (TDM) is most common for the tricyclic antidepressants (TCAs). TDM of TCAs is important due to wide inter-individual variability in pharmacokinetics, production of active metabolites, and a high risk of drug-drug interactions. In addition, TDM of some TCAs can be used to optimize dose, wherein concentration relationships are recognized for both therapeutic response and potentially life-threatening toxicity. In many clinical scenarios, TDM of TCAs is accomplished by currently available point of care or automated immunoassays that provide a "total" TCA concentration. However, these assays may not be adequately specific to meet the needs of all clinical scenarios, and hence, chromatographic separation and quantification of individual TCA parent drugs and active metabolites that may contribute to the "total" TCA concentration is sometimes required. This chapter describes an analytical method designed to detect and/or quantify clinically significant concentrations of nine TCAs (amitriptyline, nortriptyline, imipramine, desipramine, doxepin, nordoxepin, protriptyline, clomipramine, and norclomipramine) in serum or plasma, using ultra pressure liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The sample preparation employs a rapid protein precipitation with 50:50 MeOH:acetonitrile, high speed centrifugation, and injection of 5 μL of supernatant onto the instrument, with a 5 min run-time.
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To determine the efficacy of continuation pharmacotherapy with nortriptyline hydrochloride or combination nortriptyline and lithium carbonate in preventing post-ECT relapse.
Anorexia Nervosa (AN) is an illness characterised by extreme concern about body weight and shape, severe self-imposed weight loss, and endocrine dysfunction. In spite of its high mortality, morbidity and chronicity, there are few intervention studies on the subject.
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Ratios in plasma of tryptophan (Trp) and tyrosine (Tyr) to other large neutral amino acids were determined in 26 endogenous depressives before and after treatment with nortriptyline in doses adequate to achieve a steady-state serum level between 70 and 130 ng/ml, i.e., within the recommended therapeutic range. Pretreatment plasma Trp ratio and Tyr ratio were normal and did not change significantly during treatment. The plasma Trp and Tyr concentrations and the plasma Trp ratio showed no significant association with the therapeutic response. However, the pretreatment plasma Tyr ratio correlated significantly and directly with the final Hamilton rating score, and inversely with the per cent reduction of Hamilton rating score. Moreover, depressives with plasma Tyr ratio below the normal mean showed significantly greater clinical improvement than patients with higher plasma Tyr ratio with comparable serum nortriptyline levels. Evidence has been presented that biochemical variables in depressed patients are important determinants of clinical improvement following pharmacotherapeutic treatment. Moreover, the results suggest that the plasma Tyr ratio may be a guideline for antidepressant response to nortriptyline.