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Tricyclic antidepressants have notable cardiac side effects, and this issue has become important due to the recent reports of increased cardiovascular mortality in patients with depression and anxiety. Several previous studies indicate that serotonin reuptake inhibitors (SRIs) do not appear to have such adverse effects. Apart from the effects of these drugs on routine 12-lead ECG, the effects on beat-to-beat heart rate (HR) and QT interval time series provide more information on the side effects related to cardiac autonomic function. In this study, we evaluated the effects of two antidepressants, nortriptyline (n=13), a tricyclic, and paroxetine (n=16), an SRI inhibitor, on HR variability in patients with panic disorder, using a measure of chaos, the largest Lyapunov exponent (LLE) using pre- and posttreatment HR time series. Our results show that nortriptyline is associated with a decrease in LLE of high frequency (HF: 0.15-0.5 Hz) filtered series, which is most likely due to its anticholinergic effect, while paroxetine had no such effect. Paroxetine significantly decreased sympathovagal ratios as measured by a decrease in LLE of LF/HF. These results suggest that paroxetine appears to be safer in regards to cardiovascular effects compared to nortriptyline in this group of patients.
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Monitoring the plasma levels of certain antidepressant and antipsychotic drugs can be clinically helpful for certain patients. The authors discuss the particular drugs, patients, and technical conditions for effective plasma level monitoring.
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Eight healthy subjects were randomly given placebo and equimolar doses of nortriptyline (NT) and E-10-hydroxy-NT (E-10-OH-NT). Two hours after oral intake of drug, noradrenaline (NA) was infused intravenously at three consecutive rates. Before infusion of NA, E-10-OH-NT significantly increased heart rate compared to NT (p less than 0.05) and placebo (p less than 0.01). During NA infusion, the active drugs caused non-significant tendencies to augmented increase of blood pressure and decrease of heart rate. Plasma NA concentrations increased significantly due to the infused NA but were not influenced by NT or E-10-OH-NT. This absence of drug effect may have been due to several simultaneously operating factors affecting plasma NA concentrations, e.g., modification of the rates of NA release and clearance by exogenous NA or drugs and competing elimination pathways for infused NA. After stopping the NA infusion, a non-significant tendency to a slower elimination of NA was found after both active drugs.
Predictors of treatment response and recovery from depression in late life remain poorly understood. Previous studies have focused on a narrow range of response and recovery variables; namely, whether patients achieve or do not achieve a defined outcome or time to achieve the outcome. Whether patients vary in their pathways toward those outcomes--and the extent to which such variation can be anticipated by patient characteristics prior to treatment--has not been empirically examined.
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Pharmacogenetic (secondary) analysis of a randomized, placebo-controlled efficacy trial of bupropion and nortriptyline for smoking cessation.
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It is concluded that systematic evaluation of drug- and patient-related variables with the new rating scale can estimate the appropriateness of TDM. Because their rating revealed similar scores as the three reference drugs, it is proposed that TDM should be established for bupropion, buprenorphine, disulfiram or a metabolite, methadone, and naltrexone. An objective rating of drug- and patient-related characteristics could help laboratories focus their method development on the most likely drugs to require TDM along with a thorough drug use evaluation.
The popularity of selective serotonin reuptake inhibitors stems from their apparent efficacy for numerous disorders and their favorable side effect profile. However, several studies have suggested that selective serotonin reuptake inhibitors may be relatively ineffective for treating melancholia. The objective of this study was to compare the responses to fluoxetine and nortriptyline of older patients with both severe depression and heart disease.
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Overdose deaths from antidepressants have not decreased over the last 15 years. A trend away from prescribing drugs with a higher fatal toxicity index in favour of those with a lower index, would reduce the number of deaths from antidepressant poisoning.
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Cigarette smoking is the primary cause of numerous preventable diseases; as such, the goals of smoking cessation are both to reduce health risks and to improve the quality of life. Currently, the first-line smoking cessation therapies include nicotine replacement products and bupropion. The nicotinic receptor partial agonist varenicline has recently been approved by the FDA for smoking cessation. A newer product currently under development and seeking approval by the FDA are nicotine vaccines. Clonidine and nortriptyline have demonstrated some efficacy but side effects may limit their use to second-line therapeutic products. Other therapeutic drugs that are under development include rimonabant, mecamylamine, monoamine oxidase inhibitors, and dopamine receptor D3 antagonists. Inhibitors of nicotine metabolism are also promising candidates for smoking reduction and cessation. In conclusion, promising new therapeutic products are emerging and they will provide smokers additional options to assist in achieving smoking cessation.
Among patients with idiopathic gastroparesis, the use of nortriptyline compared with placebo for 15 weeks did not result in improvement in overall symptoms. These findings do not support the use of nortriptyline for idiopathic gastroparesis.
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In this model of nortriptyline poisoning, the administration of amiodarone to correct wide complex tachycardia did not have a harmful effect.
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Depression in the physically unwell is common and an important cause of morbidity. There are problems with diagnosing depression in the physically ill which may lead to under-recognition and under-treatment. In clinical practice antidepressants are available and a feasible option for treating depressive disorders. Therefore we thought it would be a reasonable first step in addressing this problem to describe the literature of randomised controlled trials in this area.
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18 studies were included, covering 838 patients with a range of physical diseases (cancer 2, diabetes 1, head injury 1, heart 1, HIV 5, lung 1, multiple sclerosis 1, renal 1, stroke 3, mixed 2). Depression was diagnosed clinically in 3 studies, otherwise by structured interview or checklist. Only 5 studies described how they performed randomisation. 1 study compared drug with no treatment, and the rest with placebo: all of the latter said they were double blind. 6 studies used SSRIs, 3 atypical antidepressants, and the remainder tricyclics. Patients treated with antidepressants were significantly more likely to improve than those given placebo (13 studies, OR 0.37, 95% CI 0.27-0.51) or no treatment (1 study, OR 3.45, 95% CI 11.1-1.10). About 4 patients would need to be treated with antidepressants to produce one recovery from depression which would not have occurred had they been given placebo (NNT 4.2, 95% CI 3.2-6.4). Most antidepressants (tricyclics and SSRIs together, 15 trials ) produced a small but significant increase in dropout (OR 1.66, 95% CI 1.14-2.40. NNH 9.8, 95% CI 5.4-42.9). The "atypical" antidepressant mianserinproduced significantly less dropout than placebo. Only 2 studies used numerical scales designed to measure effects on function and quality of life; in HIV (Karnofsky scale), drug was better than no treatment; in lung disease (Sickness Impact Profile), drug was not significantly different from placebo. Only 7 studies reported looking for changes in the physical disease. Antidepressants produced no change in immune function in HIV relative to placebo (2 studies) or no treatment (1 study). Relative to placebo, antidepressants produced no change in cardiovascular function in heart disease, in respiratory function in lung disease, or in vital signs or laboratory tests in cancer (1 study each). Nortriptyline produced worse control in diabetes. Trends towards tricyclics being more effective than SSRIs, but also more likely to produce dropout were noted, but these are based on non-randomised comparisons between trials.
A combined pharmacodynamic and pharmacokinetic approach was made to study the pharmacodynamic half-life (Pd1/2) of amitriptyline (AT). Six depressed patients were treated with 150 mg of amitriptyline as a single oral dose at night for six or more weeks. Decreased tyramine sensitivity (DTS), an index of this drug's pharmacological activity, was determined serially at various intervals after the last dose. Plasma concentrations of AT and nortriptyline (NT) were also estimated at above intervals. It was possible to detect DTS for 228-300 h after the last oral dose and the mean Pd1/2 of this decline of pharmacodynamic effect was observed to be 135 h. However, no measurable amount of AT or NT was present after 84 h and the mean elimination plasma half-life (t1/2) of AT and NT were 37.7 and 38.9 h, respectively. (In this study, pharmacokinetic parameters of NT were directly related with those of AT.) Prolonged pharmacodynamic effect of this drug after discontinuation should be borne in mind in order to avoid drug interactions and autonomic complications, especially after overdosage. Pd1/2, as assessed by DTS, correlated directly with the t1/2 (r = 0.91) and inversely with the plasma clearance rate (r = 0.60) of NT. DTS test can be used as an alternative technique to assess the biological activity of a drug which inhibits noradrenaline reuptake mechanism and/or blocks alpha-adrenoceptors at the peripheral neuronal sites, especially, where facilities to measure plasma concentrations of such drugs are limited.
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Thirty-one elderly depressed patients were treated for seven weeks with nortriptyline with plasma levels kept between 50-180 ng/ml. Electrocardiograms were taken at the third and seventh weeks of treatment. There were significant increases in the PR interval, QTc interval, and heart rate from before and after treatment. However, there were no consistent correlations between electrocardiographic changes during treatment and plasma levels of nortriptyline, 10-hydroxynortriptyline and either of its two isomers (E-10-hydroxynortriptyline, Z-10-hydroxynortriptyline). Increased QRS duration after seven weeks of treatment was correlated with daily dose of nortriptyline.
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The present findings indicate that genetic deletion or pharmacological blockade of TRPA1 produces inhibitory activity in mouse models of anxiety and depression. These results imply that TRPA1 exerts tonic control, promoting anxiety and depression, and that TRPA1 antagonism has potential as an innovative strategy for the treatment of anxiety and mood disorders.
In order to test the validity of the concept of anxiety states masking an underlying depressive illness, patients clinically diagnosed as suffering from anxiety or tension states were treated on a random double-blind basis for 4 weeks with either a pure anxiolytic, lorazepam, or an anxiolytic/antidepressant preparation, fluphenazine with nortriptyline. Patients' self-ratings were very similar to the physicians' ratings which showed that fluphenazine/nortriptyline was associated with significantly greater overall improvement(p less than 0.01), as well as significantly greater improvements in the group of symptoms specifically related to depression(p less than 0.05). These results suggest that a depressive element is present in an appreciable proportion of patients presenting with apparent anxiety states, and antidepressant as well as anxiolytic treatment is required. Patients selected on the basis that they had improved satisfactorily at the end of the 4-weeks' treatment were followed up for a further 3 months without medication, and the relapse rate was 24%, irrespective of previous treatment. More of the patients treated with lorazepam had to be excluded from the follow-up because of failure to improve, and these probably represented the proportion (19%) of this population with an appreciable depressive element to their illness.
The authors explored the relationship of cord-maternal antidepressant concentration ratios and maternal depression with perinatal events and preterm birth.
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Though selective serotonin reuptake inhibitors have revolutionized the field of psychiatry with demonstrated efficacy in affective and anxiety disorders with minimal side effects, norepinephrine-serotonin reuptake inhibitors may provide efficacy similar to tricyclic antidepressants without the adverse side effects associated with tricyclic antidepressants.
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When considering the risk-benefit profile of antidepressants in the acute treatment of major depressive disorder, these drugs do not seem to offer a clear advantage for children and adolescents. Fluoxetine is probably the best option to consider when a pharmacological treatment is indicated.
This method is rapid, sensitive, and simple for studying the metabolism of Ami and Nor.
Current evidence suggests that nortriptyline, at doses between 75 and 100 mg, is not significantly associated with serious adverse events when administered in patients without underlying cardiovascular disease.
(1) To review the literature on the risk of fetal exposure to tricyclic antidepressants (TCAs). (2) To estimate the frequency of TCA exposure in pregnant women in the Canadian province of Saskatchewan.
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The addition of intensified insulin therapy to the symptomatic treatment of painful neuropathy in type-2 diabetics, significantly enhanced the reduction of pain. The lowering of glycosilated hemoglobin was a significant predictor of success in pain reduction.
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Data were extracted independently from the trial reports by the authors. Missing information was requested from investigators wherever possible. Data were sought to allow an "intention to treat" analysis.
In this efficient extraction and isocratic liquid-chromatographic procedure for measuring eight antidepressant drugs in serum (amoxapine, 8-hydroxyamoxapine, doxepin, desmethyldoxepin, imipramine, desipramine, amitriptyline, and nortriptyline), they are extracted from serum as a group by use of disposable solid-phase cyanopropyl columns; the eluate is injected directly onto a Zorbax cyanopropyl analytical column. This sample preparation circumvents potential problems of drug instability associated with the usual evaporating/concentrating techniques. Recycling the acetic acid/acetonitrile/n-butylamine mobile phase not only maintains a stable, cost-effective system, it also prolongs column life. Standard curves for all eight drugs are linear to 1000 micrograms/L; the detection limit is 8-10 micrograms/L. For all drugs and metabolites, within-run CVs were 0.9 to 2.2%, between-run CVs 2.1 to 3.8%. Analytical recovery of the solid-phase extraction step was 85 to 100% (mean = 94.5%) for all analytes. Standards and controls, stored frozen in drug-free serum, are stable for at least six months. We also report a study of separation mechanisms.
Nortriptyline appears to attenuate the reinforcing and aversive stimulus properties of nicotine, which may mediate its anti-smoking effects. However, the results should be interpreted with caution, as non-specific effects of nortriptyline may have contributed to these findings.