It has been demonstrated that potentially corcinogenic nitroso compounds are readily formed when certain widely used drugs with secondary alkylaminostructures (e.g. nortriptyline and fenfluramine) or drug metabolities with such structures (e.g. norpropoxyphene) are reacted with nitrite in dilute acid aqueous medium or in human gastric juice under simulated gastric conditions. The reactions occur so readily in vitro that new quantitative procedures for the determination of these drugs have been developed and based on these principles. The potential hazards associated with the long term clinical use of such drugs are discussed.
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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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There was a clear relation between the C gamma P2D6 genotype and the plasma kinetics of nortriptyline and 10-hydroxynortriptyline. The proportion between the apparent oral clearances of nortriptyline in the groups with 0, 1, 2, 3, and 13 functional genes was 1:1:4:5:17. The proportions between AUC(nortriptyline) to AUC(10-hydroxynortriptyline) ratios in the groups with 0, 1, 2, 3, and 13 functional genes were 36:25:10:4:1. Oral plasma clearance of nortriptyline and AUC(nortriptyline) to AUC(10-hydroxynortriptyline) ratio both correlated significantly with the debrisoquin metabolic ratio (rS = -0.89, p = 0.0001; rS = 0.92, p = 0.0001). Although ultrarapid metabolizer subjects were given double the nortriptyline dose (50 mg), inhibition of salivation was not more pronounced compared with the other genotype groups given 25 mg nortriptyline.
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We employed a new form of solid-phase material, the Empore octyl (C8) extraction membrane (SPEM), for the efficient extraction of tricyclic drugs from patients' serum specimens. Both extraction and companion high-performance liquid chromatographic (HPLC) assay of doxepin (DOX), desmethyldoxepin (DDOX), imipramine (IMI), desmethylimipramine (DESI), amitriptyline (AMI), nortriptyline (NOR), clomipramine (CLO), and desmethylchlomipramine (DCLO) are presented here. Routinely, serum (1.0 mL or less) adjusted to pH 5.5 with phosphate buffer is passed through the SPEM secured in a MF-1 microfilter unit. Proteins and potential interferences retained on SPEM are removed with an acetonitrile-water wash. The tricyclic drugs are eluted with HPLC mobile phase and the eluate is injected directly on a Zorbax cyanopropyl (CN) HPLC column, thereby avoiding time consuming evaporation-concentration steps that can affect drug stability. Recovery for all drugs exceeds 90% and analytical responses are linear from a lower limit of sensitivity of 8 micrograms/L up to at least 1000 micrograms/L. Between-run coefficients of variation (CV) range from 2.9 to 8.3% through the concentration range of 75 to 300 micrograms/L. Performance characteristics of the SPEM are compared to those of conventional large particle silica- and polymeric-based sorbents. Within the requirements of this assay, the SPEM extraction requires less sample volume and reduces elution and solvent volumes.
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In a group of elderly depressed patients treated with imipramine (50-200 mg/day), six patients had the dose changed after 1-3 weeks of treatment. In all cases an increased dose resulted in a considerably disproportional rise in the plasma level of the active metabolite desipramine. In a group of elderly depressed patients treated with nortriptyline (40-100 mg/day) the dose/plasma level ratio could be examined in 6 patients, and there was no tendency towards a disproportional rise in plasma level, when the dose was raised. Dose changes, thus, may result in unpredictable changes in plasma levels during imipramine treatment and therapy control by plasma level monitoring may be difficult in these patients. Additional treatment with perphenazine (8-16 mg/day) to patients on imipramine (N = 3) or nortriptyline (N = 2) caused a marked rise in drug levels for imipramine in particular affecting the desipramine levels.
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Four human studies and nine experimental models were found. The human studies showed a transiently statistically significant positive association between amitriptyline and liver cancer and a negative association with pancreatic cancer; and that the antidepressants amitriptyline, nortriptyline, desipramine, and phenelzine may increase risk of breast cancer. Results of the experimental studies differed depending on which antidepressants were examined and which model was used. Amitriptyline was found to promote tumour growth, fluoxetine and clomipramine were reported to be both tumour promoters and antineoplastic agents, and imipramine and citalopram both demonstrated antineoplastic properties.
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The prevalence of TDM is generally low, more frequent, and increasing for antipsychotics, and more frequent for men and substances where TDM is strongly recommended.
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The mean SBP 10 minutes after treatment was 54+/-18 mm Hg in the control group, 134+/-21 mm Hg in the HTS group, 85+/-19 mm Hg in the NaHCO3 group, and 60+/-12 mm Hg in the HV group (P<.05). Mean QRS duration 10 minutes after treatment was 144+/-38 ms in the control group, 80+/-14 ms in the HTS group, 105+/-38 ms in the NaHCO3 group, and 125+/-46 ms in the HV group (P<.05).
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Cognitive dysfunction is common in older persons suffering from a major depression. However, the degree to which this dysfunction is reversible with successful treatment of the depression remains uncertain. The present study examined the effects that treatment (randomized double-blind design) with either an SSRI (paroxetine) or a tricyclic antidepressant (nortriptyline) had on cognition in older depressed patients. The patients' performance was compared to that of a group of normal controls of similar age and education. Patients and controls were administered measures of working memory, information-processing speed, episodic memory and attention five times over the course of a 12 week trial. At baseline, the patients performed more poorly than the elderly controls on all cognitive measures. While the patients' performance did improve over the course of their treatment, the magnitude of this improvement did not exceed that produced in the elderly controls by practice alone. The same pattern of results was evident in both intent-to-treat and responder analyses. Thus, there was no evidence that the depressed patients' cognitive performance normalized after response to antidepressant therapy. Neither the patients' age at onset nor their baseline level of cognitive functioning influenced the amount by which their performance improved over the 12 week trial. There was no difference between paroxetine and nortriptyline in the amount of cognitive change associated with treatment. The present results suggest that cognitive dysfunction persists in older depressed patients even after their mood disorder has responded to antidepressant medications.
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54 patients in five centres participated in a study of the relationship between steady-state plasma-levels of amitriptyline (AT) and its active metabolite nortriptyline (NT) and therapeutic response. The participants were inpatients who, after a 7-12 day period of assessment, were rated greater than or equal to 16 on the Hamilton rating scale for depression. They were given 75 mg of amitriptyline for 3 days and then 150 mg daily for an active-treatment period of 6 weeks. Clinical ratings and plasma-samples were obtained at baseline then at 2, 4, and 6 weeks after starting therapy. Contrary to the findings of three previous trials, no important correlations were found between steady-state plasma-levels and therapeutic outcome or corrected side-effects. Corrected side-effects correlated negatively with therapeutic outcome. There seems little advantage in routine monitoring of AT and NT, since variations in plasma-levels do not account for the considerable variation in therapeutic outcome.
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This patient's history, EEG findings, and brain imaging all point to a metabolic or toxic cause. It is likely that her three proconvulsant medications--even at therapeutic doses--synergistically lowered her seizure threshold or even precipitated her seizures. Retrospective studies and case reports portray these drugs as potentially offending agents.
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There is growing interest in investigating noradrenergic functions in obsessive-compulsive disorder (OCD) because some antidepressants with strong effects on serotonin reuptake blockade fail to relieve obsessive-compulsive symptoms. We undertook a trial to investigate whether the combination of clomipramine with nortriptyline was more effective than clomipramine alone.
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The contribution of pharmacogenetics to tailor-made pharmacotherapy, which especially might be of value for patients deviating from the average, has not yet reached the position it seems to deserve.
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The primary objective of this review was to assess the effectiveness of interventions to increase adherence to medications for smoking cessation, such as NRT, bupropion, nortriptyline and varenicline (and combination regimens). This was considered in comparison to a control group, typically representing standard care. Secondary objectives were to i) assess which intervention approaches are most effective; ii) determine the impact of interventions on potential precursors of adherence, such as understanding of the treatment and efficacy perceptions; and iii) evaluate key outcomes influenced by prior adherence, principally smoking cessation.
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The U.S. Department of Health and Human Services' Clinical Practice Guidelines have established both nicotine and nonnicotine-based pharmacotherapies as efficacious treatments for smoking cessation. Smokers attempting to quit smoking can significantly increase their chances by using one of several first-line agents, including nicotine transdermal patches, gum, nasal spray, inhalers, tablets, and the antidepressant bupropion. Those who cannot use either bupropion or nicotine replacement therapy because of contraindications or lack of effectiveness may benefit from the second-line treatment nortriptyline. This article also discusses several novel compounds for smoking cessation.
Effective pharmacotherapies are available to help people who are trying to stop smoking, but quitting can still be difficult and providing higher levels of behavioural support may increase success rates further.
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Amongst patients taking escitalopram (n=223), the genotype CYP2C19 was significantly associated with escitalopram serum concentrations and desmethylescitalopram:escitalopram ratio. For those taking nortriptyline (n=161), the CYP2D6 genotype was significantly associated with nortriptyline and 10-hydroxynortriptyline serum concentrations and 10-hydroxynortriptyline:nortrip-tyline ratio. CYP450 genotypes conferring greater enzyme activity were linked to lower drug serum concentrations and higher metabolite:drug ratios. Nonetheless, no significant association was found between either CYP450 genotype or antidepressant serum concentration and treatment response.
Overdosing of several drugs, such as tricyclic antidepressants, salicylates, and opiates, is known to induce effects like those seen in patients with adult respiratory distress syndrome. By exposing isolated perfused and ventilated rat lungs via the perfusate to six different tricyclic antidepressants (amitriptyline, nortriptyline, imipramine, desipramine, mianserine, and maprotiline), we investigated possible effects on ventilation (conductance and dynamic compliance), lung perfusion flow, and edema formation. The effects of these substances were pronounced and appeared within 15 min after exposure. Amitriptyline was studied in greater detail and caused a dose-related (0.01-1.0 mM) reduction in ventilation and perfusion flow. At the highest drug concentration pronounced lung edema was observed. Morphological studies were conducted with a transmission electron microscope. The microscopic preparations showed dose-related edema (amitriptyline 0.1 and 1.0 mM). The effects noted in our experimental studies are similar to those described in patients who have taken an overdose of tricyclic antidepressants. This emphasizes the possibility of a noncardiogenic edema component in these patients.
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Psychological interventions and pharmacological interventions with SSRIs may have a small yet clinically meaningful effect on depression outcomes in CAD patients. No beneficial effects on the reduction of mortality rates and cardiac events were found. Overall, however, the evidence is sparse due to the low number of high quality trials per outcome and the heterogeneity of examined populations and interventions.
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Genome-wide RNA expression data from the hippocampal tissues of four inbred mouse strains (129S1/SvlmJ, C57LB/6J, DBA/2J and FVB/NJ) were treated with varying doses of either nortriptyline (NRI) or escitalopram (SSRI) and subjected to two different depressogenic protocols. Following robust multichip average normalization, we applied the nonparametric RankProd approach to identify differentially expressed genes in response to drugs across the four strains. Pathway analysis was subsequently carried out on top-ranking genes to gain further biological insights.
The results suggest that the efficacy of nortriptyline is superior to fluoxetine in this group of major depressed patients. No significant differences were observed between dropout rates in the two groups but anti-cholinergic side-effects were significantly more frequent with nortriptyline than with fluoxetine but there was no significant difference in cardiovascular effects in particular QTc prolongation.
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TENS seemed to be equivalent in efficacy to nortriptyline. A significant decrease in visual analog scale scores of pain and/or sensory complaints of the upper extremities occurred in both groups. Of the 29 people treated with TENS, the mean (SD) intensity of pain and/or sensory complaints decreased from 5.3 (1.6) at baseline to 2.8 (1.5) at 8 weeks follow-up (P < 0.001). Correspondingly in the 30 people treated with nortriptyline, the mean (SD) intensity of pain and/or sensory complaints decreased from 4.9 (1.9) to 3.3 (2.1) (P < 0.001). The mean difference in visual analog scale score at 8 weeks follow-up was not significant between the 2 groups (mean difference -0.5; 95% confidence interval, -1.5-0.5).
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The population approach is a general term covering different aspects of kinetic and dynamic data collected mainly from drug-treated patients and new techniques allowing evaluation of sparse observations from each subject. Such data originate from clinically relevant conditions and can give information on several qualities of a drug. An example is given with the tricyclic antidepressant nortriptyline for which the kinetics and the concentration-effect relationship have been thoroughly documented previously with conventional techniques. We have evaluated retrospective data from a therapeutic drug monitoring service using a nonparametric population kinetic method (NPML) that allows description of kinetic outliers and nonlinear relationships between kinetic parameters and covariates. In addition, drug interactions, nonlinear kinetics and dosing habits were studied with other techniques corroborating previous results and adding new information. The concentration-effect relationship could not be evaluated from our data as information on efficacy and adverse effects was of too low quality. However, several controlled studies have defined a therapeutic concentration interval and a discussion on dosing strategies is based on this interval. Collection of sparse data in patients during phases II-IV of drug development as a complement to conventional studies is highly recommendable.
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To quantify the effect of clinical and demographic factors on the risk of elevated and toxic tricyclic antidepressant (TCA) plasma concentrations (Cp) and to describe the rates of elevated and toxic TCA Cp.
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The limited use of nortriptyline for smoking cessation is likely due to concerns about its serious adverse effects.
The internight variability in REM latency in 92 drug-free inpatients with major depressive illness was recorded for 4 consecutive nights and subsequently assessed. Individual coefficients of variation in REM latency [CV = (standard deviation of mean REM latency for 4 recording nights/4-night mean REM latency) X 100] ranged from 5.1 to 121.7, with a mean of 37.0 (SD = 27.3) and a median of 27.4. CV was positively correlated with both age (p less than 0.05) and age at onset of depressive illness (p less than 0.01). Male patients showed more variability in REM latency than female patients (p less than 0.05); likewise, the subgroups of patients who either were incapacitated or had bipolar II illness showed greater variability in REM latency in comparison with the remainder of the sample (p less than 0.05). When the entire patient sample was stratified by CV into three equal subgroups, the subgroup of patients defined by the highest CV presented the longest sleep latency (p less than 0.05) and the shortest REM latency (p less than 0.0001). No other clinical or polysomnographic correlates of REM latency variability were noted nor was REM latency variability related to severity of illness, other subtypes of illness, or clinical response to antidepressant therapy. In selecting REM latency data for assessment of diagnostic sensitivity, the use of the shortest REM latency from at least 3 consecutive nights yielded a higher sensitivity (74%-81%) than did the use of any one individually specified night (50%-56%) or different internight means (49%-52%). The same conclusion applied when patient age was taken into account. These results have implications for standardizing the use of REM latency as a biological correlate in major depression.
Spirometry for early detection of chronic obstructive pulmonary disease (COPD) and smoking cessation is criticised because of the potential negative effects of labelling with disease.
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A method for the quantitative determination of the tricyclic antidepressant drug amitriptyline (AT) and its active major metabolite, nortriptyline (NT), in plasma is described. The method involves a three-step extraction procedure, no derivatization, and a rapid run on a gas--liquid chromatograph equipped with a nitrogen detector. The standard curves were linear in the range of 25-1,000 ng/ml. The lower detection limit was 2-5 ng/ml for both drugs. The method is specific for AT and NT, with a recovery of AT and NT of 68 and 71%, respectively. The precision of the method, expressed as the coefficient of variation, was 10.7% for AT and 12.9% for NT within 25--1,000 ng/ml. The method has proven to be suitable for monitoring plasma levels of AT and NT in patients, and in animals during experimental studies on pharmacokinetics after therapeutic and toxic doses of NT.