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Psychotropic medications are an important treatment approach to mental health disorders; such disorders are common in the elderly population. Elderly patients are more likely to experience adverse effects from these agents than their younger counterparts due to age-related changes in pharmacodynamic and pharmacokinetic parameters. Because of these factors, inappropriate use of psychotropic medications in elderly patients has become a focus of concern. In general an agent is considered inappropriate if the risk associated with its use exceeds its benefit. Implicit and explicit criteria for inappropriate use of medications in the elderly have been created and include psychotropic agents. These criteria vary in their make-up but the explicit criteria tend to agree that amitriptyline, doxepin, and benzodiazepines that have long half-lives are not appropriate. Although explicit inappropriate medication criteria have been in existence since 1991, elderly patients continue to receive inappropriate psychotropic medications. A wide array of factors may be responsible for this practice. Provider-related causes include deficits in knowledge, confusion due to the lack of a consensus on the inappropriate psychotropic criteria, difficulties in addressing an inappropriate medication started by a previous provider, multiple prescribers and pharmacies involved in the care of a patient, negative perceptions regarding aging, and cost issues. Patients may contribute to the problem by demanding an inappropriate medication. Finally, the healthcare setting may inadvertently contribute to inappropriate prescribing by such policies as restrictive formularies or lack of reimbursement for pharmacists' clinical services. Successful approaches to optimising prescribing have been either educational or administrative. Educational approaches (e.g. one-on-one sessions, academic detailing) seek to influence decision making, while administrative approaches attempt to enforce policies to curtail the undesired practice. The US Omnibus Budget Reconciliation Act of 1987, which improved psychotropic medication use in long-term care, is an excellent example of administrative intervention. More research specifically focused on the causes of inappropriate psychotropic medication use and methods to avoid this practice is needed before targeted recommendations can be made.
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Herein, we present a case of a parkinsonism-hyperpyrexia syndrome (PHS) in a 58-year-old man with a 10-year history of Parkinson's disease. The patient presented with a 2-week history of fever and increasing confusion, in the context of a number of changes to his medication regimen. On presentation, he was noted to be febrile with autonomic instability, diaphoresis and marked rigidity. He was disoriented and responding to visual hallucinations. Investigations revealed an elevated creatine kinase and a provisional diagnosis of PHS was made. After the patient failed to respond during a 2-week period to supportive measures, electroconvulsive therapy (ECT) treatment was commenced. A good response to eight bilateral ECT treatments was achieved, with resolution of his confusional state and associated psychotic phenomena. We discuss the nosological and management issues associated with this case and discuss the role of ECT as a treatment modality in this condition.
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The doxepin N-demethylation was studied by means of pooled human liver microsomes and chemical inhibitors, recombinant human (rh)-CYPs, and geno- and phenotyped human liver microsomes.
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A 46-year-old man suffering from neurotic depression complicated by alcohol and benzodiazepine dependence developed Coombs'-positive hemolytic anemia and thrombocytopenia with acute renal failure after 5 weeks of monotherapy with doxepin at a final dosage of 100 mg daily. The patient recovered completely after discontinuation of doxepin, blood exchange transfusion, and repeated hemodialyses. He had no history of hematologic abnormalities, exposure to other toxins, or glucose-6-phosphate dehydrogenase deficiency. Because other etiologic factors were ruled out, the short interval between the onset of the patient's hemolytic crisis and the administration of doxepin highly suggests that doxepin was associated with the complication. To the best of our knowledge, ours is the first report of this adverse effect following doxepin administration.
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Laboratory testing in CUA patients referred for an Allergy and Immunology evaluation rarely lead to changes in management resulting in improved outcomes of care.
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The kinetics of protriptyline were examined in 8 subjects after a single oral dose of 30 mg protriptyline hydrochloride. Peak protriptyline levels ranged from 10.4 to 22.3 ng/ml and were reached 6 to 12 hr after the oral dose. The mean protriptyline half-life (t1/2) was 74.3 hr and ranged from 53.6 to 91.7 hr in individual subjects, confirming the long t1/2 of protriptyline reported by Moody and associates. The estimated first-pass metabolism of protriptyline was relatively small, ranging from 10% to 25% of the oral dose, assuming complete absorption. The mean volume of distribution was 22.5 L/kg and ranged from 15.0 to 31.2 L/kg. No relationship was found between the kinetics of protriptyline and those of doxepin studied previously in 7 of the 8 subjects.
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Patients placed on indomethacin obtained relief more consistently and more completely. Patients on pentoxifylline had the fewest side effects of all oral therapies. Patients on antihistamines with or without doxepin had the highest incidence of side effects, although more of these patients reported a greater degree of relief than patients on pentoxifylline. All patients on oral therapy overall had greater relief than patients using topical steroids.
An excellent therapeutic result was obtained by treating TMEP with the 585-nm flashlamp-pumped dye laser, although the response was temporary. The therapeutic effect of the laser appears to be secondary to reduction of the vasculature with no apparent effect on the mast cells. Physicians treating TMEP with laser therapy must use proper H1 and H2 receptor blockade to avoid potential complications from laser-induced mediator release.
A variety of antidepressants of different chemical classes were tested for their in vivo and in vitro activity at 5-HT1C receptors in the brain. Conventional tricyclic antidepressants (imipramine, desipramine, maprotiline, clomipramine, trimipramine, amitriptyline, nortriptyline, doxepin, amoxapine) as well as mianserin and trazodone were found to display high to low nanomolar affinity for 5-HT1C receptors. Antidepressants of other chemical classes and with other mechanisms of action (affecting amine uptake systems: fluoxetine, citalopram, sertraline, fluvoxamine, nomifensine, amineptine; or monoamine oxidase inhibitors: moclobemide, iproniazid) had negligible affinities (micromolar range) for 5-HT1C receptors, except fluoxetine. When tested in an in vivo rat model thought to reveal functional agonistic or antagonistic properties at 5-HT1C receptors, all antidepressants displaying high affinity for this receptor type (except clomipramine and trimipramine) were antagonists at 5-HT1C receptors. Antidepressants with a lower affinity for 5-HT1C receptors (except nomifensine) were inactive in this functional in vivo model. Taken together, these results suggest that antagonism at brain 5-HT1C receptors is a component of the antiserotonergic properties of a number of established antidepressants. In addition, the study confirmed that 5-HT1A receptors functionally interact with 5-HT1C receptors, which suggests that some degree of activity at 5-HT1A receptors may also be an important property for antidepressant activity.
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In blood platelets of untreated patients with endogenous depression a significantly lower concentration of serotonin (5-HT) was found than in healthy persons (P less than 0.05). The patients were afterwards divided into two groups: group I with mild symptoms of depression (total scores by Hamilton Depression Rating Scale below 40) and group II with severe depression (total scores above 40). The gradual diminishing of symptoms in both groups was accompanied by no change in 5-HT level in the first group and by progressive and well marked increases in platelet 5-HT content in the second one, attaining average normal values at the end of week 3 of treatment with maprotiline. In in vitro experiments maprotiline inhibited the uptake of 5-HT into blood platelets of healthy persons less than doxepin. After injection of maprotiline in rats (50 mg/kg IP) the turnover rate of 5-HT in the brain was only marginally affected if measured by 5-HT rise and 5-hydroxyindoleacetic acid (5-HIAA) decline after administration of the MAO inhibitor pargyline, or by estimation of 5-HIAA increase after blocking active transport with probenecid. However, after treatment with maprotiline alone, the 5-HIAA level in the rat brain was significantly increased, although the concentration of 5-HT was not altered. These results suggest: a) the possibility of an action of maprotiline on serotoninergic neurons and b) the suitability of blood platelets as a model for such an investigation.
We aimed to assess the efficacy and safety of pharmacological interventions for daytime sleepiness and sleep disorders in PD.
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Considering time and frequency derived measures, which are rather independent of heart rate, the patients showed significantly decreased heart rate variability parameters (p < 0.0001), as compared with the normal subjects. Of the patients presenting delirious symptoms 6 showed coefficients of variation more than 4 standard deviations below the mean control value.
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Psoriasis is a common chronic inflammatory skin disease observed in about 1-3% of the general population. About 60-90% of patients with psoriasis suffer from itching. Interestingly, in the past itch was not considered as an important symptom of psoriasis. Despite the high frequency of itch in psoriasis, the pathogenesis of this symptom is still not fully elucidated. Although most studies indicate neurogenic inflammation and the role of neuropeptides, other mediators may be important as well. The majority of psoriatic patients consider itch as the most bothersome symptom of the disease as it significantly alters daily functioning and psychosocial well-being. Patients with itch showed greater impairment of their health-related quality of life compared to those without itch, and the intensity of itch correlated with the degree of quality-of-life reduction. However, treatment options for itch in psoriasis are limited. Therapy of itch in patients with psoriasis should be directed toward the resolution of skin lesions, as disease remission usually is linked with itch relief. Recent studies have clearly pointed to an important role of apremilast and biologic agents in itch intensity reduction in subjects suffering from psoriasis. Other treatment modalities include antihistamines, especially with a sedative effect, narrowband ultraviolet B, and antidepressants (doxepin, mirtazapine, paroxetine). Support by family members and/or health professionals may also be of importance in helping psoriatic subjects cope with itch.
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There at least two reasons to believe antidepressants might help in smoking cessation. Depression may be a symptom of nicotine withdrawal, and smoking cessation sometimes precipitates depression. In some individuals, nicotine may have antidepressant effects that maintain smoking. Antidepressants may substitute for this effect.
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A randomized evaluation of fluoxetine and doxepin measured a 50% change in the Hamilton Depression Rating Scale (HDRS) score as a response to therapy and was correlated with measures of standard deviation of the mean of all 5-minute segments of normal electrocardiographic R-R intervals (SDANN), standard deviation of all normal R-R intervals (SDNN), root mean square of successive differences in R-R intervals (r-MSSD), and percentage difference between adjacent normal R-R intervals that are greater than 50 msec (pNN50) from 24-hour electrocardiogram (ECG) tapes.
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Male Wistar rats received acute and four-week intraperitoneal injections of doxepin (3, 5, and 10 mg/kg) or its vehicle (0.9% saline). One hr after the last injection, animals were exposed to a 5 min swim stress session. In other cohorts of animals, the CB1 receptor antagonist AM251 (0.25, 0.5, and 1mg/kg) was injected 30 min before the administration of doxepin. Plasma corticosterone concentration was measured by enzyme-immunoassay at 45 min following stressing. 1, 5, and 12 hr after the last injection of doxepin, the contents of endocacannabinoids (anandamide and 2-arachidonylglycerol) within the lipid extracts of the prefrontal cortex, amygdala, hippocampus, and hypothalamus were determined using isotope-dilution liquid chromatography-mass spectrometry.
Existing studies were not able to define the best approach for the treatment of BPS/IC. The lack of standardized treatment may be related to the diversity of interventions used; therefore, further studies with better methodological quality are needed.
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In the double-blind study of 51 patients with duodenal ulcer the effect of doxepin and placebo was evaluated. Complete healing of the ulcer was found in 19 of 23 patients after 4 weeks of treatment with 50 mg doxepin (83%) and in 14 of 27 patients given placebo (52%) (p less than 0.05). Two patients in the placebo group developed complications necessitating surgical intervention. No serious side effects were registered in the doxepin group.
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The cases had taken dothiepin (16 patients), doxepin (six patients), thioridazine (five patients), amitriptyline (five patients), nortriptyline (three patients), imipramine (one patient) and a combination of dothiepin and thioridazine (three patients). In 20 of the 39 patients with arrhythmias, the arrhythmia had been a presumed ventricular tachycardia. Of the other 19 patients, 15 patients had a supraventricular tachycardia, two patients had cardiac arrests (one asystole, one without ECG monitoring) and two patients had insufficient data recorded to make classification of the arrhythmias possible. The QRS was >/= 100 ms in 82% of cases but also in 76% of controls. QRS >/= 160 ms had a sensitivity of only 13% and occurred in 2% of controls. QRS > 120 ms, QTc > 500 and the R/S ratio in aVR appeared to have a stronger association with the occurrence of arrhythmia: QRS > 120 ms (odds ratio [OR], 3.56; 95% confidence interval [CI], 1.46-8.68), QTc > 500 (OR, 3.07; 95% CI, 1.33-7.07), and R/S ratio in aVR > 0.7 (OR, 16; 95% CI, 3.47-74). Excluding thioridazine overdoses and performing the analysis for tricyclic antidepressant overdoses alone gave increased odds ratios for QRS > 120 ms (OR, 4.83; 95% CI, 1.73-13.5) and QTc > 500 (OR, 4.5; 95% CI, 1.56-13) but had little effect on that for the R/S ratio in aVR > 0.7 (OR, 14.5; 95% CI, 3.10-68).
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We extracted data in duplicate on the type of study population, the nature of the drug therapy, the outcome measures, method of randomization, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline, expressed as an odds ratio (OR). We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model.
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Using an isocratic high-performance liquid chromatography (HPLC) system and UV detection, a simple and precise analytical procedure was developed to quantify levels of the CB(1) receptor antagonist rimonabant in the plasma of rhesus monkeys. Rimonabant was extracted from plasma samples into 5% isopropanol in hexane. After separation, the isopropanol-hexane fractions were dried to residue, redissolved in mobile phase, and then injected into the HPLC. The HPLC system included an acetonitrile-phosphate buffer (62:38, v/v) mobile phase (pH 6.7), flow rate of 1.5 mL/min, C(18) column (4.6 mm i.d. x 150 mm length, 5 microm), and UV detection at 280 nm. Retention times for rimonabant and doxepin (internal standard) were 9.9 and 2.4 min, respectively. The regression of the spiked calibrator curve was linear from 60 to 4000 ng/mL (r(2) = 0.996). The lower limit of quantification was 60 ng/mL, and recovery was 83.6%. Rimonabant was stable in stock solutions and monkey plasma across a range of temperatures and concentrations. To demonstrate utility, plasma rimonabant was measured in six rhesus monkeys at 60 and 240 min after intramuscular administration of 1 mg/kg rimonabant. Rimonabant levels ranged from 175 to 1290 ng/mL. The analytical assay described here provides a simple and accurate procedure for multiple within-subject measurements of the CB(1) antagonist rimonabant.
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Hemoperfusion over cellulose-coated activated charcoal was used to treat a patient with severe doxepin overdose. Noncardiogenic pulmonary edema (NCPE) developed temporally in relation to the procedure. In this case, NCPE may have been from complement activation by the cellulose-coated charcoal column.