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A gas-liquid chromatographic procedure is presented for the determination of therapeutic and toxic serum levels of doxepin and loxapine, using a nitrogen-phosphorus-sensitive detector. Amitriptyline is used as the internal standard. The method is accurate, sensitive and specific with no derivatization required prior to analysis. An advantage of the procedure is the small serum sample size needed for analysis and the selectivity and sensitivity of the detector, with the limit of detection being 3 and 2 microgram/l for doxepin and loxapine, respectively. Nine cases of doxenin and loxapine misuse are presented. Serum doxepin concentrations ranged from 113 to 439 microgram/l, with a loxapine concentration of 192 microgram/l observed in one patient. The presence of the tricyclics was identified and confirmed by gas chromatography-mass spectrometry and the mass spectrum of loxapine is reported.
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In Finland the majority of the users of antidepressants are women and old age people. In the 80's the number of fatal poisonings has increased. During the years 1985-1987 58% of these poisonings were women who belonged to the younger age group of the users. The older tricyclic drugs are known to be more toxic, at least in overdose, than the newer antidepressants especially when they are compared to mianserin. Of the latter, however, lately more serious side effects have been reported. For this reason the use of the different kinds of antidepressants in Finland had changed: the sales of doxepin and amitriptyline have increased and those of maprotiline and mianserin have decreased. To study the role of antidepressants in sudden and unexpected deaths the fatality ratio (defined as fatalities divided by defined daily doses per 1000 inhabitants/day) was calculated for four most prescribed antidepressants. As to the sales, amitriptyline has to be considered to be the leading antidepressant followed by doxepin, mianserin and maprotiline. As a detection in the forensic toxicological screening the sales related ratios showed that maprotiline was most commonly found followed by doxepin, amitriptyline and mianserin. When an antidepressant was the cause of death the fatality ratio was highest for doxepin (6.4) followed by maprotiline (4.3), amitriptyline (4.0) and mianserin (1). In cases of established suicides the order was the same again.(ABSTRACT TRUNCATED AT 250 WORDS)
There was no evidence of an excess likelihood of presentation with overdose with SSRIs, and the likelihood was reduced with sertraline. There was a small excess of both admissions and poisons inquiries for mirtazapine and venlafaxine. This is a concern in view of the increased toxicity of venlafaxine in overdose in comparison with SSRIs.
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Fluoxetine, imipramine, doxepine and opipramol after liquid-liquid extraction were separated by TLC on silica gel 60 GF254 by ascending and horizontal technique using suitable mobile phases. The substances were identified by UV irradiation at 254 nm and by spraying of Amelinka's reagnet (up to the amount 0.25 microgram fluoxetine and 0.05 microgram imipramine, doxepine and opipramol).
Phantom pain phenomenon is a poorly understood but relatively common sequela of limb amputation that may result in significant psychological and physical morbidity. In this review, proposed pathoneurophysiological mechanisms for the development of phantom pain are reviewed as well as psychological mechanisms that may be involved. The authors recommend an integrated approach to management of chronic phantom pain that takes into consideration the multiple factors that may contribute to its etiology.
Our review describes potential weight-altering effects of psychotropic medications (antipsychotics, antidepressants, anti-anxiety medications, mood stabilizers, sedative-hypnotics, medications for attention-deficit/hyperactivity disorder, and other psychotropic medications) and offers guidance on switching a medication if its weight-altering effect becomes problematic. For second-generation antipsychotics, the risk of weight gain is high with clozapine and olanzapine, low with amisulpride, aripiprazole, and ziprasidone, and medium with other second-generation antipsychotics. Switching from a high-risk antipsychotic to a low-risk antipsychotic usually mitigates or reverses weight gain. For second-generation antidepressants, there may be modest weight loss with bupropion and modest weight gain with mirtazapine and paroxetine. Other second-generation antidepressants are weight neutral but individual variations can occur. If significant change in weight occurs, switching to or adding a low-risk second-generation antidepressant should be considered. Mood stabilizers include lithium, valproate, carbamazepine, lamotrigine, oxcarbazepine, and most second-generation antipsychotics. Risk of weight gain is high with lithium and valproate and low with carbamazepine, lamotrigine, and oxcarbazepine. Given the complexity of bipolar disorder and its management, a switch of a mood stabilizer would be best done by a psychiatrist. Benzodiazepines, non-benzodiazepine and melatonergic hypnotics, doxepin, and trazodone are weight neutral. Diphenhydramine may cause weight-gain and can be switched to a weight-neutral hypnotic if needed. Stimulants can cause varying degrees of weight loss and switching to atomoxetine or bupropion may reverse this problem. If that fails, switching to clonidine or guanfacine can be tried. Switching must be evidence-based and take into account status of the condition being treated, efficacy, side effect profile, potential drug-drug interactions, required laboratory monitoring and cost of the drug(s) being considered, and patient's pregnancy status or plan. Non-pharmacological interventions both for mental disorders and overweight/obesity must be fully availed.
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The aim of this study was to apply microextraction by packed sorbent (MEPS) to the isolation of six tricyclic antidepressants (TCADs): nordoxepin, doxepin, desipramine, nortriptyline, imipramine, and amitriptyline from human oral fluid. Samples were collected from healthy volunteers via free spillage from the oral cavity to disposable test tubes. A method of oral fluid sample pretreatment was developed and optimized in terms of suitability for MEPS extraction and removing of interfering agents (protein, food debris, or air bubbles). Moreover, it was short and simple to perform with limited sample consumption (150μL). Extracts were analysed by UHPLC-MS. The MEPS/UHPLC-MS method was validated at three concentration levels (2.00, 4.00 and 8.00ng/mL) of all analytes in the range 1.25-10.0ng/mL. The following parameters were determined: limit of detection, limit of quantification, precision, and accuracy. For all tested concentration levels, the intra- and inter-day repeatability did not exceeded 8.1% and 12.2%, respectively. Gained LOQ value, 0.50ng/mL, made the MEPS/UHPLC-MS method to be a useful tool in clinical and forensic laboratories, which was demonstrated on the basis of analysis of real samples.
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Paroxetine is the first selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitor (SSRI) to be approved for the treatment of patients with panic disorder with or without agoraphobia. It is a highly selective inhibitor of presynaptic serotonin reuptake and does not interact with adrenergic, dopaminergic, histaminergic or serotonergic receptors to any significant extent. Oral paroxetine 10 to 60 mg/day is significantly more effective than placebo in reducing the frequency of panic attacks and improving associated symptoms, as shown in short term trials in patients with panic disorder with or without agoraphobia. The efficacy of the drug was maintained during up to 6 months'; treatment, and continued therapy reduced the risk of relapse. Oral paroxetine 10 to 60 mg/day was at least as effective as clomipramine 10 to 150 mg/day, but appeared to have a more rapid onset of effect, in a placebo-controlled trial. The tolerability profile of paroxetine is similar to that established for other SSRIs and is characterised by adverse events such as nausea, headache, somnolence, dry mouth, tremor, insomnia, asthenia, sweating, constipation, dizziness and sexual dysfunction. Paroxetine was better tolerated overall than clomipramine and was associated with a lower incidence of certain anticholinergic events (such as dry mouth and constipation) in a comparative trial. It is not associated with the type of dependence seen with benzodiazepines, and it appears to be safer in overdose than the tricyclic antidepressants. Paroxetine 20 or 30mg does not significantly impair psychomotor function or interact with alcohol (ethanol). In conclusion, the good tolerability profile of paroxetine, including lack of dependence potential and relative safety in overdose, makes it attractive for the treatment of patients with panic disorder. It appears to be at least as effective as clomipramine in reducing panic attacks and associated symptoms. Although further trials to compare the efficacy and tolerability of paroxetine with that of other tricyclic agents (especially Imipramine), high-potency benzodiazepines and monoamine oxidase inhibitors are needed, the drug appears to have the potential to become a first-line treatment for panic disorder.
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These data indicate a significant influence of the CYP2D6 genotype, minor influence of the CYP2C19 genotype and no influence of the CYP2C9 genotype on plasma concentrations of patients taking mainly second-generation antidepressants. Because of the good tolerability of the latter and the flat dose-response relationship, genotyping should only be considered in cases of suspected side effects.
Although tricyclic antidepressants remain a principal mode of treatment of depression in the elderly, concomitant medical illness in this subgroup creates particular concern regarding the safety of these drugs. Doxepin has gained favour for use in the geriatric population due to claims of low cardiovascular side effects. This perceived safety has been questioned, however, since few investigators have actually reviewed plasma levels. A recent finding of interest revealed that two patients on 150 mg of doxepin daily with assured compliance had undetectable levels of doxepin or desmethyldoxepin in their plasma. A prospective study was consequently undertaken to compare oral doses and plasma levels of doxepin with desipramine as a standard reference compound. Data was collected for 19 females (12 on doxepin, seven on desipramine) and 12 males (five on doxepin, seven on desipramine) with a mean age of 76. Eight patients on doxepin showed undetectable plasma levels as compared with none on desipramine. This is a highly significant difference. Although the therapeutic plasma range for doxepin remains controversial, it is unlikely that patients can respond to levels of zero. The authors recommend routine monitoring of doxepin levels in the elderly and question poor bioavailability or absorption of this tricyclic antidepressant in some patients.
A sensitive and specific direct-injection high-performance liquid chromatography-atmospheric pressure chemical ionization tandem mass-spectrometry (HPLC-APCI-MS-MS) method has been developed for the rapid identification and quantitation of seven tricyclic antidepressants-amitriptyline, nortriptyline, doxepin, dosulepin, dibenzepin, opipramol, and melitracen-in human plasma. After the addition of the internal standard lofepramine and dilution with 0.1% formic acid, plasma samples were injected into the LC-MS-MS system. Proteins and other large biomolecules were removed during an on-line sample cleanup using an Oasis extraction column (1 x 50 mm, ID, 30 microm) with a 100% aqueous mobile phase at a flow rate of 4 mL/min. The extraction column was subsequently brought in-line with the analytical column by automatic valve switching. Analytes were separated on a 5-microm Symmetry C18 (Waters) analytical column (3.0 x 150 mm, ID) using a step gradient of acetonitrile-0.1% formic acid at a flow rate of 0.6 mL/min. The total analysis time was only 12 minutes per sample. The interday and intraday coefficients of variation for all compounds were =11%. The assay was sufficiently sensitive to monitor all seven compounds within their therapeutic ranges. The proposed method has been in routine use for more than 1 year and permits direct analysis of plasma samples without time-consuming sample preparation, which may be especially advantageous for clinical laboratories.
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A sensitive method for the simultaneous determination of doxepin and its active metabolite desmethyldoxepin in plasma was established, using high-performance liquid chromatographic separation with tandem mass spectrometric detection. The samples were extracted with hexane-isoamyl alcohol, separated on a Phenomenex Luna C18 5 microm, 150x2.1 mm column with a mobile phase consisting of methanol-water-formic acid (600:400:0.5, v/v) at a flow-rate of 0.25 ml/min. Detection was achieved by a Perkin-Elmer API 2000 mass spectrometer at unit resolution in multiple reaction monitoring mode monitoring the transition of the protonated molecular ions m/z 280.2, 266.2 and 250.1 to the product ions m/z 107.1, 107.1 and 191.0 for analyte, metabolite and internal standard (benzoctamine-HCl), respectively. TurbolonSpray ionisation was used for ion production. The mean recovery for doxepin and desmethyldoxepin was 90% and 75%, respectively, with a lower limit of quantification at 0.320 ng/ml and 0.178 ng/ml for the analyte and its metabolite, respectively, using 0.5 ml plasma for extraction. This is the first assay method described for the simultaneous determination of doxepin and desmethyldoxepin in plasma using LC-MS-MS. The method is sensitive enough to be used in drug bioavailability studies with doxepin.
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Paroxetine is well absorbed after oral administration. It undergoes extensive first-pass metabolism and is rapidly distributed into tissue. Only about 1% of the paroxetine dose remains in the systemic circulation. Approximately 95% of paroxetine is protein bound in the plasma. Steady-state concentrations are reached after 7 to 14 days of oral administration and the terminal elimination half-life (t1/2βr) is approximately 24 hours. However, there is a great deal of interindividual variation in the pharmacokinetics of paroxetine. Paroxetine is metabolised by at least 2 enzymes of the cytochrome P450 (CYP) system, one of which is CYP2D6. This enzyme is subject to genetic polymorphism, and thus the pharmacokinetics of paroxetine differ between individuals who have the enzyme (extensive metabolisers) and those who do not (poor metabolisers). The metabolites of paroxetine are essentially inactive. Metabolism of paroxetine by CYP2D6 is saturable. Consequently, with repeated administration, bioavailability of paroxetine increases and pharmacokinetics may become nonlinear in some patients, especially when the dosage of paroxetine is increased. Approximately two-thirds of a paroxetine dose is eliminated in the urine and the remainder is excreted in faeces. Almost all of the dose is eliminated as metabolites; lt3% is excreted as unchanged drug. The plasma concentration and area under the plasma concentration-time curve of paroxetine are greater, and the t1/2βr prolonged, in elderly patients and those with hepatic or severe renal impairment compared with the general population. Paroxetine distributes into breast milk to produce concentrations similar to those in plasma.
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The effects of various tricyclic antidepressants on clonidine-induced electroencephalographic changes were investigated in rats. The EEG pattern of conscious rats was recorded by means of bipolar electrodes, implanted chronically. Clonidine (50, 150 and 300 micrograms/kg) not only synchronized cortical EEG pattern but also evoked signs of behavioural depression within 15 min of its administration. Pretreatment with imipramine, desipramine, trimipramine, amitriptyline, nortriptyline and doxepin reduced clonidine-induced EEG synchrony without showing any effects per se. Acute treatment with tricyclic antidepressants failed to modify but, chronic treatment abolished the clonidine-induced behavioural depressive signs. Chronic administration of tricyclic antidepressants (10 mg/kg/day) evoked more pronounced antagonism of the EEG effects of clonidine. Yohimbine (200 micrograms/kg) pretreatment inhibited both, clonidine-induced EEG synchrony and behavioural effects. Guanfacine as well as B-HT 920, elicited clonidine-like effects on cortical EEG pattern and behaviour. The present data suggests that antagonism of clonidine-induced EEG synchronization in conscious animals could serve as a useful test for screening of antidepressant drugs.
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We describe a single procedure for assay of seven tricyclic antidepressant drugs and metabolites in serum or plasma: protriptyline, nortriptyline, amitriptyline, desmethyldoxepin, doxepin, desipramine, and imipramine. With the Technicon "FAST-LC" system, samples are aspirated directly into the unit and pretreated via double extraction; the concentration of each drug is then determined by "high-performance" liquid chromatography. Final chromatograms are monitored at 205 nm, at analysis rates of 7.5 samples/h. Concentration and absorbance are linearly related for each drug from 0 to 1400 micrograms/L. Day-to-day CVs averaged 5 to 6% for each drug, and there is good correlation of FAST-LC values with those obtained by gas-chromatographic methods. Total sample volume is 750 microliters.
There are two reasons to believe anxiolytics might help in smoking cessation. Anxiety may be a symptom of nicotine withdrawal. Second, smoking appears to be due, in part, to deficits in dopamine, serotonin and norepinephrine, all of which are increased by anxiolytics and antidepressants.
Plasma levels of doxepin and its metabolite desmethyldoxepin were determined in 7 depressed patients treated with doxepin hydrochloride in 3 divided doses at 1000, 1600, and 2200 hours (t.i.d.), and repeated after changing the dosage schedule to a single daily bedtime (h.s.) dose at 2200 hours. Doxepin and its metabolite were measured at 9000, 1200, 1500, and 1800 hours. None of the individual patients showed clinically significant changes in their plasma concentration of tricyclic antidepressant on the 2 dosage schedules. No difference in the clinical condition of the patients was detected on the 2 dosage schedules using the Zung Self Rating Depression Scale, however patients experienced more morning sedation while on the single h.s. dosage. This study provides pharmacological support for the prescription of doxepin on a once daily basis.
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Measurement of H1RO is a sensitive and absolute method to characterize the non-sedating property of drugs with H1 antagonistic activity.
Guidelines including level of evidence and grade of recommendation were recently published for chronic urticaria (CU).
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It is surprising that a large amount of sedating antihistamines was prescribed. In many instances these were prescribed as needed. This fact could have a negative impact on urticaria control and patient satisfaction. It seems difficult for the nonexpert to differentiate between CU and any kind of physical urticaria.
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A method of microextraction by packed sorbent (MEPS) followed by liquid chromatography with diode array detection has been developed and optimized for the extraction of six tricyclic antidepressants (amitriptyline, nortriptyline, imipramine, desipramine, doxepin, nordoxepin) from human serum. The optimal parameters of MEPS extraction (type of sorbent, volume of sample, composition, and volume of washing and elution solutions) for these drugs in spiked samples were defined. The developed MEPS procedure was validated and then successfully applied to the analysis of serum reference material. The limit of detection (0.02-0.05 μg/mL), intraday (2.7-8.8%) and interday (4.4-11.6%) precision (RSD), and the accuracy of the assay (94.5-108.8%) at three concentration levels-0.2, 0.5, and 0.8 μg/mL-were estimated. The accuracy of the method was evaluated by the analysis of certified reference material. Moreover, the validated procedure was compared with the solid-phase extraction technique. Finally, microextraction by packed sorbent was assessed as a suitable tool in forensic and clinical methods for serum sample preparations.
There are two reasons to believe antidepressants might help in smoking cessation. First, depression may be a symptom of nicotine withdrawal, and smoking cessation sometimes precipitates depression. Second, nicotine may have antidepressant effects that maintain smoking for some smokers. Antidepressants may substitute for this effect.
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Cutaneous lymphoid hyperplasia (CLH) has been proposed to be the benign end of a continuum of lymphoproliferative disorders with cutaneous lymphoma at its malignant extreme. An intermediate condition, known as "clonal CLH," was first recognized by us and shown to be a transitional state capable of eventuating in overt lymphoma. To better determine the prevalence of dominant clonality and risk of lymphoma among CLH cases, we studied the immunohistology and clonality of fresh-frozen samples from 44 CLH patients referred to a multidisciplinary cutaneous lymphoproliferative disorders program. Using a large panel of lymphoid markers, the cases were divided into 38 typical mixed B-cell/T-cell type CLH and 6 T-cell-rich type (T-CLH), the latter containing > 90% T cells. Of the 44 patients, 38 had solitary or localized lesions (4 cases of T-CLH), and 6 had regional/generalized lesions (2 cases of T-CLH). Forty cases were of idiopathic etiology. Suspected etiologies among 4 other cases included mercuric tattoo pigment, doxepin, clozapine, and bacterial infection. Immunoglobulin heavy chain (IgH) and T-cell receptor (TCR)-gamma gene rearrangements (GR) were studied using polymerase chain reaction assays, which are approximately 80% sensitive. Overall, 27 cases (61%) showed clonal CLH: 12 IgH+ (27%; 3 cases of T-CLH); 13 TCR+ (30%; 1 case of T-CLH); and 2 IgH+/TCR+ (4%; neither case was T-CLH). Two cases (4%; 1 case of T-CLH) progressed to cutaneous B-cell lymphoma. Both of these patients presented with regional lesions. Our findings indicate that clonal overgrowth is common in CLH, links CLH to lymphoma, and probably involves both B- and T-cell lineages (although TCR GR by B cells and vice versa could not be ruled out). The high prevalence of dominant clonality in our series may have resulted from the sensitivity of our PCR assays as well as patient selection.
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2193 homebound people older than age 60.
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1. A possible coupling of the rat cerebral cortex 5-hydroxytryptamine (5HT)-1A receptors to isletactivating protein (IAP, pertussis toxin) sensitive Gi protein was investigated by studying the effects of a guanosine 5'-triphosphate (GTP) and IAP injection to the rat ventricle. 2. Scatchard analysis showed that Bmax value of the high-affinity componentin [3H]8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) binding was decreased by pretreatment with IAP. 3. GTP caused a significant decreased Bmax of the high affinity site for [3H]8-OH-DPAT binding. It was noted that the IAP suppressed the cyclic AMP production by 5HT, VIP and Forskolin. 4. These results suggest that the rat cortex 5HT-1A receptors are linked to the Gi protein. 5. After 3 weeks chronic administration of amitriptyline (5mg/kg), desipramine (5mg/kg), imipramine (5mg/kg), doxepin (5mg/kg) and trazodone (10mg/kg), the receptor binding assay was carried out on 5HT-1A receptors. 6. It was observed that all the antidepressant drugs except for imipramine increased the number of high-affinity sites of the 5HT-1A receptors in the frontal cortex. 7. These results suggested that the increase of the Bmax for the 5HT-1A receptor might be related to the effectiveness of the antidepressant drugs.
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Solutions containing drugs (amitriptyline, clomipramine, or doxepin) and variable amount of AC or SPS were incubated for 30 minutes.
Antihistamines often are self-administered at night as over-the-counter (OTC) sleep aids, but their next-day residual sedative effect has never been evaluated using a reliable quantitative method such as positron emission tomography (PET). We performed a double-blind, placebo-controlled, crossover study in which we evaluated the residual effect the next day after nighttime administration of diphenhydramine, a commonly used OTC sleep aid, in terms of brain H₁ receptor occupancy (H₁RO) measured using ¹¹C-doxepin-PET. We also compared the results of diphenhydramine with those of bepotastine, a second-generation antihistamine. Eight healthy adult male subjects underwent PET measurement the morning (11:00) after random oral administration of diphenhydramine (50 mg), bepotastine (10 mg), or placebo the night before (23:00). Binding potential ratios and H₁ROs were calculated in different brain regions of interest such as the cingulate gyrus, frontotemporal cortex, and cerebellum. Subjective sleepiness and plasma drug concentration also were measured. Calculation of binding potential ratios revealed significantly lower values for diphenhydramine than for bepotastine or placebo in all regions of interest (P < 0.01). Cortical mean H₁RO after diphenhydramine treatment was 44.7% compared with 16.6% for bepotastine treatment (P < 0.01). Subjective sleepiness was not significantly different among the subjects treated with each test drug or the placebo. In conclusion, the next-day residual sedative effect after nighttime administration of the OTC sleep aid diphenhydramine was verified for the first time by direct PET measurement of H₁RO. Taking into account the possible hangover effect of OTC antihistamine sleep aids, care needs to be taken during their administration.