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PubMed1989

Bulimia: independence of antibulimic and antidepressant properties of desipramine.

The purpose of this study was to identify variables useful for predicting a positive response to the tricyclic antidepressant desipramine, amongst bulimic subjects. Using a randomized double-blind cross-over design, 24 normal weight bulimics completed a 15-week protocol in which they received either desipramine (150 mg/day) for six weeks, no drug for three weeks, followed by placebo for six weeks, or the reverse sequence. At weeks 0, 2, 4, 6, 9, 11, 13, and 15, each subject was assessed using the EDI, SCL-90, POMS and binge records. The DST, Diagnostic Interview Schedule (DIS), and a personal and family medical-psychiatric history questionnaire were administered at initial assessment, while plasma desipramine levels were obtained at weeks 4 and 13. Responders were defined in terms of both binge frequency reduction, and decrease in depressive symptoms. In the sample of 24 subjects, desipramine was significantly more effective than placebo in reducing the frequency of weekly binging and vomiting, as well as causing a reduction in the fatigue scale of the POMS. No significant effect of the drug was obtained on the EDI or the SCL-90. In terms of reduction in binge frequency, seven responders were identified; another seven were found to be borderline responders, while 10 were labeled as non-responders. The three groups did not differ in terms of their initial scores on the SCL-90, POMS, DST, DIS results, or psychological subscales of the EDI. However, responders were found to have lower EDI bulimia subscale scores, but a higher frequency of purging episodes than were non-responders. Eight patients were identified as borderline responders with respect to depressive symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Comparative plasma levels of doxepin and desipramine in the elderly.

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.

Administration, Oral↗

PubMed1981

A pilot study of the mechanism of action of desipramine.

To test the hypothesis the desipramine alters alpha adrenoceptor function in depressed patients, the effects of clonidine upon growth hormone sedation and blood pressure have been measured in depressed patients before and after treatment with desipramine. After three weeks of treatment the hypotensive and sedative effects of clonidine were inhibited in all patients even though plasma desipramine concentrations at this time varied from 42 to 560 micrograms/l. Growth hormone responses to clonidine were enhanced in five of the six patients but this effect was not statistically significant. These findings are consistent with the hypothesis that in these patients desipramine altered alpha adrenoceptor function: other explanation are discussed.

Adult↗

PubMed1982

The effect of desipramine upon central adrenergic function in depressed patients.

Eleven drug free patients meeting Research Diagnostic Criteria for Major Depressive Disorder have been treated with desipramine and given a clonidine infusion after 0, 1 and 3 weeks of treatment. The sedative and hypotensive effects of clonidine were significantly inhibited after three weeks of treatment with desipramine: a similar interaction was seen after one week of treatment although this just failed to reach statistical significance. The growth hormone (GH) response to clonidine was initially impaired, but increased significantly after one week of treatment. A significant reduction in the GH response occurred during the second and third weeks of treatment with desipramine. This last finding is interpreted as evidence of adaptive change of alpha 2 adrenoceptors: the other changes can be explained by the known ability of desipramine to block the re-uptake of noradrenaline.

Adult↗

PubMed1984

Effects of desipramine treatment upon central adrenoceptor function in normal subjects.

Six normal subjects were given clonidine infusions after 0, 1 and 3 weeks of treatment with desipramine (2 mg/kgm) and at 1 and 3 weeks after withdrawal from desipramine. The sedative and hypotensive effects of clonidine were inhibited after one and three weeks of desipramine treatment, and returned to normal after stopping treatment without any rebound increase. Such a time-course can be explained in terms of the acute effects of the drug, no adaptive changes at receptors need be invoked. By contrast, the growth hormone response to clonidine tended to be increased after one week of desipramine, reduced after three weeks of treatment, and further reduced after discontinuation. Such a time-course is consistent with an adaptive down regulation at alpha 2 adrenoceptors in response to their acute stimulation, due to noradrenaline re-uptake blockade.

Adult↗

PubMed1995

Effects of yohimbine and desipramine on adrenal catecholamine release in response to splanchnic nerve stimulation in anesthetized dogs.

The effects of yohimbine and desipramine on adrenal catecholamine (CA) release in response to splanchnic nerve stimulation (SNS) were examined in anesthetized dogs. SNS and 3 Hz produced frequency-dependent increases in epinephrine (EPI) and norepinephrine (NE) output determined from adrenal venous blood. Yohimbine (30 and 100 micrograms/kg, i.v.), a selective alpha 2-adrenoceptor antagonist, enhanced the SNS-induced increases in both EPI and NE output. Desipramine (100 and 300 micrograms/kg, i.v.), an amine pump inhibitor, enhanced the SNS-induced increases in NE output, whereas no enhancement of EPI output was produced. After desipramine treatment, yohimbine further enhanced the SNS-induced increases in EPI and NE output. After yohimbine treatment, desipramine further enhanced the SNS-induced increase in NE output. These results suggest that the release of adrenal CA in response to SNS is inhibited by alpha 2-adrenoceptors, and that released NE, rather than EPI, is predominantly taken up into the dog adrenal medullary cells.

Adrenal Glands↗

PubMed2006

A double-blind, multicenter, parallel-group study of paroxetine, desipramine, or placebo in breast cancer patients (stages I, II, III, and IV) with major depression.

OBJECTIVE: This study compared the efficacy and safety of paroxetine and desipramine with those of placebo in the treatment of depressive disorders in adult women with breast cancer, stages I-IV. METHOD: In a double-blind, placebo-controlled study, 35 female outpatients with breast cancer and DSM-III-R major depression or adjustment disorder with depressed mood were randomly assigned to treatment with paroxetine (N=13), desipramine (N=11), or placebo (N=11) for 6 weeks. Primary efficacy was assessed by change from baseline in score on the 21-item Hamilton Rating Scale for Depression (HAM-D), and the secondary outcome measure was change from baseline in the Clinical Global Impressions-Severity of Illness scale (CGI-S) score. RESULTS: Mean changes in the total HAM-D and CGI-S scores from baseline to 6-week endpoint for the paroxetine and desipramine groups were not significantly different than those for the placebo-treated group. An unusually high rate of response (defined as >or=50% improvement in the HAM-D score) in the placebo group was observed (55% [N=6]); adverse events precipitated patient discontinuation in the active treatment groups (9% [N=1] for desipramine, 15% [N=2] for paroxetine) similar to that in the placebo-treated patients (18% [N=2]). Improvement on symptom dimensions within the HAM-D and Hamilton Rating Scale for Anxiety (depressive, anxiety, cognitive, neurovegetative, or somatic) was also similar between groups. CONCLUSION: The small number of women in this study most likely contributed to the lack of observed differences in efficacy observed during the 6 weeks of treatment. Randomized, placebo-controlled trials of adequate power seeking to determine efficacy of antidepressants in the United States for the treatment of women with breast cancer and comorbid depression remain of paramount importance.

Adult↗

PubMedDate not supplied

Comparison of desipramine or carbamazepine to placebo for crack cocaine-dependent patients.

The authors compared the effects of desipramine or carbamazepine to placebo in an intensive outpatient program for cocaine abuse. Subjects recruited from an urban drug treatment program were randomly assigned to a double-blind, placebo-controlled, eight-week trial of desipramine, carbamazepine, or placebo. Patient ratings, urine drug screens, and blood samples were obtained weekly. Using survival analysis, the three groups did not differ in time to drop out of treatment. While subjects improved over time on all self-ratings related to cocaine use, mood, and craving, only two items related to mood were significantly different over time as a function of treatment group. Subjects in the two treated groups reported significantly more improvement on self-ratings of depression and irritability. No treatment differences were noted for sustained abstinence or for proportion of positive urine drug screens. Desipramine subjects who attained a minimum blood level were retained in treatment significantly longer than placebo or other non-compliant treatment groups. This finding supports previous reports of a possible role for desipramine in cocaine abuse treatment.

Adult↗

PubMed1991

Meta-analysis of desipramine as an adjunct in the treatment of cocaine addiction.

Many pharmacologic regimens have been recommended as supplemental treatment strategies for cocaine abuse. Using the technique of meta-analysis, we compared and combined the data from six studies to examine the efficacy of desipramine as an adjunctive treatment approach for cocaine addiction. These studies were randomized, placebo-controlled clinical trials of desipramine and involved a total of 200 cocaine-addicted patients. We found that desipramine is no better than placebo in retaining patients in treatment. However, while patients are in treatment, desipramine is helpful in promoting abstinence (p less than 0.001). There were several compromises made to use meta-analysis for these studies. These included comparing patient populations with different psychiatric and substance use diagnoses, comparing studies that used varying amounts of psychotherapy, and comparing studies that defined certain outcome variables in diverse ways. There are other limitations in the use of meta-analysis that were not specific to the studies we compared. These include such issues as statistical bias and publication bias. The purpose of this paper is to suggest the use of meta-analysis as one way to help the clinician evaluate the literature and to point out the areas of difficulty when assessing the literature.

Cocaine↗

PubMed1990

[Methoxyflurane and ethanol do not inhibit the neuronal uptake of noradrenaline (uptake 1) at the desipramine binding site].

We recently demonstrated that the net accumulation of 3H-norepinephrine in the rat pheochromocytoma cell line PC12 was reduced by anesthetic concentrations of n-alkanols and the volatile anesthetics halothane, enflurane, isoflurane, and methoxyflurane. In PC12 cells, as in adrenergic neurons, norepinephrine is transported across the plasma membrane by a saturable, high-affinity, carrier-mediated mechanism (uptake1), which follows Michaelis-Menten kinetics, is energy- and sodium-dependent, and is inhibited by low concentrations of cocaine and the tricyclic antidepressant desipramine. Although uptake1 is the most important process for the removal of norepinephrine from the synaptic cleft, the net accumulation of norepinephrine within the neuron also depends on other factors including its vesicular uptake and storage within the granules, its metabolism by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT), and the efflux of its more lipophilic metabolites. In our previous report we could not exclude the contribution of any of these factors to the observed inhibitory effects of volatile substances. Therefore, the aim of the present study with ethanol and methoxyflurane was: (1) to elucidate further the exact mechanism responsible for the reduction of the norepinephrine accumulation; and (2) to investigate the anesthetics' interaction with the substrate recognition site, which is identical with the desipramine binding site on the norepinephrine carrier. METHODS. For 3H-norepinephrine uptake experiments, PC12 cells were cultured on dishes (60 mm, Nunc) coated with polyornithine. Reserpine (10 microM) was added to the culture 24 h before the experiment to deplete endogenous norepinephrine. The initial carrier-mediated transport rate (60 s) was measured as previously described. 3H-desipramine equilibrium binding was determined with isolated plasma membranes prepared from PC12 cells grown in suspension culture. The carrier-mediated uptake of 3H-norepinephrine and the specific 3H-desipramine binding were defined as those inhibited by 1 microM nisoxetine. All buffers contained 10 microM pargyline and 10 microM U-0521 to inhibit MAO and COMT. Incubations were done in the presence and absence of methoxyflurane (1% and 2% vol/vol in synthetic air containing 5% CO2) or ethanol (5% vol/vol). Media had been equilibrated with methoxyflurane by bubbling (30 min) and were routinely checked by gas chromatography. RESULTS AND DISCUSSION. Methoxyflurane and ethanol inhibited uptake1. However, reduction of uptake1 was far less pronounced than that previously found for the net accumulation of norepinephrine. Even at a vaporous concentration of 2% (corresponding with an over 15-fold half-maximal inhibitory concentration for norepinephrine accumulation), methoxyflurane produced only 58% inhibition of the high-affinity uptake...

Adrenal Gland Neoplasms↗

PubMed1989

Chemical delivery systems for drugs containing an amino group: synthesis and properties of some pyridine derivatives of desipramine.

Seven chemical delivery systems (CDS) based on a dihydropyridine<-->quaternary pyridinium salt type redox system and analogous to the naturally occurring NADH<-->NAD+ coenzyme system were applied in the case of the antidepressant drug desipramine. The pyridine moiety-containing carriers were linked to the amino function of desipramine either as amides or substituted carbamates. Lipophilic properties were expressed in terms of chromatographic Rm values. Oxidative stability of the dihydropyridine forms of the CDSs were determined in vitro. The amide type derivatives were stable toward hydrolysis in buffers and in biological fluids, whereas the carbamates released the parent drug in a very efficient manner. In a behavioral despair test, the CDSs did not show improved activity when compared to desipramine. In vivo distribution studies of one of the CDS did not show more efficient delivery of the desipramine into the rat brain but did show a prolonged presence at a constant level.

Animals↗

PubMed1989

Hypersensitivity myocarditis and hepatitis associated with imipramine and its metabolite, desipramine.

We present two cases of myocarditis and hepatitis with histologic characteristics of hypersensitivity-mediated drug reactions associated with imipramine and its metabolite, desipramine. In one case, death was directly attributed to myocarditis; in the second case, the patient died of an acute myocardial infarct, but myocarditis may have played a contributory role. One patient was taking imipramine, and therapeutic concentrations of imipramine and desipramine were documented in postmortem blood. The other patient was receiving desipramine documented by in-patient hospital medication records. Both cases had liver lesions associated in the medical literature with adverse drug reaction to imipramine. Although myocarditis has been previously associated with amitriptyline, these cases appear to be the first reported in association with imipramine/desipramine. The fact that one patient was taking only desipramine suggests that it may be the offending agent.

Aged↗

PubMed1986

Symptom exacerbation in psychotically depressed adolescents due to high desipramine plasma concentrations.

The pharmacological treatment of two female adolescent patients meeting DSM-III criteria for psychotic depression is described. A combined antipsychotic and tricyclic antidepressant regimen led to clinical remission. However, a recrudescence in both psychotic and depressive symptoms developed as plasma desipramine levels rose 4 times higher than anticipated from the oral doses prescribed. Clinical improvement occurred in both cases when plasma desipramine levels were reestablished below 200 ng/ml. Thus, we recommend prospective monitoring of desipramine plasma levels, especially when an antipsychotic agent that inhibits the metabolism of the tricyclic antidepressant is also used. We further suggest that deterioration with the reemergence of the presenting clinical syndrome, without signs of delirium, represents a distinct manifestation of antidepressant toxicity. Finally, these cases support the existence of a therapeutic upper limit for desipramine plasma concentrations, above which clinical deterioration occurs.

Adolescent↗

PubMed1988

Treatment of bulimia with fenfluramine and desipramine.

Desipramine and fenfluramine were administered to bulimic patients in a 15-week study of double-blind, placebo-controlled, crossover design. The 22 patients in the study met DSM-III criteria for bulimia and were of normal weight. Twelve subjects were randomly allocated to the fenfluramine group, and 10 subjects received desipramine. Half the subjects in each group received the active drug in the first 6 weeks and half received placebo. There was a 3-week washout period, after which subjects were crossed over for the remaining 6 weeks. The Eating Disorder Inventory, profile of Mood States, bulimia symptom checklists, and Hopkins Symptom Checklist were administered at weeks 0, 2, 4, 6, 9, 11, 13, and 15. Subjects maintained a daily record of bingeing, vomiting, and laxative/diuretic abuse. Results indicated that both drugs had beneficial effects on bingeing and vomiting frequency, although a greater proportion of patients were identified who responded to fenfluramine than to desipramine. Fenfluramine and desipramine were also effective in reducing the psychological symptoms of bulimia, such as the urge to binge, and feelings of depression. Results suggest that direct alteration of central food intake regulatory centers can effectively control bulimia.

Adolescent↗

PubMed1986

Double-blind comparison of desipramine and placebo for treatment of phencyclidine or amphetamine dependence.

Open clinical trials have suggested that desipramine may be an effective agent for treatment of phencyclidine (PCP) or amphetamine dependence. Four pairs (eight subjects) with PCP and two pairs (four subjects) with amphetamine dependence were studied. One subject in each pair was given desipramine or placebo under double-blind conditions. Although desipramine clearly was no more effective than placebo in treatment of PCP dependence, subjects with amphetamine dependence who received desipramine remained in treatment longer and submitted more urine samples absent of amphetamine than did subjects who received placebo.

Amphetamines↗

PubMed1988

Desipramine and testicular swelling in two patients.

Two patients are described who developed testicular swelling and pain during treatment with desipramine. The symptoms disappeared when desipramine was discontinued and in one case returned when desipramine treatment was reinitiated. The observations suggest that testicular swelling and pain are side effects of desipramine.

Bipolar Disorder↗

PubMed1978

[Differential indications for desipramine--results of a controlled multiclinical study].

The antidepressants desipramine and imipramine were compared within the framework of a multiclinical study performed under the conditions of a controlled clinical experiment. There has been found a time-different remission of affective symptoms, which was not detectable for the inhibition of drive. The tachythymoleptic action of desipramine is discussed with reference to these results. Evaluation of the possibility of controlling affects shows different ranges of activity of desipramine and imipramine, with desipramine influencing especially negative psychoenergetic symptoms in the area of drives and emotions and imipramine, restrictive symptoms in addition to differential phenomena of the psychomotor expression.

Clinical Trials as Topic↗

PubMed1987

The effect of desipramine on body weight in depression.

Twenty-six patients with major depressive disorder were treated with desipramine for 4 weeks to determine the effect of the drug on body weight. Responders to desipramine showed a weight gain only at Weeks 3 and 4; nonresponders had a nonsignificant loss of weight. The increase in body weight of the responders was independent of dosage, sex, and hospitalization status. These findings suggest that the small increase in body weight that occurs in patients taking desipramine is associated with treatment response. In addition, desipramine may be a valuable treatment alternative for those patients in whom excessive weight gain is undesirable.

Adult↗