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Biomedical subjects

S Vandel

Publications and source records attributed to S Vandel.

At least 19 recordsLinked to original sources
PubMed1992

Tricyclic antidepressant plasma levels after fluoxetine addition.

After a review of a pharmacokinetic interaction between tricyclic antidepressants (TCA) and fluoxetine the authors report their own data. They confirm the existence of an interaction of TCA with fluoxetine, in clinical practice, but the fluoxetine was not associated in all cases with a marked increase of TCA plasma levels. The increase appeared especially high with clomipramine (n = 4) and imipramine (n = 3), and lower or dose-dependent with amitriptyline (n = 4). The pharmacokinetic change did not induce side effects in the patients, even when the total TCA plasma level increased to 965 (clomipramine) or 785 (imipramine) ng/ml. The authors then discuss the clinical implication and the possible mechanism of action.

Adult↗
PubMed1992

Clomipramine plasma levels among depressed outpatients in Benin, west Africa: drug compliance and comparison with Caucasian patients.

A 75 mg/day clomipramine treatment was prescribed for 4 weeks to 92 outpatients with major depression at the Neuropsychiatric Clinic of the National University Hospital of Cotonou in Benin, West Africa. Among them, only 42 followed the treatment during the 4 weeks and had a clomipramine and desmethylclomipramine plasma level measure (gas chromatography technique). The rate of noncompliance appeared high: 10 patients had no trace and another 2 had only traces of antidepressant in their plasma. For the remaining 29, a comparison with 29 Caucasian patients treated by clomipramine (the two samples are matched for sex and age, and the variables of weight, dosage and drug association are controlled) shows no significantly higher plasma levels in the Beninese sample.

Ambulatory Care↗
PubMed1991

[Prediction of suicide risk].

Suicide is a great problem for public health. In France it causes more than 12,000 deaths every year, and it has been estimated that 45 to 70% of these subjects were suffering of affective disorders. Some epidemiological aspects of the links between suicide and depression are analytic and concern the risk factors of suicide among depressed patients: sociodemographic factors: risks are more important for men and for people living alone or suffering of social and affective isolation. Violent suicides increase with age; clinical and evolutive characteristics of the illness: the risk of suicide is correlated with the global severity of the depression, whatever are the nosographic subtypes, with anxiety, sleep disorders and anhedonia, with personal and familial history of suicide; among biological factors, a decrease of 5-HT transmissions has been implicated, but it seems to be more correlated with a modification of the ability to delay, with a poor impulse control. The association of several of these factors increases suicidal risk but it is impossible to describe a specific picture of the depressed suicidal patient, and clinical scales to estimate suicide risk are of limited interest. Finally, the clinical vigilance adapted to each individual case and the quality of the therapeutical relation remain the most important point for preventing suicide.

Causality↗
PubMed1990

Desipramine induces cardiac beta-adrenergic sensitivity decrease in major depressed patients without relationship to therapeutic response.

Nineteen major depressed inpatients were treated over three weeks with desipramine. Cardiac beta-adrenergic receptor sensitivity was evaluated by an isoproterenol test before and after the three-week treatment. Desipramine induced a beta-adrenergic sensitivity decrease in most of the patients: I 20 (isoproterenol dose necessary to increase by 20 beats/min. the basal heart rate) before treatment: 89 +/- 37 ng/kg (mean +/- SD); after treatment: 170 +/- 135 ng/kg; p(t) less than 0.03. Despite a linear relationship between pretreatment beta-adrenergic sensitivity and post-treatment clinical state, there was no relation between post-treatment cardiac beta-adrenergic sensitivity and therapeutic response or even desipramine plasma levels.

Depressive Disorder↗
PubMed1989

Debrisoquine oxidative phenotyping and psychiatric drug treatment.

The debrisoquine/sparteine phenotype was determined in 51 patients with depression, who were subdivided into 3 groups in terms of their drug treatment. Log (MR) for each group was compared. Patients treated with benzodiazepines had the same distribution of log (MR) as the healthy population, but the distribution was shifted towards higher values in patients treated with neuroleptics and antidepressants. It appears that the phenotypic expression of debrisoquine oxidation may be modified by drugs whose metabolism follows the same route as debrisoquine. The debrisoquine test must be carefully interpreted in patients receiving several drugs in the same time.

Adolescent↗
PubMed1989

Amitriptyline: linear or nonlinear kinetics in every day practice?

The linearity of the (AMT) kinetics of amitriptyline has been tested in 135 depressed dosed twice daily by measuring plasma. Their (AMT) and nortriptyline (NT) levels under steady-state conditions. The AMT concentration/dose ratios at low and high dosages were not significantly different and there was a linear relationship between the dose ratios and the concentration ratios. No change in the metabolic ratio (AMT/NT) was observed between the two dosages. Although the results are consistent with linear AMT kinetics, there may have been nonlinear kinetics in some patients as the ratio between the concentration/dose ratios in them at low and high dosages was greater than one. Those patients were characterized by a low concentration/dose ratio at low dosage. No clinical adverse effect appeared in the study.

Amitriptyline↗
PubMed1989

Desipramine dose prediction based on 24-hour single-dose levels: feasibility and validity.

The authors present a prospective study of a rapid desipramine dose adjustment on the basis of a 24-hour plasma concentration after a single 150 mg dose. For this, they use a prediction table constructed from data in the literature showing strong correlation between steady-state plasma levels and 24-hour single-dose levels. Despite the fact that desipramine action is not always linear, the method appears to be feasible and valid. In an attempt to reach a 150 ng/ml level, the authors obtained steady-state levels ranging from 85 to 317 ng/ml, with 14 of the 19 patients in the range between 125 and 250 ng/ml. Moreover, 11 of the 19 patients received a daily dose of 250 mg or more desipramine from the third day of treatment onward; in ten of these cases, this dose had been adapted.

Adult↗
PubMed1989

Cardiac beta-adrenergic sensitivity in depression: relation with endogenous subtype and desipramine response.

The authors studied the responsiveness of cardiac beta-receptors to isoproterenol, a noradrenergic agonist, in 29 depressed patients and 13 control subjects. They showed a significantly lower sensitivity in depressed patients as compared with the control subjects. Focussing on the group of depressed patients without antidepressant treatment in the month preceding the study (n = 15) in order to avoid a bias, the following significant results were obtained: cardiac beta-adrenergic receptor sensitivity was lower in patients suffering from endogenous depression than in those suffering from reactive depression (as classified by Newcastle Scale). There was a negative linear relation between cardiac beta-adrenergic sensitivity and the posttreatment clinical state (as expressed by the MADRS score) for the 9 patients who ended a 3-week desipramine treatment period.

Adjustment Disorders↗
PubMed1988

Valpromide increases the plasma concentrations of amitriptyline and its metabolite nortriptyline in depressive patients.

The effects of valpromide on amitriptyline (AMT) and nortriptyline (NT) plasma levels were examined in 20 depressed inpatients. They all were treated with AMT, 125 mg once daily, and 10 patients also received 600 mg of valpromide daily after 10 days on AMT. In the 10 patients receiving valpromide in addition to AMT, the mean AMT level increased from 70.5 +/- 35 to 105.5 +/- 49 ng/ml (p less than 0.0003) and the mean NT level from 61.0 +/- 34 to 100.5 +/- 65 ng/ml (p less than 0.01). This increase was not related to valpromide metabolite plasma levels, nor to the age of the patients. The addition of valpromide to a stable AMT regimen may result in an increase of antidepressant plasma level with clinical implications.

Adult↗