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Biomedical subjects

D Sechter

Publications and source records attributed to D Sechter.

At least 55 records · Page 3Linked 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↗
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

Diagnostic and therapeutic value of testing stimulation of thyroid-stimulating hormone by thyrotropin-releasing hormone in 100 depressed patients.

The thyrotropin-releasing hormone (TRH) test was performed in 100 depressed patients, including 73 patients with a major depressive episode (MDE) according to DSM-III. Thirty-one patients subsequently received an antidepressant with a predominant serotoninergic action (indalpine or citalopram), and 27 patients received a noradrenergic antidepressant (maprotiline). The diagnostic value of the TRH test was not conclusive for any of the subgroups of depressed patients: MDE, MDE with melancholia or MDE in bipolar patients. Similarly, the value of the TRH test in the choice of antidepressant treatment according to the monoaminergic action was not convincing. These results are discussed in the light of the data of the international literature.

Adult↗
PubMed1987

Changes in [3H]5-HT uptake and [3H]imipramine binding in platelets after chlorimipramine in healthy volunteers. Comparison with maprotiline and amineptine.

In the platelets of normal healthy volunteers (n = 8) taking chlorimipramine (50 mg/day) for 1 week, the saturable uptake of [3H]5-hydroxytryptamine (5-HT) was fully inhibited at the end of the week, but returned to control values after 2 weeks washout. The Bmax of [3H]imipramine binding was decreased by 63% at the end of the treatment and remained significantly decreased below control values after 1 week washout, whereas the Kd values were increased at the end of the treatment, but had returned to baseline values after 1 week washout. The time course of recovery following the administration of chlorimipramine showed some variation between subjects, but it was necessary to wait up to 4 weeks of washout before the Bmax of [3H]imipramine returned to baseline levels. In contrast, neither 1-week treatment with maprotiline (50 mg/day) nor with amineptine (100 mg/day) changed the parameters of [3H]5-HT uptake or [3H]imipramine binding in platelets from healthy volunteers. These results support the following conclusions. (1) [3H]Imipramine binding in platelets can be down-regulated by relatively low, subtherapeutic doses of chlorimipramine. (2) It is possible to dissociate [3H]imipramine binding parameters from [3H]5-HT uptake because the time course of recovery was clearly different, indicating that [3H]imipramine labels a site linked with, but different from, the 5-HT recognition site in the transporter complex. (3) A washout of antidepressants of 4 weeks may be needed when studying the parameters of [3H]imipramine binding in platelets from depressed patients if the previous medication involved chlorimipramine. For antidepressants like maprotiline or amineptine, that act through mechanisms other than inhibition of 5-HT uptake, the time of washout appears to be less critical, although it is not possible to rule out the existence of some secondary modifications influencing the 5-HT transporter complex.

Adult↗
PubMed1987

Association of [3H]-imipramine and [3H]-paroxetine binding with the 5HT transporter in brain and platelets: relevance to studies in depression.

[3H]-Imipramine and [3H]-paroxetine label with high affinity a site which is associated with the serotonergic transporter in brain and platelets. The pharmacological profile of inhibition by drugs of [3H]-imipramine and [3H]-paroxetine binding is highly correlated with the potency of the drugs to inhibit the uptake of 5HT. Denervation of serotonergic neurons by electrolytic lesions or with 5,7-dihydroxytryptamine produces marked decreases in the density of [3H]-imipramine as well as [3H]-paroxetine binding. Dissociation kinetic experiments support the view that the substrate recognition site for 5HT is different from the modulatory site which is labelled by [3H]-imipramine or [3H]-paroxetine. The existence of an endogenous ligand acting on the [3H]-imipramine recognition site to modulate the 5HT transporter was proposed by several laboratories. [3H]-Imipramine binding in platelets appears to be a biological marker in depression. Studies carried out in several laboratories report a significant decrease in the Bmax of platelet [3H]-imipramine binding without changes in Kd, when severely depressed untreated patients are compared with healthy volunteers matched for age and sex. The Bmax of platelet [3H]-imipramine binding appears to be a state-dependent biological marker in depression. It is tempting to speculate that the endocoid of the [3H]-imipramine recognition site may play a role in the pathogenesis of depression.

Animals↗
PubMed1986

Electroconvulsive shock therapy and maximum binding of platelet tritiated imipramine binding in depression.

We studied the tritiated imipramine binding values in platelets from 12 hospitalized untreated patients with endogenous depression and found a significant decrease in maximum binding (Bmax) values compared with a control population of the same age and sex. There were no changes in the equilibrium dissociation affinity constant values between the untreated depressives and the control population. After at least six sessions of electroconvulsive therapy and at the time when a significant clinical improvement of depression was confirmed, the Bmax value of tritiated imipramine binding in platelets was slightly increased but was still significantly below that of the control values. However, when six of these patients were reexamined after 12 to 18 months, at a time when they were euthymic, the Bmax of tritiated imipramine binding in platelets was found in the same range as the values of the control population. Our results indicate that clinical improvement precedes the changes in Bmax of tritiated imipramine binding in platelets from depressed patients. The tritiated imipramine binding in platelets is a useful biologic marker in affective disorders. Furthermore, our results suggest that tritiated imipramine binding in platelets may be a state-dependent biologic marker in depression.

Aged↗
PubMed1986

Reduced Bmax of [3H]-imipramine binding to platelets of depressed patients free of previous medication with 5HT uptake inhibitors.

The high-affinity binding sites for [3H]-imipramine (IMI) present in human platelets are associated with the neuronal uptake system for 5HT. It was recently demonstrated that previous antidepressant therapy with drugs which inhibit 5HT uptake could down-regulate [3H]-IMI binding and that this effect could persist up to 1 month after the end of treatment. We therefore re-examined the reported differences in Bmax of [3H]-IMI binding in platelets between control and depressed untreated patients, to evaluate the residual influence of previous antidepressant medication. The saturation characteristics of [3H]-IMI binding were compared in platelets from 17 depressed patients carefully selected according to previous antidepressant therapy and washout period, who were closely matched, for age and sex, with a group of control healthy volunteers. The results reveal a significant decrease by 47% in the Bmax of [3H]-IMI binding in platelets of untreated depressed patients when compared with controls. There was no significant modification of Kd values for platelet [3H]-IMI binding between the depressed and the control groups. Our results support the view that platelet [3H]-IMI binding is a useful tool as a biological marker in depression.

Adult↗
PubMed1986

Lack of seasonal variation in platelet [3H]imipramine binding in humans.

The Bmax of [3H]imipramine (IMI) binding has been reported to be reduced in platelets of depressed untreated patients as compared with normal controls. However, it has also been suggested that this difference could be related to the failure to take into account seasonal variations in the binding parameters for [3H]IMI recognition sites in platelets. For this reason, [3H]IMI binding was studied throughout 1 year in platelet membranes from 11 control volunteers, with blood samples collected once a month. The Bmax and Kd values of [3H]IMI binding showed no significant variation throughout the 12-month period of the study. These results indicate that in the control population, the platelet [3H]IMI binding parameters remain stable, and that the decrease in Bmax observed in depressed untreated patients reflects a genuine difference, which may be considered to be a biological marker in depression.

Adult↗
PubMed1986

Lack of correlation between plasma DOPEG and urinary MOPEG levels in depressed patients.

Twenty-four-hour urinary excretion of 3-methoxy,4-hydroxyphenylethyleneglycol (MOPEG) and levels of free and conjugated plasma 3,4-dihydroxyphenylethyleneglycol (DOPEG) were measured in 56 depressed patients to find a possible correlation between these two peripheral indices of cerebral noradrenergic activity. Plasma DOPEG was measured at 9:00 AM on the same day that urine was collected for the measurement of MOPEG. All depressed patients were diagnosed as having affective disorders according to DSM-III. No correlation was found between plasma free or conjugated DOPEG levels and urinary MOPEG output. This lack of correlation was found in the total sample of depressed patients (56), in 45 patients diagnosed as having major depressive episodes, and in 24 depressed patients diagnosed as major depressive with melancholia. The authors discuss the significance of this lack of correlation between two peripheral indices of central noradrenergic metabolism.

Adult↗
PubMed1985

[Study of the metabolism of cerebral noradrenaline in depressed patients by the assay of plasma dihydroxyphenylethylene glycol].

Dihydroxy-phenyl-ethylene-glycol (DOPEG or DHPG), a deaminated catabolite of noradrenaline formed after presynaptic re-uptake, is a good marker of metabolic activity in noradrenergic pathways. Plasma levels of free, conjugated and total DOPEG were measured by a radioenzymatic method in 45 patients with major depression selected according to the DSM 3 criteria and in 45 matched controls. A significant decrease in man DOPEG levels was observed in all depressive patients. A dexamethasone suppression test performed in these patients showed no difference in DOPEG levels between responders and non-responders, thus failing to support the hypothesis that subjects with low noradrenergic drive escape suppression. There was no correlation between plasma DOPEG levels and urinary excretion of methoxy-hydroxy-phenylglycol (MOPEG), another marker of noradrenaline metabolic activity. Thirty-one patients were treated with a specific monoaminergic antidepressant: maprotiline or indalpine; contrary to urinary MOPEG levels, plasma DOPEG levels had no predictive value concerning the response to this category of antidepressants. The various possible reasons for the fall in DOPEG observed in depressive patients are discussed.

Adult↗
PubMed1984

[3H]Imipramine binding and [3H]5HT uptake in human blood platelets: changes after one week chlorimipramine treatment.

In platelets of normal volunteers taking chlorimipramine (50 mg/day) for one week, the saturable uptake of [3H]5HT was fully inhibited at day 8, but returned to control values at day 15. The Bmax of [3H]imipramine binding was decreased by 65% at day 8 and remained significantly below control values at day 15. If the present findings can be extrapolated to other antidepressants, the reported decreases in [3H]imipramine binding in depression may partly reflect residual treatment effects. It cannot be excluded that, in depression, the platelet [3H]imipramine receptor already is down-regulated maximally which would preclude a further down-regulation due to antidepressant drug therapy.

Adult↗
PubMed1983

3H-Rauwolscine binding in platelets from depressed patients and healthy volunteers.

3H-Rauwolscine binds specifically and with high affinity to alpha 2-adrenoceptors in human platelets. In a study comparing the binding of 3H-rauwolscine in platelets obtained from 26 control volunteers with 19 hospitalised, untreated, severely depressed patients, the mean maximal binding (Bmax) and mean dissociation constant (Kd) of 3H-rauwolscine binding were found to be identical in both groups. After 7-12 days, treatment with different tricyclic antidepressant drugs there was a significant improvement in the depressive symptoms but no change in the 3H-rauwolscine binding. After an average of 23 days treatment with tricyclic antidepressants, and when the Hamilton Depression Rating Scores had returned to normal, the Kd and Bmax of 3H-rauwolscine binding were still unchanged.

Adjustment Disorders↗
PubMed1982

[Biochemistry of schizophrenia and mechanism of action of neuroleptics].

Among the biochemical theories proposed for schizophrenia the best-founded appears to be the dopaminergic theory. Dopaminergic agonists exacerbate schizophrenic symptoms. Neuroleptics, which are the most effective drugs in schizophrenia, are dopaminergic-blocking agents. Other biochemical disorders have been demonstrated in some cases of schizophrenia but results are not always consonant. The presence of abnormal compounds, i.e. methylated derivatives or phenylethylamine, has often been mentioned. Several disorders of enzymes have also been reported, such as a defect in beta-dopamine hydroxylase or an abnormal activity of the MAO which metabolizes the indolamines and catecholamines. Disorders of the metabolism of noradrenaline and serotonin have also been suggested, mainly on experimental evidence. Other compounds have been incriminated, such as endorphins, gamma-aminobutyric acid, lysine-8 vasopressin or prostaglandins. The action of neuroleptics can be ascribed to dopaminergic respector blockade, as a safe approximation. However, the demonstration of several dopaminergic pathways and of several types of receptors makes the understanding of their mode of action all the more difficult that they interplay with many other neurotransmittors.

Antipsychotic Agents↗
PubMed1982

[Clinical study of bromazepam. Thirty cases (author's transl)].

The anxiolytic activity of a new benzodiazepine derivative, bomazepam, was investigated in 30 ambulatory patients treated for psychotic or neurotic disorders. The effectivenss and safety of the drug were assessed at the different stages of the study by means of Hamilton's anxiety scale and Guelfi and Pull somatic scale. As all tranquillizers of the benzodiazepine group, bromazepam proved effective against anxiety and associated somatic symptoms. Indoses ranging from one to three 6 mg tablets per day (6-18 mg), the drug was extremely well tolerated, even by elderly patients.

Adolescent↗
PubMed1982

[Anxiety and psychotherapies (author's transl)].

The two words "anxiety" and "angoisse" are now generally used in the same sense in the french psychiatric literature. S. Freud distinguished anxiety neurosis from neurasthenia, providing a detailed clinical description and developing a psychopathological theory of anxiety. All forms of mental disease include to the same extent, anxiety. The treatment of anxiety depends upon the clinical background. Various approaches--psychotherapy psychopharmacology--are often simultaneously necessary.

Anxiety Disorders↗