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Biomedical subjects

S Vandel

Publications and source records attributed to S Vandel.

90 records · Page 5Linked to original sources
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[Drug interactions and new antidepressive agents].

The mechanism of action of new antidepressants is characterized by a specific inhibition of the serotonin reuptake at synaptic level. In France, fluoxetine, fluvoxamine, and more recently paroxetine are extensively used. Based on a review of the literature, the authors report the interactions of these new antidepressants with psychotropic and other drugs, that are frequently associated with them. All studies report the frequent occurrence of interaction when the new serotonergic antidepressants are associated with tricyclic ones. The increase of tricyclic drug plasma levels is often high with side effects as a consequence. If the pharmacodynamic aspects of these interactions are not well known, the pharmacokinetics are easier to understand, due to the power of these new antidepressants to inhibit cytochrome P450.

Antidepressive Agents↗
PubMedDate not supplied

[Undesirable effects of drugs. Epidemiologic study at a psychiatric service of a university hospital].

The authors reviewed the drug side effects observed in their ward during the 5 last years (1988-92). These alleged effects occurred at a very low incidence, 3 per cent, (116 cases on 3809 hospitalizations). As mentioned in the literature, the occurrence was higher in females (60 per cent), than in males. The age seemed not to be a risk factor in that population, the mean age being 44 for the men and 45 for the women. All side effects disappeared after decreasing or stopping the suspected drug. In 6 cases the suspected drug was not a psychotropic agent. The authors presented some of the more often reported cases, and some of the more recently known, such as extrapyramidal side effects with antidepressants, increase of the libido with serotonergic antidepressants. The problem fo polytherapy is discussed. In half (59/116) of the cases there was a psychotropic association. The side effect may be due to a pharmacokinetic interaction in 16 cases, either with enzymatic inhibitors like dextropropoxyphene, valpromide, valproic acid, fluvoxamine and fluoxetine, or with enzymatic inducers like carbamazepine. The authors compared the side effects of the antidepressants mainly used in their ward (amitriptyline, clomipramine, fluvoxamine and fluoxetine).

Adult↗
PubMedDate not supplied

[A case of metabolic interaction: amitriptyline, fluoxetine, antitubercular agents].

Polytherapy is often used in clinical practice. The drug associations may lead to pharmacokinetic and/or pharmacodynamic interactions, with clinical implications. The authors reported a quantified illustration of 2 types of interactions in a depressed patient: between antidepressants, amitriptyline and fluoxetine, between these antidepressants and antituberculosis. Firstly, when fluoxetine was added to amitriptyline, it was observed, as expected, an increase of the tricyclic and its metabolite plasma levels, despite a decrease of its dosage. Secondly, when antituberculosis were added to the 2 antidepressants, it was observed a decrease of the tricyclic drug plasma levels. These levels remained below the therapeutic window even when the tricyclic antidepressant dosage was increased. It seems that the fluoxetine interaction disappeared. The competition between the inhibitory effect of fluoxetine and the induction of rifampicin, on the metabolism of amitriptyline is discussed.

Adult↗
PubMedDate not supplied

[Thyroid function in depressed patients].

This preliminary report compares the FT3, FT4, TSH basal levels and FT4/FT3 ration of depressed patients (DSM III-R criteria) with those of a healthy control group. Authors have also studied thyroid parameters in function of some clinical depression data (polarity, intensity and endogenous character) and other factors as age and sex. 81 depressed patients (31 men, 50 women), with mean age of 44.85 years were studied. 44 patients suffered of an endogenous depression and 37 of a non endogenous depression (Newcastle criteria). 60 patients had an unipolar depression while 21 patients had a bipolar depression. The control group was constituted of 36 healthy subjects (20 men, 16 women), with mean age of 40.94 years. There is no significant difference between the two groups for sex and age, besides the different size of the two groups. FT3 mean of depressed patients was 4.39 pmol/l. There was a significant difference between unipolar group FT3 mean (4.51 +/- 1.01 pmol/l) and bipolar FT3 mean (4.03 +/- 0.91 pmol/l; t = 2.02, p < 0.05). Depression intensity was correlated negatively to FT3 mean (r = -0.23; t = 2.10, p < 0.005). FT4 mean in the depressed group was 12.62 +/- 4.14 pmol/l. The only significative result for FT4 was its correlation to TSH levels (r = -0.36; t = 3.43, p < 0.001). TSH mean in depressed patients was 1.43 +/- 0.85 microIU/ml. When we have compared these results with those of control group we concluded that FT3 and TSH levels were significantly lower in the depressed group (FT3: t = 4.83, p < 0.0001; TSH; t = 2.44 p < 0.02) and that FT4 was slightly but not significantly increased in the depressed group. FT3 decrease and the slight FT4 increase in depression may be the consequence of a metabolic deviation of FT4 transformation into FT3. Its link with intensity and polarity of depression suggests that it can be considered as a biological marker of this disease.

Adult↗
PubMedDate not supplied

[Fluoxetine and tricyclic antidepressants: clinical tolerance in short-term combined administration].

The tricyclic SSRI antidepressant association is often used in the treatment of resistant depressive illness. The pharmacokinetic interaction existing between these two types of drugs is well known, with as result, an increase of tricyclic antidepressant plasma levels. The aim of this work was to assess the clinical tolerance of the association of fluoxetine and tricyclic antidepressants, prescribed at usual doses. In 10 patients, having a bad response to a tricyclic antidepressant treatment, with in the therapeutic window adjusted plasma levels since 3 weeks, an association of fluoxetine (20 mg/d) to the tricyclic was prescribed. The other associated treatments were unmodified. The clinical evolution was recorded with the MADRS and the UKU scale for side effects, before the tricyclic antidepressant treatment adjustment (D-21) and just before the fluoxetine association (D1) and every 7 days after this association too. The tricyclic plasma levels (amitriptyline and clomipramine) and the patient phenotype CYP 2D6 and 2C19 were determined before and 7 days after the fluoxetine addition. A good clinical evolution was noted since the 7th day after the fluoxetine association to tricyclic (mean MADRS scores on D-21, D1, D7 and D14; 35.4, 33.1, 23.9, 16.8 respectively). In 3 patients, an anxiety increase on day 6, 14 and 16 respectively, after fluoxetine addition, induces a stop of the serotonergic antidepressant. In one patient all the treatment was stopped due to the appearance of a mood inversion. In another patient, after 14 days of antidepressant association, EC were prescribed as asked by the patient, due to an insufficient mood improvement, with a good clinical result and tolerance. The evolution of the side effects was surprising. There was no increase of the UKU score mean during the associated treatment, despite an increase of the tricyclic plasma levels that reached, in three patients, the toxic level (510, 605 and 860 ng/ml of amitriptyline + nortriptyline or clomipramine + demethylclomipramine). The UKU psychic score mean significatively decreased (7.7, 6.8, 5.3, 4 on D-21, D1, D7, D14 respectively). The fluoxetine association did not modify the neurological, neuro-endocrinologic and the skin side effects. None increase of headheck was noted. The increase of anxiety, observed in 3 patients, was not considered as a side effect of the antidepressant association, but an effect of the stimulant potency of fluoxetine in anxious patients. The pharmacogenetic results confirmed the strong inhibition potenty of fluoxetine on the CYP 2D6 isoenzyme. In 5 patients indeed, the extensive metabolizer phenotype was modified in a poor metabolizer phenotype, seven days after the association of fluoxetine. The CYP 2C19 phenotype was unchanged after this association. The patient phenotype did not seem to interfere with the clinical results. In conclusion, in this group of patients, the short-term clinical tolerance of the tricyclic antidepressant and fluoxetine association was very good, despite the pharmacokinetic interaction existing between these two types of drugs.

Adult↗
PubMedDate not supplied

[Maprotiline versus fluvoxamine: comparison of their effects on the hypothalamo-hypophyseal-thyroid axis].

The TRH test has been used in psychiatry these last 20 years. One of the most promising results is that concerning the possibility to use it to identify the best moment to stop a treatment after clinical recovery of the depressive episode. For that it is necessary to demonstrate an absence of intrinsic action of antidepressants on the HPT axis physiology. This overt, randomized study has compared the actions on T3, T4, basal TSH and its response to the TRH test after 75 mg/day of maprotiline and 100 mg/day of fluvoxamine, both administrated in depressed patients during 28 days. Forty patients (20 men and 20 women) were studied, 20 patients per treatment. The inclusion criteria were those of DSM III-R for major depression and dysthymia as well a minimum score of 25 at MADRS scale. Blood samples for T3, T4 and basal TSH dosages were made before TRH intranasal administration (2 mg) at days 1 and 28 of the treatment. We haven't observed any difference before treatment between the 2 groups for clinical and biological studied parameters. After treatment both antidepressants produced equivalent improvement of depression evaluated by MADRS (fluvoxamine:dMADRS = 16.95 +/- 7.11; maprotiline: dMADRS = 17.10 +/- 6.84. t = 0.07, NS). T3 and T4 variations between the beginning and the end of the study weren't also significantly different between the 2 groups. Basal TSH was increased in the maprotiline group but decreased in the fluvoxamine group resulting in a significant difference (fluvoxamine: dTSH = 0.31 +/- 0.76 mUI/l. Maprotiline : dTSH = -0.23 +/- 0.66 mUI/l. t = 2.40, p < 0.02). The TSH response to TRH was decreased in the fluvoxamine group (ddTSH = 0.24 +/- 6.65 mUI/l. dAUC = 103.98 +/- 596.84 mUI/l) while it was increased in the maprotiline group (ddTSH = -3.59 +/- 5.88 mUI/l. dAUC = -355.80 +/- 505.67 mUI.min/l). The difference between the 2 treatments was not significant when evaluated by ddTSH (t = 1.53, NS) but it became significant if evaluated by dAUC (t = 2.63, p < 0.01). As we could demonstrate an absence of influence of the clinical evolution between both groups in the hormonal variations observed, we concluded to a intrinsic difference action on HPT axis between fluvoxamine and maprotiline. This difference could be linked to the different aminergic action of these 2 antidepressants.

Adult↗