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Exploration de l’influence noradrénergique (par le dosage du MHPG urinaire) sur le test de freinage à la dexaméthasone chez les déprimés

Published online by Cambridge University Press:  28 April 2020

H. Lôo
Affiliation:
Professeur de Psychiatrie. Chef du Service Hospitalo-Universitaire de Santé Mentale et de Thérapeutique Hôpital Sainte Anne, 1, rue Cabanis – 75674 , Paris Cédex 14
M.F. Poirier
Affiliation:
Chargé de Recherehe Inserm. Service Hospitalo-Universitaire de Santé Mentale et de Thérapeutique Hôpital Sainte Anne, 1, rue Cabanis – 75674 , Paris Cédex 14
T. Dennis
Affiliation:
Ph. D. Groupe de Biochimie Pharmacologique, Laboratoires d'Études et de Recherches Synthélabo 31, avenue Paul Vaillant Couturier – 92220 , Bagneux
C. Benkelfat
Affiliation:
Attaché de Recherche. Service Hospitalo-Universitaire de Santé Mentale et de Thérapeutique Hôpital Sainte Anne, 1, rue Cabanis – 75674 , Paris Cédex 14
J.M. Vanelle
Affiliation:
Assistant des Hôpitaux Psychiatriques, Service du Docteur Pascal – 60 Clermont de L'oise
J.P. Olié
Affiliation:
Praticien du cadre Hospitalier. Service Hospitalo-Universitaire de Santé Mentale et de Thérapeutique Hôpital Sainte Anne, 1, rue Cabanis – 75674 , Paris Cédex 14
S. Askienazy
Affiliation:
Chef du Service de Médecine Nucléaire, Hôpital Sainte Anne, 1, rue Cabanis – 75674Paris Cédex 14
B. Scatton
Affiliation:
Ph. D. Groupe de Biochimie Phamiacologique, Laboratoires d'Études et de Recherches Synthélabo 31, avenue Paul Vaillant Couturier – 92220 , Bagneux
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Résumé

Une hyperactivité de l’axe hypothalamo-hypophyso-cortico-surrénalien est souvent objectivée dans les dépressions majeures ou endogènes, particulièrement par le test de freinage à la dexaméthasone (DST).

Certaines hypothèses évoquent un dysfonctionnement noradrénergique pour expliquer cette anomalie.

Afin de rechercher les liens entre l’axe HPA et une anomalie du métabolisme de la noradrénaline (NA) cérébrale, 47 déprimés majeurs ont été étudiés.

Pour chaque déprimé étaient mesurés l’excrétion urinaire du MHPG de 24 heures et un test de freinage à la dexaméthasone était effectué.

Aucune corrélation n’est retrouvée entre l’âge et la sévérité de la dépression d’une part et d’autre part, l’excrétion du MHPG et les chiffres de cortisolémie pré et post dexaméthasone. Par contre, il existe une corrélation positive entre l’âge et l’excrétion du MHPG et entre l’âge et la cortisolémie post dexaméthasone, entre la durée du sevrage thérapeutique et la cortisolémie pré dexaméthasone et surtout, entre la cortisolémie pré DST et post DST.

Aucune corrélation ne peut âtre retrouvée entre l’excrétion du MHPG et la cortisolémie maximale post dexaméthasone.

Il n’y a pas de différence d’excrétion urinaire du MHPG entre les suppresseurs et les non suppresseurs qui sont au nombre de 19 (40 %).

Lorsque les déprimés sont séparés en hauts excréteurs et bas excréteurs de MHPG, il existe une tendance significative des déprimés hauts excréteurs à présenter un pourcentage supérieur de non suppresseurs.

L’étude ne confirme pas l’hypothèse hyponoradrénergique de l’échappement à la dexaméthasone. Elle tend plutôt à démontrer une association entre une hyperactivité de l’axe HPA et une excrétion urinaire élevée de MHPG.

De nombreux facteurs peuvent peut-âtre expliquer les difficultés à mettre en évidence les liens entre l’échappement au freinage par la dexaméthasone et une anomalie du métabolisme de NA cérébrale lorsque des mesures biologiques périphériques sont utilisées.

Summary

Summary

A hyperactivity of the hypothalamic -pituitary - adrenocortical axis (H.C.A.) has often been substantiated in major or endogenous depressions, particurlarly in the Dexamethasone Suppression Test (D.S.T.). Some authors have hypothesized noradrenergic (NA) dysfunctioning to explain this abnormality.

In order to define the links between the H.P.A. axis and abnormal brain NA metabolism, 47 major depressed patients were studied.

For each depressed patient 24 h. urinary M.H.P.G. excretion was measured and a D.S.T. was performed.

No correlation was found between age and severity of depression on the one hand, and M.H.P.G. excretion and pre and post Dexamethasone plasma cortisol on the other hand.

However, there was a positive correlation between age and M.H.P.G. excretion, between age and post Dexamethasone plasma cortisol, between therapeutic washout duration and pre Dexamethasone plasma cortisol and, above all, between pre D.S.T. plasma cortisol and post D. S. T. plasma cortisol.

No correlation could be found between M.H.P.G. excretion and maximal post Dexamethasone plasma cortisol.

There was no difference in the M.H.P G. urinary excretion between suppressors and non suppressors (N = 19.40%). When depressed patients were distributed into high and low M.H.P.G. excretors, high excretors significantly included a higher percentage of non suppressors.

This study did not confirm the hypothesis of a link between NA deficiency and escape to Dexamethasone. Rather it tends to point out an association between a hyperactivity of the H.P.A. axis and a high excretion of urinary M.H.P.G. A number of factors may explain the difficulties in clarifying the links between the escape to D.S.T and abnormal brain NA metabolism as evidenced by peripheral biological measures.

Type
Research Article
Copyright
Copyright © European Psychiatric Association 1986

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