Hostname: page-component-78c5997874-dh8gc Total loading time: 0 Render date: 2024-11-10T14:05:21.588Z Has data issue: false hasContentIssue false

De regulatie van de hypothalamus-hypofyse-bijnier-as in de pathogenese van depressieve stoornissen

Published online by Cambridge University Press:  16 January 2019

Samenvatting

De dexamethason-corticotrofin-releasing-hormoon (DEX-CRH)-test is de meest gevoelige test voor veranderingen in de regulatie van de hypothalamus-hypofyse-bijnier-as bij stemmingsstoornissen. Zowel in de premorbide toestand als tijdens de acute episoden van stemmingsstoornissen komt onder deze conditie een verhoogde cortisolreactie voor. Een irreversibele lage GAHA-concentratie kan aan dit regulatietekort een bijdrage leveren. Verhoogde noradrenerge en vasopressinerge activiteiten kunnen in de overgang naar hogere DEX-CRH-reacties tijdens de acute episode een rol spelen. De dexamethason-suppressie-test verschilt van de DEX-CRH-test door de afwezigheid van een externe CRH-belasting en ‘early escape’ in deze test is op specifieke wijze geassocieerd met het melancholische subsyndroom. Dit suggereert dat een endogeen verhoogde CRH-activiteit bij de overgang naar deze subcategorie is betrokken. Verhoogde CRH-activiteit is aangetoond en toenames van noradrenerge activiteit en 5-HT2a-receptoren en afnames van glucocorticoïd-receptor-functie, tryptofaan-concentratie en serotonine-afgifte kunnen een bijdrage leveren. De uiteindelijk resulterende hoge cortisol-concentraties lijken de ontwikkeling te kunnen bevorderen van een resttoestand met ‘early escape’ na herstel.

Summary

Summary

The dexamethasone-corticotrophin-releasing-honnone (DEX-CRH) test is the most sensitive lest to detect dysregulations of the hypothalamic-pituitary-adrenal axis. An enhanced cortisol release has been found in both the premorhid stage as in most acute episodes of mood disorders. An irreversibly low GABA concentration may be involved in the DEX-CRH response in the premorbid stage of a subgroup of unipolar and bipolar disorders. Increased noradrenaline and vasopressin concentrations may play a role in the change to higher DEX-CRH responses in acute episodes. The dexamethasone-suppression-test differs from the DEX-CRH-test by the absence of exogenous CRH, and early escape in this condition is specifically associated with the melancholic subtype. This means that an increased endogenous CRH-activity is involved in the change to this subcategory. Increased CRH-activity has been demonstrated and increased noradrenergic activity and upregulated 5-HT2a receptors as well as a decreased glucocorticoid receptor function, reduced tryptophan concentration and serotonin release may be involved. The eventually resulting increases in cortisol concentration seem to be involved in the development of a residual condition with early escape.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1998

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Literatuur

1. Holsboer, F, Lauer, ChJ, Schreiber, W, et al. Altered hypothalamic-pituitary-adrenocortical regulation in healthy subjects at high familial risk for affective disorders. Neuroendocrinology 1995:62: 340-7.Google Scholar
4. Ribeiro, S, Tandon, R, Grunhaus, L, et al. The DST as a predictor of outcome in depression: A Meta-Analysis. Am J Psychiat 1993; 150: 1618–29.Google Scholar
5. Thompson, L, Rubin, RT, McCracken, JT. Neuroendocrine aspects of primary endogenous depression: Receiver operating characteristic and kappa analyses of serum and urine cortisol measures in patients and matched controls. Psychoneuroendocrinol 1992; 17: 507–15Google Scholar
9. Holsboer, F, Barden, N. Antidepressants and hypothalamic-pituitary-adrenocortical regulation. Endocrine Rev 1996; 17: 187205.Google Scholar
11. Von Bardeleben, U, Holsboer, F, Stalla, GK, et al. Combined administration of human corlicolropin-releasing factor and lysine vasopressin induces cortisol escape from dexamethasone suppression in healthy volunteers. Life Sci 1985; 37: 1613–8Google Scholar
12. Sapolsky, RM, Plotzky, PM. Hypercortisolism and its possible neural bases. Biol Psychiat 1990; 27: 937–52.Google Scholar
14. Petty, F, Kramer, GL, Fulton, M, et al. Stability of plasma GABA at four year follow-up in patients with a primary unipolar depression. Biol Psychiat 1995; 37: 806–10.Google Scholar
18. Altamura, CA, Mauri, MC, Perrera, A, et al. Plasma and platelet excitatory amino acids in psychiatric disorders. Am J Psychiat 1993; 150: 1731–3.Google Scholar
19. Roy, A, Pickar, D, De Jong, J, et al. Norepinephrine and its metabolites in cerebrospinal fluid, plasma and urine. Relationship to hypothalamo-pituitary-adrenal-axis function in depression. Arch gen Psychiat 1988; 45: 849–57.Google Scholar
21. Schatzberg, AF, SAmson, JA, Bloomingdale, KL, et al. Toward a biochemical classification of depressive disorders. Arch gen Psychiat 1089; 46: 2608.Google Scholar
22. Asnis, GM, Sanderson, WC, Van Praag, HM. Cortisol response to intramuscular desipramine in patients with a major depression and normal control subjects: a replication study. Psychial Res 1992; 44: 237–50.Google Scholar
23. Trestman, RL, Coccaro, EF, Mitropoulou, V, et al. The cortisol response to clonidine in acute and remitted depressed men. Biol Psychiat 1993; 34: 3739.Google Scholar
28. Leseh, KP, Mayer, S, Disselkamp-Tietze, , et al. 5-HTla receptor responsivity in unipolar depression: evaluation of ipsapirone-induced ACTH and cortisol secretion in depressed patients. Biol Psychiat 1990; 28: 6208.Google Scholar
31. Anand, A, Charney, DS, Delgado, PL, et al. Neuroendocrine and behavioral responses to intravenous m-chlorophenylpiperazine (mCPP) in depressed and healthy comparison subjects. Am J Psychiat 1994; 151: 1626–30.Google Scholar
33. Yates, M, Leake, A, Candy, JM, et al. 5HT2 receptor changes in major depression. Biol Psychiat 1990; 27; 489-96.Google Scholar
34. Hrinda, PD, Demeter, E, Vu, TB, et al. 5-HT2 receptors in brain of suïcide victims/depressives: increase in 5-HT2 sites in cortex and amygdala. Brain Res 1993; 614: 3744.Google Scholar
38. Meltzer, HY, Maes, M. Effect of pindolol on the L-5-HTP-induced increase in plasma prolactin and cortisol concentrations in man. Psychopaharmacol 1994; 114: 635–43.Google Scholar
39. O'Keane, V, Dinan, TG. Prolactin and cortisol responses to d-fenfluramine in major depression: Evidence for diminished responsivity of central serotonergic function. Am J Psychiat 1991; 148: 1009–15.Google Scholar
40. Mann, JJ, Malone, KM, Diehl, DJ, et al. Demonstration in vivo of reduced serotonin responsivity in the brain of untreated depressed patients. Am J Psychiat 1996; 153: 174–82.Google Scholar
45. Maes, M, Minner, B, Suy, E. The relationship between the availability of L-tryptophan to the brain, the spontaneous HPA-axis activity and the responses to dexamethasone in depressed patients. Amino Acids 1991; 1: 5765.Google Scholar
51. Young, EA, Haskelt, RG, Grunhaus, L, et al. Increased evening activation of the hypothalamie-piluitary-adreual axis in depressed patients. Arch gen Psychiat 1994; 51: 7017.Google Scholar
56. Wodarz, N, Rupprecht, R, Kornhuber, J, et al. Cell-mediated immunity and its glucocorticoid-sensitivity after clinical recovery from severe major depressive disorder. J affect Disord 1992; 25: 318.Google Scholar
60. Van, Louden, Kerkhof, GA, Van den Berg, F, et al. Plasma arginine-vasopressin and motor activity in major depression. Biol Psychiat (in druk)Google Scholar
61. Van Louden, L, Goekoop, JG, Van Kempen, GMJ, et al. Plasma levels of arginine-vasopressin elevated in patients with major depression. Neuropsyehopharmaeol 1997; 17: 283–92.Google Scholar
66. Joyce, PR, Mulder, RT, Cloninger, CR. Temperament and hypereortisolemia. Am J Psychiat 1994; 151: 1958.Google Scholar