Circadian Rhythm of Plasma 11-Hydroxycorticosteroids in Psychiatric Disorders

Conroy, R. T. W. L.; Hughes, Bronwen; Mills, J. N.

doi:10.1136/bmj.3.5615.405

Cited by 18 publications

(8 citation statements)

References 18 publications

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“…The participation of calcitonin cannot be ruled out because acute treatment decreased calcitonin levels in rats [Komoda et al" 1987], although the scrum levels have not been determined in this study. Hypersecretion of glu cocorticoid seems less possible because acute and chronic treatment with neuroleptics does not affect the serum glu cocorticoid levels both in patients [Conroy et al, 1968] and in rats [Komoda et al, 1987], It is suggested that antiepileptic drugs accelerate the breakdown of vitamin D by liver enzyme induction [Stamp et al, 1976]. The differences of abnormal find ings between patients treated with neuroleptics and those with antiepileptic drugs are that the latter demon strated reduced serum Ca and P levels and raised ALP activity, while the former showed increased urinary Ca levels and reduced ALP activity.…”

Section: Discussionmentioning

confidence: 99%

Certain Neuroleptics Reduce Bone Mineralization in Schizophrenic Patients

Higuchi

Komoda²,

Sugishita³

et al. 1987

Neuropsychobiology

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A significant increase of urinary Ca and hydroxyproline levels and a decrease of urinary alkaline phosphatase activity were found in 12 schizophrenic patients receiving certain neuroleptic drugs. In these patients, the levels of active metabolites of vitamin D3 were decreased, while the levels of midmolecule parathyroid hormone were within the normal range, except for 2 cases. These results suggest that certain neuroleptics induce the increased urinary Ca excretion through suppression of active vitamin D₃ formation and that chronic treatment with certain neuroleptics may induce abnormal bone mineralization.

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Section: Discussionmentioning

confidence: 99%

Certain Neuroleptics Reduce Bone Mineralization in Schizophrenic Patients

Higuchi

Komoda²,

Sugishita³

et al. 1987

Neuropsychobiology

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“…It has since been reported (Butler and Besser, 1968;Conroy et al, 1968) that levels of plasma cortisol at midnight are higher in depressed patients than in normal subjects. Both these abnormalities are reversible.…”

Section: Acth Feedback Controlmentioning

confidence: 99%

Clinical Research in Depression

Carroll¹

1968

Aust N Z J Psychiatry

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reflect changes in the body as a whole and not just in the brain. Moreover, urinary levels of noradrenaline and normetanephrine, the product formed from noradrenaline by catechol-0-methyltransferase, are in very small part derived from brain metabolism as the blood-brain barrier is not permeable to hydroxylated amines. Schildkraut? and his associates found that urinary levels of normetanephrine were increased in patients with mania or cyclic manicdepressive psychosis and were also increased in patients in whom imipramine was an effective antidepressant whereas urinary levels of vanillylmandelic acid ( V M A ) were decreased. Normetanephrine is regarded as the breakdown product of noradrenaline which is thought to reflect chiefly extracellular metabolism whereas V M A levels reflect intracellular deamination. The fact that imipramine blocks the reuptake of noradrenaline is in accord with these findings. However the source of the noradrenaline could be from autonomic adrenergic neurones rather than from the central nervous system. In this case, the observations would have more relevance to sideeffects than to the desired effect of imipramine.The metabolism of indoleamines in depression has been studied by Coppen and his associates6. They found that urinary excretion of tryptamine and its metabolic product indoleacetic acid was decreased during depression and increased upon recovery with treatment. Here, as in studies with catecholamine metabolites, interpretation is difficult for similar reasons, namely that urinary changes may not reflect brain changes especially as indoleamines and their metabolites are not freely transported across the blood-brain barrier.While much of this evidence for the role of biogenic amines seems to fit into a satisfactory pattern, Dewhurst has criticized the methodology of the clinical and laboratory studies*. He put forward an alternative theory of cerebral amine action based on studies of the behavioural effects of sixty amines and related compounds in various species and proposed that amines can be divided according to their cerebral actions into two distinct and opposing categories: type A (excitant) and type C (depressant). The determinant of type of action is lipid solubility, type A amines (substituted ethylamines) being both lipophilic and hydrophilic, and type C amines (substituted ethanolamines) being hydrophilic only. Other variations in the chemical structure affect potency and duration of action but not type of action. Naturally occurring amines of type A are tryptamine and B-phenylethylamine. The excitant action of type A amines is specifically antagonized by methysergide, and this drug is reported to be of use in the treatment of manian. Naturally occurring type C amines are noradrenaline and adrenaline. S-hydroxytryptamine has a biphasic (excitant then depressant) action and is classed as type B. Dewhurst's conclusions have obvious points of difference from the catecholamine theory, but he is examining the role of monoarnines in cerebral function from a different standpo...

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“…Generally, 1 mg dexamethasone was given at 11 p.m. to patients and cortisol concentrations in plasma during the next day were compared to those measured in matched normal controls. Through such protocols, the known overproduction of cortisol during major depressive episodes (Doig et al 1966;Conroy et al 1968;Fullerton et al 1968) has been confirmed in subgroups of patients.Circadian rhythms of cortisol sercretion might be abnormal, i.e. phase-advanced by a few hours, during major depressive episodes (Jarrett et al 1983;Sachar et al 1973), though other authors did not confirm this observation (Claustat et al 1984).…”

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confidence: 99%

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Influence of the time of administration of dexamethasone 0.25 MG on cortisol secretion in normal humans

Schulz¹,

Costa²,

Widmer³

et al. 1986

Psychopharmacology

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Single low doses (0.25 mg) of dexamethasone were given at 11 p.m., 2, 5 and 8 a.m. on separate days to five normal subjects. The concentrations of cortisol in plasma on the next day were significantly decreased compared to results after placebo administration, and cortisol suppression was maximal after dexamethasone had been given at 8 a.m. Our findings suggests that the postulated phase-advance of circadian rhythms is not a major cause of cortisol non-suppression in depressives given dexamethasone.The utility of the dexamethasone suppression test (DST) in psychiatry has been the subject of numerous studies. Generally, 1 mg dexamethasone was given at 11 p.m. to patients and cortisol concentrations in plasma during the next day were compared to those measured in matched normal controls. Through such protocols, the known overproduction of cortisol during major depressive episodes (Doig et al. 1966;Conroy et al. 1968;Fullerton et al. 1968) has been confirmed in subgroups of patients.Circadian rhythms of cortisol sercretion might be abnormal, i.e. phase-advanced by a few hours, during major depressive episodes (Jarrett et al. 1983;Sachar et al. 1973), though other authors did not confirm this observation (Claustat et al. 1984). If there exists a phase-advance of cortisol rhythms in depressives, then one could conclude that administering dexamethasone at 11 p.m. to depressives would correspond to giving the drug between 1 and 3 a.m. to normal subjects. We therefore studied the influence on cortisol secretion of the time of dexamethasone administration in normal subjects, to establish whether chronobiological changes in the sensitivity of the hypothalamic-pituitaryadrenal axis (HHAA) might lead to a false positive nonsuppression. Materials and methodsSeven normal subjects of 25-38 years of age participated. The study was conducted in May and June. A pilot study in two subjects revealed complete suppression after 1 mg dexamethasone (Millicortene R, Ciba) given at 2 or 5 a.m.Offprint requests to: P. Schulz (with the exception of the 8 a.m. samples drawn after the 5 a.m. administration). Partial suppression was obtained after 0.25 mg given at 11 p.m. or 3 a.m. to the same two subjects. Therefore, 0.25 mg dexamethasone was administered orally to the other five subjects, at 11 p.m., 2 a.m., 5 a.m. and 8 a.m., using a cross-over latin square design. An identical placebo was administered once at 11 p.m. Each drug or placebo administration was separated by at least 5 days. According to Yerevanian et al. (1985), weekly administration of dexamethasone to normal subjects does not lead to false positive non-suppression. Venous blood samples were drawn through an indwelling catheter (BectonDickinson), using no heparin, every 2 h from 8 a.m. to 8 p.m. after dexamethasone and plasma was stored at -20 ° C pending analysis. The concentration of cortisol in plasma was measured using a commercial kit (Bio-M6rieux) based on the competition for transcortin. There was an excellent concordance between cortisolaemia measured with this assay a...

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Circadian Rhythm of Plasma 11-Hydroxycorticosteroids in Psychiatric Disorders

Cited by 18 publications

References 18 publications

Certain Neuroleptics Reduce Bone Mineralization in Schizophrenic Patients

Certain Neuroleptics Reduce Bone Mineralization in Schizophrenic Patients

Clinical Research in Depression

Influence of the time of administration of dexamethasone 0.25 MG on cortisol secretion in normal humans

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