Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old man with depression, Cushingoid features and hypogonadism was found to have simultaneous pituitary-dependent Cushing's disease and marked elevation of serum prolactin (PRL). CT-scan revealed a macroadenoma with suprasellar extension. Transphenoidal surgery cured the patient's Cushing's disease, but failed to correct his hyperprolactinemia, which was controlled by subsequent bromocriptine therapy. Immunostaining of the pituitary tumor was positive for PRL as well as for ACTH, and ACTH-related peptides beta-lipotropin and beta-endorphin in two distinct tumor cell lines. This pituitary tumor is one of the few mixed PRL- and ACTH-secreting tumors documented by immunostaining. It is the second reported in a macroadenoma, in which PRL-secreting tumoral cells are much more abundant than ACTH-secreting cells.
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PMID:Cushing's disease and hyperprolactinemia due to a mixed ACTH- and prolactin-secreting pituitary macroadenoma. 165 8

The cardiovascular and metabolic responses to treatment with ACTH(1-24) were investigated in a porcine model of septicaemia. Sixteen anaesthetised, instrumented animals were infused with live Escherichia coli over 2 hr. During the first hour of the infusion, significant reductions in cardiac index, mean arterial pressure, and pH were observed together with a significant increase in mixed venous blood lactate concentrations and packed cell volumes. ACTH(1-24) 160 micrograms kg-1, given 1 hr after starting the E. coli infusion (n = 8), had no significant effect on these haemodynamic or metabolic measurements when compared with the control group (n = 8). These results do not support the suggestion that intravenous ACTH(1-24) reverses cardiovascular depression in septicaemic shock.
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PMID:Lack of effect of ACTH in porcine Escherichia coli septic shock. 166 41

A 7-day infusion with neurotensin (NT) (10 micrograms.kg-1.day-1) stimulated adrenal growth in intact female rats, and raised ACTH blood concentration, without altering corticosterone (B) plasma level and output by adrenal homogenates. For a week dexamethasone (Dx) administration (125 micrograms.kg-1.day-1) caused a notable adrenal atrophy, a marked lowering of ACTH and B blood concentrations, and a profound depression of B output by adrenal homogenates. NT infusion reversed Dx-induced adrenal atrophy and plasma ACTH-level drop, but not the impairment in adrenal-cortex secretory activity. In vitro studies showed that NT (10(-6) mol/l) significantly reduced basal, but not ACTH-stimulated B release by isolated rat inner adrenocortical cells. These findings suggest that NT exerts a direct inhibitory effect on B production by rat adrenals, while it is able to enhance ACTH secretion and consequently adrenal growth. Moreover, they indicate that NT evokes a striking, and at present unexplained dissociation between structure and function in the adrenal cortex of Dx-suppressed rats.
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PMID:Effects of neurotensin on the pituitary-adrenocortical axis of intact and dexamethasone-suppressed rats. 166 3

Twenty-six institutionalized elderly subjects, selected as healthy according to the SENIEUR protocol, were compared to adult controls to establish correlations between affective disorders and immune abnormalities and to investigate underlying neuroendocrine mechanisms. After an extensive psychodiagnostic examination, 35% of the aged subjects were classified as depressed. Cutaneous delayed hypersensitivity tests showed reduced responses in the aged, but no correlation was found with the psychological status. Examination of the peripheral blood lymphocyte subsets revealed no imbalance in the percentages of CD3+, CD4+, CD8+ cells in the aged. A slight reduction in the CD4+/CD8+ cell ratio could however be detected in the non-depressed aged, as compared to adult controls. The CD4+/CD45R+ cell subset was reduced in non-depressed aged. The percentage of B lymphocytes was reduced in the aged, mostly in the non-depressed subjects. No changes were detected in the percent of OKDR+ cells. The percentage of CD16+ cells was found unchanged, while that of Leu7+ cells was significantly higher in the aged than in the adults and in the non-depressed than in the depressed aged. Leu7+ cell levels were negatively correlated with the depression score. On double labelling, the percent of CD16+/Leu7+ cells appears increased in the subgroup of depressed aged and positively correlated with age. Plasmatic and urinary cortisol levels were both positively correlated with depression score. Urinary cortisol level was higher in the depressed aged. These parameters, as well as plasmatic ACTH, beta-endorphin and urinary catecholamines, were not correlated with immune responses. Based on these findings, we recommend that the neuroendocrinological conditions should be taken into account when healthy subjects are examined in studies of immune senescence.
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PMID:Immune parameters in a population of institutionalized elderly subjects: influence of depressive disorders and endocrinological correlations. 174 60

Stress can be defined as a "reaction by living beings to any relevant impairment". The effect of anaesthesia on endocrine function is closely related to the actual stress concept based on the works by Cannon and Selye. Cannon described the role of catecholamines in stress and characterised the fight-flight reaction. Selye emphasised the role of the adrenocortical reaction defining the "general adaptation syndrome", which evolves in three stages ("alarm reaction", "stage of resistance", "stage of exhaustion"). Later, Henry postulated the dual stress concept. The sympathetic-adrenomedullary system is activated during the fight-flight reaction, thus representing an active role of the organism. The pituitary-adrenocortical system is activated during loss of control, submission and depression, especially in a social context. Main valid parameters of this endocrine stress response are adrenaline, noradrenaline, ADH, ACTH and cortisol. In the perioperative period, both pathways are "stressed". The most important factors are patient, operation, and anaesthesia. Anaesthesia can influence the stress response by afferent blockade (local anaesthesia), central modulation (general anaesthesia) or peripheral interactions with the endocrine system (etomidate). Up to now, a total peripheral blockade of the nociceptive system is impossible, due to surgical technique (destruction of nerve fibres) and release of mediator substances. With regard to reduction of endocrine stress response, inhalation anaesthesia with volatile anaesthetics and nitrous oxide may be less effective than neuroleptic, spinal or epidural anaesthesia. Immediately after extubation, rapid increases of endocrine parameters are observed. In addition to central modulation of pain and stress, both halothane and enflurane inhibit catecholamine release from the adrenal medulla. Neuroleptic anaesthesia and total intravenous anaesthesia are very potent and sufficient to control the increases in endocrine parameters even during major surgery, due to their central effects. Spinal and epidural anaesthesia alone as well as in combination with general anaesthesia can reduce the endocrine stress response more than necessary. This is due to the sympathetic blockade, combined with an afferent blockade of central cord fibers which modulate the pituitary-adrenocortical system. Only few data are available concerning the stress response during infiltration anaesthesia or nerve block, but additional sedation seems to be beneficial. Peripheral interactions with the endocrine system like blockade of the adrenal cortex by etomidate is dangerous and has caused a high mortality in intensive-care patients if the substance was admitted for a longer period. Assessment of endocrine stress response in anaesthesia and surgery is controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The endocrine stress reaction in anesthesia and surgery--origin and significance]. 175 50

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.
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PMID:Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression. 181 84

Sleep EEG and neuroendocrine disturbances have been described in the acute phase of affective illness. The question arises as to whether these biological marker disturbances are state- or trait-related. This important issue can be addressed by evaluating changes in sleep EEG and neuroendocrine parameters from a chronobiological approach before and after antidepressant treatment. Among the circadian variables explored in affectively ill patients are REM sleep and slow wave sleep, as well as circadian secretion of plasma GH, cortisol, ACTH and prolactin. Our studies show that depressed patients mainly of the unipolar type secrete more GH and cortisol during the circadian period than control subjects do. GH hypersecretion appears mainly during wakefulness while cortisol hypersecretion is observed during the 24 h space. Temporal disorganization of hormonal secretion is also present since an advance of the quiescent period of the ACTH-cortisol rhythm as well as pre-sleep GH spikes were described in our depressed unipolar patients before treatment. After antidepressive treatment, these chronobiological anomalies tend to normalize, as state biological markers. These observations are giving support to the phase-advance hypothesis of depression.
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PMID:Sleep-related chronobiological markers of affective illness. 184 28

In seventy-two patients affected by hyperphagic obesity and forty age-matched, normal weight volunteers we performed a psychological assessment, through various mental tests, and evaluated the beta-endorphin (B-Ep), ACTH and cortisol circulating levels, in basal condition and following an overnight short dexamethasone suppression test (DST). The hormones were measured by radioimmunoassay either directly in the serum (cortisol) and the plasma (ACTH), or after affinity gel column chromatography (B-Ep). In obese subjects B-Ep levels in basal conditions were four times greater than in normal weight controls and showed significantly less reduction after DST. ACTH and cortisol levels, in contrast, were in the normal range and were suppressed following dexamethasone as was also true in the control group. Psychological evaluation on M.M.P.I. (Minnesota Multiphasic Personality Inventory) revealed a trend toward hypochondria, depression, hysterias, psychoasthenia and schizophrenia. However, no significant correlation has been found between M.M.P.I. clinical scale scores and circulating levels of B-Ep and cortisol either in basal conditions or after DST. In conclusion, these data do not support the hypothesis that abnormalities of the hypothalamus-pituitary-adrenal axis in hyperphagic obesity are related to affective disorders.
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PMID:Hyperendorphinemia in obesity is not related to the affective state. 196 3

Hypersecretion of cortisol is associated with depression. Because corticosterone may show greater responsiveness than cortisol to exogenous ACTH in depression and it has behavioural effects in rodents, we determined whether depression is also associated with hypersecretion of corticosterone. Both cortisol and corticosterone were significantly elevated in depression, with greatest differences from control subjects during the afternoon and evening. The ratio of corticosterone/cortisol was constant and similar throughout the day in both depressed patients and controls. We conclude that there is no disproportionate endogenous hypersecretion of corticosterone in depression.
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PMID:Diurnal variation of plasma corticosterone in depression. 196 3

There is current controversy over the mechanisms underlying hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in depression. Pro-gamma-MSH, a portion of the N-terminal region of POMC, has been shown to act synergistically with ACTH in stimulating corticosteroid secretion in vitro and in vivo. Pro-gamma-MSH and ACTH plasma levels were measured in 30 drug-free male patients with a DSM-III-R major depressive disorder and 21 healthy controls. The baseline levels were similar in the two groups. After single-dose metyrapone stimulation, both hormones increased, but pro-gamma-MSH was significantly higher in control subjects than in depressives. After overnight 1 mg dexamethasone, ACTH was significantly less suppressed in depressives than controls. These results suggest that HPA axis dysregulation in depression may involve peptides other than ACTH and be more complex than previously reported.
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PMID:Effects of metyrapone and dexamethasone on pro-gamma-MSH and ACTH levels in depressed patients. 196 19


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