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)

Twenty patients with fibromyalgia syndrome and 20 patients with rheumatoid arthritis (RA) were assessed as outpatients over a 3 day period with respect to peak and trough levels of plasma cortisol, growth hormone, prolactin, ACTH and thyroid stimulating hormone. Patients with fibromyalgia syndrome had loss of diurnal variation in plasma cortisol (trough levels 347.3 +/- 254.7 vs 232.8 +/- 70.0 nmol/l, p less than 0.001) compared with RA patients. Thirty-five percent (7/20) of patients with fibromyalgia syndrome and only 5 percent (1/20) of those with RA exhibited abnormal dexamethasone suppression tests (p less than 0.001). No differences were noted in the diurnal variation of other hormones tested. Beck Depression Inventory scores were similar in both groups and no patient exhibited clinical evidence of depression. These data suggest alteration in the pituitary hypothalamic axis with respect to cortisol secretion in fibromyalgia syndrome, perhaps as a consequence of chronic pain.
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PMID:Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. 260 9

Four hypotheses have been proposed to explain why nonsuppression on the dexamethasone suppression test occurs in patients with major depression. These include 1) increased metabolism of dexamethasone, 2) decreased sensitivity of pituitary glucocorticoid receptors to dexamethasone, 3) hyperresponsivity of the adrenal gland to ACTH stimulation, and 4) increased central drive of the pituitary from hypothalamic/limbic structures that overrides the action of the dexamethasone. A critical review of the literature suggests that the last hypothesis is most closely supported by the data. Despite this conclusion, factors other than depression may be involved in hypothalamic-pituitary-adrenal axis dysfunction.
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PMID:Pathophysiology of HPA axis abnormalities in patients with major depression: an update. 264 93

Considerable research over the past 20 years has documented alterations in the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenal (HPA) axes in patients with affective disorders, especially depression. Although plasma concentrations of thyroid hormones (T3, T4) are generally unaltered in patients with major depression, plasma thyroid stimulating hormone (TSH) responses after intravenous administration of thyrotropin-releasing hormone (TRH) are blunted in approximately 25% and abnormally elevated in approximately 15% of depressed patients. Data are presented supporting the hypothesis that TSH blunting may be secondary to central nervous system (CNS) hypersecretion of TRH, and that the enhanced TSH response may be secondary to subclinical hypothyroidism associated with autoimmune thyroiditis. The HPA axis has received considerable scrutiny in depressed patients and there is universal agreement that 50% to 75% of patients with major depression exhibit hyperactivity of the HPA axis characterized by hypercortisolemia, ACTH hypersecretion, and nonsuppression of plasma cortisol concentrations after administration of the synthetic glucocorticoid dexamethasone. Evidence is presented that hypersecretion of corticotropin-releasing factor (CRF) contributes, at least in part, to HPA axis hyperactivity and perhaps to certain of the signs and symptoms of major depression.
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PMID:Clinical significance of psychoneuroendocrinology in psychiatry: focus on the thyroid and adrenal. 265 28

Cortisol and hypophyseal hormones contents were measured in the blood serum of circular, schizophrenic and psychogenic depressed patients during pharmacotherapy. Distinct nosological differences in hypophyseal hormone secretion were noted. The increase in blood serum levels of ACTH, prolactin and somatotropic hormones were obligatory stages of the positive therapeutic effect in circular depressions. The ACTH and prolactin decrease was characteristic of schizophrenic depression. The cortisol level decreased in any depression with positive therapeutic effect.
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PMID:[Changes in hormonal indicators during the treatment of depression of different types]. 275 Mar 67

Plasma ACTH and serum cortisol levels were measured at 20-min intervals for 24 h in six young women with unipolar endogenous depression and in eight normal women during the early follicular phase of the menstrual cycle. The women with depression had a marked increase (P less than 0.005) in mean ACTH pulse frequency [14.5 +/- 0.6 (+/-SE) pulses/24 h] compared with normal women (9.9 +/- 0.7 pulses/24 h), while mean ACTH pulse amplitude and 24-h transverse mean ACTH levels were similar in the two groups. In contrast, 24-h transverse mean cortisol levels were higher (P less than 0.02) in the depressed women (242 +/- 28 nmol/L) than in the normal women (163 +/- 10 nmol/L). This hypercortisolemia in the depressed women was accompanied by markedly increased (P less than 0.001) episodic cortisol secretion (286 +/- 24 X 10(2) nmol/L X min) compared with that in normal women (155 +/- 17 X 10(2) nmol/L X min), and the secretory episodes were both longer in duration (P less than 0.05) and of higher amplitude (P less than 0.05) in the depressed women. The circadian variations in ACTH and cortisol were maintained in these depressed women, and the times of the circadian nadir, as determined by cosinor analysis, were similar to those in the normal women. However, the mean length of the evening quiescent period of cortisol secretion was far shorter (P less than 0.005) in the depressed women (27 +/- 8 vs. 202 +/- 40 min). Moreover, the postlunch rise in serum cortisol was significantly higher (P less than 0.02) in the depressed women (204 +/- 29 vs. 111 +/- 15 nmol/L). These results provide evidence that the hypercortisolism in depressed women is associated with an increase in ACTH pulse frequency, expanded cortisol secretory episodes, including a greater postlunch rise in cortisol, and a shortened evening quiescent period of cortisol secretion. Our findings provide evidence for centrally mediated activation of the ACTH-cortisol system in women with depression without a phase shift in circadian rhythm.
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PMID:Pulsatile rhythms of adrenocorticotropin (ACTH) and cortisol in women with endogenous depression: evidence for increased ACTH pulse frequency. 282 56

The ACTH response to arginine vasopressin was the same in patients with depression while cortisol response was significantly greater in patients with depression when compared to the control population. These findings are consistent with the hypothesis that vasopressin corticotroph receptors are not downregulated in depression and that there is increased adrenal responsiveness in patients with depression to endogenous ACTH.
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PMID:Stimulation of the pituitary-adrenal axis with arginine vasopressin in patients with depression. 282 65

Plasma concentrations of ACTH and prolactin were measured in psychiatric inpatients at 8 a.m. and 4 p.m. before and after the standard 1 mg overnight Dexamethasone Suppression Test (DST). Plasma concentrations of cortisol were measured at 8 a.m. and 4 p.m., and 11 p.m. before and after 1 mg dexamethasone. Dexamethasone suppressed plasma concentrations of ACTH, prolactin and cortisol in the subject group as a whole. "Cut Points" obtained using Fisher's Exact Test identified plasma ACTH values at 8 a.m. baseline, 4 p.m. baseline and 8 a.m. post-dexamethasone and plasma prolactin values at all four times that significantly differentiated patients with bipolar depressive disorder and major depressive disorder from other psychiatric patients. There were no cut points found at any of the six times for plasma levels of cortisol that significantly differentiated between these two diagnostic groups. Of interest in this subject population, basal (pre-dexamethasone) plasma concentrations were of more diagnostic information than post-dexamethasone values. These pilot findings suggest that monitoring plasma prolactin and ACTH concentrations before and after dexamethasone might increase the sensitivity and specificity of this laboratory test for depression.
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PMID:Measurement of ACTH and prolactin in the dexamethasone suppression test. 282 9

The authors present a critical overview of the multiple and contradictory studies of cortisol production in depressed patients. Some notions of physiology are first recalled. A main part of the review discusses the dexamethasone suppression test, but studies of the cortisol secretion profile and of other dynamic tests are also presented. One can describe in depressed people: cortisol overproduction, an impaired negative feedback mechanism, an adrenocortical hyperreactivity to ACTH and a phase advance in the circadian rhythm of cortisol secretion. These anomalies are more frequently encountered in patients exhibiting severe depressions of the endogenomorphic type. However, none of them can be considered as a biological marker of depression, nor as a marker for a particular type of depression. The relation between endocrine disturbances and the clinical parameters of depression is still controversial.
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PMID:[Cortisol secretion in depressed patients. Review of the literature]. 283 59

A substantial body of data suggests that excessive cortisol secretion in depression may result from a dysregulation at several sites within the hypothalamic-pituitary-adrenocortical (HPA) axis. These alterations in regulatory mechanisms are thought to be the result of a hypothalamic 'overdrive' of corticotropin-releasing hormone (CRH). Previous studies have demonstrated a diminished adrenocorticotropin (ACTH) secretory response, as well as a heightened adrenocortical responsiveness after ovine-CRH administration in depressed patients. In the present investigation, we examined pituitary and adrenocortical responsiveness after an ovine-CRH stimulation test before and during clinical recovery in seven depressed patients. Cumulative ACTH responses increased significantly during clinical recovery (P = 0.014). Paradoxically, maximum and peak cortisol responses increased after recovery, suggesting that heightened adrenocortical responsiveness to ACTH during depression may take longer to 'normalize' than abnormal pituitary responsiveness to ovine-CRH stimulation.
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PMID:The oCRH stimulation test before and after clinical recovery from depression. 283 38

To explore the integrity of the hypothalamic-pituitary-adrenal (HPA) system in major depressive disorder, 12 patients and normal controls matched for sex, age, and body weight received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Compared to controls, depressed patients showed an elevation in baseline cortisol and a significant attenuation of net adrenocorticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. These abnormalities in HPA axis function and apparent discordances in the interrelationships of ACTH and cortisol baseline and net stimulation responses between depressed patients and normal controls indicate, at least in part, a derangement of the glucocorticoid-dependent negative feedback circuitry and support the hypothesis that HPA hyperactivity in depression involves neurotransmitter-mediated hypothalamic hypersecretion of CRH.
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PMID:Corticotropin and cortisol response to human CRH as a probe for HPA system integrity in major depressive disorder. 283 59


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