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)

Urinary androgen fractions, with other parameters of adrenal function, were assessed in renal transplant patients on long-term alternate-day steroid therapy. Urinary 17-ketosteroids and plasma cortisol values were low normal or slightly reduced in female patients and normal in male patients. In female patients the following urinary androgen fractions were depressed to less than the normal range: androsterone, dehydroepiandrosterone, etiocholanolone and 11-ketoetiocholanolone; 11-hydroxyetiocholanolone was not detectable. In male patients dehydroepiandrosterone and 11-ketoetiocholanolone were depressed to less than the normal range. Adrenal scan using 131I-19-cholesterol failed to image the adrenal glands in 5 of 7 patients studied, confirming the lack of an adrenocorticotropic hormone effect, with corresponding depression of the hypothalamic-pituitary-adrenal axis. These studies demonstrate the value of fractionating urinary 17-ketosteroids in assessing adrenal reserve and are a more sensitive index of adrenal suppression than the total 17-ketosteroids alone.
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PMID:The effects of long-term alternate-day steroids on parameters of adrenal function in renal transplant patients. 77 34

We evaluated potential pituitary-adrenal influences on postoperative reticuloendothelial (RE) function. Male dogs, 13 to 18 kg (28.6 to 39.6 lb), were used and the operative procedure was hemicolectomy. The RE function was evaluated by a colloid clearance technique and circulating opsonin levels were quantified by bioassay. Normal animals manifested RE depression three hours following incision (49 percent decline in the global phagocytic index K and an associated 30 percent decline in the circulating opsonic activity). Dexamethasone sodium phosphate pretreatment over a three-day preoperative period prevented the postoperative RE clearance failure (control K = 0.69; postoperative k = 0.79) however, a slight (18 percent) but not significant decrease in opsonic activity occurred. Cortisone acetate or adrenocorticotropic hormone over a wide-dosage range manifested no depressing effect on in vitro phagocytosis. These studies, in conjunction with our previous findings of Kupffer cell activation following adrenalectomy, as well as the demonstration of opsonin depletion and RE phagocytic depression following surgery in the absence of the adrenal glands suggest that the pituitary-adrenal system modulates postoperative RE phagocytosis.
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PMID:Hepatic reticuloendothelial host defense failure following surgical trauma. 116 88

Graded doses arginine-vasopressin (AVP) were administered to depressed patients and control subjects to compare the sensitivity of the pituitary-adrenal system of these subjects for this compound. The plasma levels of cortisol, adrenocorticotropic hormone (ACTH) and beta-endorphin were measured before and after intravenous AVP injection. The hormonal output was taken as a measure of pituitary-adrenal function. In control subjects 3 doses AVP and placebo were used, whereas in patients two doses AVP, a low and a high dose, and placebo were tested. All tests were carried out in the afternoon when the pituitary-adrenal system is stable and more susceptible for stimulation. Patients were subdivided into dexamethasone suppressors and nonsuppressors based on their DST status before testing to look for differences among these groups. Control subjects showed no response of the hormones to the lowest dose AVP and a moderate response to the higher doses. Interestingly, depressed patients as compared to controls responded more to the lowest dose AVP in particular with respect to ACTH. DST status did not influence the results. These findings suggest an enhanced sensitivity of the pituitary to low doses AVP in depressed patients. Thus, AVP might play a role in HPA dysfunction in depression.
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PMID:Stimulation of the pituitary-adrenal axis with a low dose [Arg8]-vasopressin in depressed patients and healthy subjects. 133 98

In order to investigate pituitary alpha-melanocyte-stimulating hormone (alpha-MSH), intact (1-39 structure) adrenocorticotropic hormone (ACTH), and adrenal cortisol secretion, we measured 8 a.m. plasma levels of those hormones before and after administration of 1 mg dexamethasone in 39 depressed inpatients and 10 healthy controls. We found a significantly lower baseline alpha-MSH secretion in melancholic patients as opposed to healthy controls. There were no significant relations between alpha-MSH secretion on the one hand and ACTH or cortisol secretion on the other. Dexamethasone did not affect the 8 a.m. alpha-MSH circulating levels. The post-dexamethasone intact ACTH and cortisol values were significantly higher in melancholics as compared with healthy, minor and simple major depressed subjects. ACTH non-suppression was defined as post-dexamethasone intact ACTH greater than or equal to 12 pg/ml. ACTH non-suppression was found to be more sensitive (70%) and specific (100%) for melancholia than cortisol non-suppression. By means of pathway analysis we have established that cortisol non-suppression during a severe depression is completely determined by an augmented ACTH escape from suppression by dexamethasone. It is concluded that the assay of post-dexamethasone intact ACTH could, in the future, replace post-dexamethasone cortisol determination.
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PMID:Abnormal pituitary function during melancholia: reduced alpha-melanocyte-stimulating hormone secretion and increased intact ACTH non-suppression. 165 52

Human corticotropin releasing hormone (h-CRH) was administered to 14 patients with major depression, after premedication with an overnight dose of 1.5 mg dexamethasone. Cortisol response, expressed as area under the time course curve (AUC), was significantly higher in the 14 patients than in a group of 13 age-matched control subjects (9.4 +/- 7.6 ng x min x 1,000/ml vs. 3.1 +/- 3.6 ng x min x 1,000/ml). Corresponding AUC values for plasma adrenocorticotropic hormone (ACTH) were also significantly higher in patients than in control subjects (4.9 +/- 1.4 pg x min x 1,000/ml vs. 2.6 +/- 0.9 pg x min x 1,000/ml). After patients were treated with trimipramine (200 mg/day) for 6 weeks, the combined dexamethasone/h-CRH test was repeated. At that time, depression scores were significantly improved and the patients' cortisol response pattern became indistinguishable from that of controls. While plasma cortisol output normalized during treatment with trimipramine, ACTH release remained exaggerated. The combined dexamethasone/h-CRH challenge test may be of particular value in the detection of state-dependent changes of pituitary-adrenocortical neuroregulation.
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PMID:Repeated administration of the combined dexamethasone-human corticotropin releasing hormone stimulation test during treatment of depression. 166 30

There is current controversy over the mechanisms underlying hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in depression. Pro-gamma-melanocyte-stimulating hormone (MSH), a portion of the N-terminal region of pro-opiomelanocortin, has been shown to act synergistically with adrenocorticotropic hormone (ACTH) in stimulating corticosteroid secretion both in vitro and in vivo. Pro-gamma-MSH and ACTH plasma levels were measured in 30 drug-free male patients with a DSM-IIIR 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 upon pro-gamma-MSH plasma levels in depressed patients and healthy controls. 217 Apr 84

1. The plasma levels of L-tryptophan (L-TRP) and the sum of five competing amino acids (CAA) namely tyrosine, phenylalanine, valine, leucine, isoleucine, were determined in 79 depressed females categorized according to the DSM-III. 2. In these patients the authors measured several parameters known to affect the availability of the above amino acids, i.e. triidothyronine (FT3) and thyroxine (FT4), vanilylmandelic acid (VMA), noradrenaline and adrenaline in 24 hr urine, the sex hormonal and nutritional state. 3. The 1 mg dexamethasone suppression test was performed and the pre and postdexamethasone cortisol and adrenocorticotropic hormone (ACTH) levels were determined at 8 a.m. 4. L-TRP and the ratio L-TRP/CAA were significantly lower in severely depressed females (296.X3, 296.X4) as compared with minor (300.40, 309.00) and simple major depressives (296.X2). The ratio L-TRP/CAA performed well as a clinical tool separating melancholic from minor depression. 5. FT3, FT4, VMA and noradrenaline were significantly increased in the severely depressed females, but these data did not correlate with the availability of L-TRP. Neither baseline cortisol nor the sex hormonal, nor the nutritional state related to the L-TRP data. The ratio L-TRP/CAA was significantly and negatively correlated with the postdexamethasone cortisol and ACTH values.
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PMID:The decreased availability of L-tryptophan in depressed females: clinical and biological correlates. 217 60

A substantial body of data suggests that excessive cortisol secretion in depression may result from dysregulation at several sites within the hypothalamic-pituitary-adrenocortical (HPA) axis. The alterations in regulatory mechanisms are thought to result from a limbic system-hypothalamic "overdrive" of corticotropin-releasing hormone (CRH). We also have demonstrated that excessive secretion of cortisol may result from an abnormal adrenocortical responsiveness to adrenocorticotropic hormone (ACTH), and we have postulated that corticotropic cells within the pituitary mediate between excessive secretion of CRH from the hypothalamus and hypercortisolemia secondary to adrenocortical hyperplasia and enhanced sensitivity to ACTH at the adrenal cortex. The present report describes a series of clinical experiments utilizing several neuroendocrine probes, as well as computer-assisted tomography, to examine the complexities of the HPA axis dysregulation in depression. These studies support the hypothesis that a limbic system-hypothalamic disturbance results in excessive CRH secretion as well as enhanced adrenocortical activity, and that these factors contribute to excessive cortisol secretion in patients with depression. These data further support the hypothesis that endogenous affective disorders are best characterized in the framework of a generalized biological disturbance of HPA axis function which involves both central and peripheral endocrine sites.
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PMID:The assessment of abnormalities in hormonal responsiveness at multiple levels of the hypothalamic-pituitary-adrenocortical axis in depressive illness. 254 2

To investigate the relationships between dexamethasone (DEX) and post-DEX cortisol and adrenocorticotropic hormone (ACTH) levels, the authors measured DEX at 8.00 a.m. and post-DEX cortisol and ACTH levels at 8.00 a.m. and 4.00 p.m. in 72 depressed patients categorized according to DSM-III. Cortisol non-suppressors exhibited significantly (P = 0.0006) decreased levels of DEX compared to suppressors. DEX levels at 8.00 a.m. explained 21.1% of the variance in the post-DEX cortisol values at 8.00 a.m. and 34.5% of those at 4.00 p.m. DEX levels were not significantly different among minor depressives (300.40, 309.00), major depressives without melancholia (296.X2) or with melancholia and/or psychotic features (296.X3, 296.X4). In the latter the post-DEX cortisol was significantly increased compared to all other depressives and these differences remained significant even after adjusting for the variations in DEX (by means of regression analysis). Also the diagnostic performance of the post-DEX cortisol values for major depression with associated features versus minor depression was not substantially affected when the DEX levels were accounted for. ACTH levels after DEX were shown to correlate significantly (P less than 0.05) and negatively with DEX. Although post-DEX ACTH levels did not differ among the DSM-III diagnostic categories, cortisol non-suppressors averaged significantly (P = 0.0004) higher ACTH levels than suppressors.
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PMID:The influences of dexamethasone levels on the predictive value of the DST for unipolar major depression and the relationships between post-dexamethasone cortisol and ACTH levels. 254 36

The influence of glucocorticoid administration and limited nursing on piglet carbohydrase enzyme development and subsequent growth was examined in three experiments using 371 piglets. Treatments in the first two experiments were formed by the factorial arrangement of hydrocortisone (-HYD or +HYD) and limited nursing (-LN or +LN) imposed form d 14 to weaning (d 28). Hydrocortisone was replaced by adrenocorticotropic hormone (ACTH) in the third experiment. Growth rates were severely depressed by HYD (P less than .01), LN (P less than .001) and to a lesser extent (P less than .06) by ACTH during the last 2 wk of lactation. During the first 14 d postweaning, piglets continued to grow more slowly following HYD treatment (P less than .01), whereas LN piglets grew more rapidly than those allowed to suckle normally. Although piglets were smaller at weaning after HYD injection (P less than .01), relative weights of liver, pancreas and small intestine were increased (P less than .05). Only adrenal weights were increased by ACTH (P less than .09). Pancreatic and intestinal amylase activities were increased two- to three-fold by HYD injection (P less than .05) but were unaffected by ACTH or LN (P greater than .10). Sucrase and maltase activity increased linearly with age (P less than .001). This rate of increase was numerically enhanced by glucocorticoid treatment and LN. The normal decrease in lactase activity was accelerated by LN and HYD injection, with the greatest depression caused by the combination of LN and either HYD or ACTH administration (P less than .05). Glucocorticoid administration to nursing piglets can evoke premature elevation of the carbohydrase enzymes necessary for initiating the hydrolysis of starch.
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PMID:Effect of glucocorticoids and limiting nursing on the carbohydrate digestive capacity and growth rate of piglets. 255 55


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