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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty depressed inpatients aged 7-16 yrs were compared for salivary hypercortisolism with a control group of 16 inpatients of mixed diagnosis matched for age and sex. Four cortisol samples were taken over a 48 hr period: 8 a.m. and 11 p.m. on the first day; then, with 1 mg of dexamethasone given immediately after the second sample, at 4 p.m. and 11 p.m. on the second day. All except the 8 a.m. value were significantly greater (P less than 0.03) in the depressed group. A 4 nmol/l cutoff for the 4 p.m. sample gave 48% sensitivity and 91% specificity for discriminating depressed cases (P = 0.03). The results indicate that the salivary method for estimating cortisol levels in children and adolescents with depression warrants further study.
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PMID:Salivary cortisol hypersecretion in juvenile depression. 341 7

To study the pathophysiology of hypercortisolism in anorexia nervosa, we measured the cerebrospinal fluid (CSF) levels of corticotropin-releasing hormone (CRH) in patients when they were underweight and at intervals after weight restoration. CSF CRH levels were significantly elevated in hypercortisolemic underweight patients. Both CSF CRH levels and pituitary-adrenal function normalized after weight recovery. A significant positive correlation was found between CSF CRH levels and depression ratings in weight-corrected patients. We conclude that the hypercortisolism of anorexia nervosa reflects a defect at or above the hypothalamus which results in the hypersecretion of endogenous CRH. The positive correlation between CSF CRH and depression in the weight-restored patients is compatible with previous data indicating increased CRH secretion in the depressed phase of primary affective disorder and supports the notion of a relationship between CRH and depressive symptomatology. Moreover, these data are compatible with observations that depression is part of the anorexia nervosa syndrome.
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PMID:Elevated cerebrospinal fluid levels of immunoreactive corticotropin-releasing hormone in anorexia nervosa: relation to state of nutrition, adrenal function, and intensity of depression. 349 30

Hypercortisolism due to Cushing's syndrome or glucocorticoid therapy induces disturbances in several other endocrine systems and may also cause mental changes, predominantly depression of various degrees. On the other hand, it has repeatedly been shown that endogenous depression is often accompanied by hypercortisolemia, usually of a modest degree, and/or by changes in other hormonal systems similar to those observed in Cushing's syndrome and during treatment with glucocorticoids. Research performed at the MPIP on 327 psychiatric patients and 103 healthy subjects has demonstrated that, in contrast to Cushing's syndrome, the circadian rhythm in depression is usually well preserved, and that diurnal variation in mood is correlated with that rhythm. Furthermore, it was found that a modest hyperactivity of the HPA system, as indicated by enhanced UFC excretion and nonsuppression in the DST, is not specific for depression in general or its endogenous subtype. It can also be observed in many other psychiatric disorders and seems to mirror stress and the influence of other factors, such as weight loss due to anorexia, rather than a particular nosology. TSH blunting in the TRH test appears as a consequence of hypercortisolemia in psychiatric disorders as is the case in Cushing's syndrome and in the course of glucocorticoid therapy. Differences in the patterns of neuroendocrine abnormalities in depressives and other psychiatric patients probably reflect differences in the individual responsiveness of the various hormonal axes to stress rather than nosological subtypes of the disorder. A comparison of these results with the past and current literature reveals remarkable changes in the concepts of neuroendocrine dysfunctions in depression and leads to suggestions of new strategies for research on this subject.
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PMID:Neuroendocrinological studies on depression with special reference to research at the Max-Planck-Institute of Psychiatry. 354 21

Corticotropin releasing factor (CRF) is a 41 amino acid peptide first isolated from sheep hypothalami and thought to be a principal modulator of the hypothalamic-pituitary-adrenal cortical (HPA) axis. We report herein a series of clinical studies with CRF in healthy volunteers and in patients with abnormalities in HPA function, including depression, Cushing's disease, Cushing's syndrome, and Addison's disease. Our data indicate that CRF can be a diagnostic aid in distinguishing various disorders of the HPA axis from one another, including Cushing's disease from depression and secondary from tertiary adrenal insufficiency. Moreover, the hormone responses to CRF help clarify the pathophysiology of the HPA abnormalities in several disorders. For instance, our data indicate that hypercortisolism in Cushing's disease results principally from a defect at the level of the pituitary; in contrast, in depression the defect seems to be hypothalamic, possibly involving hypersecretion of endogenous CRF. This latter possibility is of particular interest in light of clinical observations that depression often can be precipitated by stress. Moreover, data from experimental animals show that CRF may influence several processes known to be altered in the overall symptom complex of depression, including not only pituitary-adrenal function, but also motor activity, appetite regulation and sexual behavior.
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PMID:Clinical studies with corticotropin releasing factor: implications for the diagnosis and pathophysiology of depression, Cushing's disease, and adrenal insufficiency. 387 72

One hundred and ten patients with Research Diagnostic Criteria (RDC) diagnoses of major depressive disorders were assessed for present or recent suicidal ideation and behavior and for suicidal acts earlier in life before current depression using the Schedule for Affective Disorders and Schizophrenia (SADS). Suicidal scores were correlated uni- and bivariately with levels of CSF monoamine metabolites (HVA, 5HIAA, MHPG), urinary MHPG, the proportion post-/predexamethasone plasma cortisol at 1100 h, and platelet MAO activity (all standardized to same sex, age, height and weight). Results indicate that all 3 monoamine metabolites and their interactions are involved in various aspects of suicidality, at least in unipolar patients. MHPG and 5HIAA (both low or both high) were involved in current or recent suicidal ideation, and low HVA was mainly associated with past potential lethality of suicidal acts. Current hypercortisolism was found in patients that earlier in life had tried to commit dangerous suicides. Bipolar patients (depressives with a history of manic or hypomanic episodes) had earlier in life significantly more, and more dangerous, suicidal attempts than the unipolars.
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PMID:Life at risk: markers of suicidality in depression. 620 42

Naturally-occurring hyperadrenocorticism was diagnosed in an 11-year-old female Dachshund with signs of polydipsia, polyuria, pendulous abdomen, weakness, depression and lethargy, and laboratory test abnormalities comprising lymphocytopaenia, eosinopaenia, hypercholesterolaemia and increased plasma alkaline phosphatase concentration. While awaiting hormonal test results, an adrenocorticolytic drug (o,p'-DDD) was administered for 14 days, during which the patient deteriorated. Hormonal assays suggested a functioning adrenocortical tumour, but the poor condition of the patient precluded adrenalectomy. An adrenocortical carcinoma with hepatic metastases was found at necropsy.
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PMID:Functioning adrenocortical tumour in a dog. 628 91

Measures of neuroendocrine function--plasma cortisol and its response to dexamethasone, and plasma thyroid-stimulating hormone (TSH) and its response to thyrotropin-releasing hormone (TRH)--were employed in 50 hospitalized male veteran psychiatric patients with diagnoses of unipolar or bipolar melancholia, secondary depression, or schizophrenia. Of 20 cases of unipolar melancholia, 17 (85%) exhibited hypercortisolism; 14 (70%) failed to suppress plasma cortisol after dexamethasone; and 4 (31%) of 13 tested had an abnormal TSH response to intravenous TRH. Two patients with secondary depression also exhibited hypercortisolism; no other patients evinced abnormal neuroendocrine test results. These measures were repeated in 14 unipolar depressed patients after a course of electroconvulsive therapy (ECT). Improvement in psychopathology was directly related to normalization of measures of hypothalamic-pituitary-adrenal (HPA) function. The TSH response to TRH was not systematically altered. After a followup period of 1 to 9 months, there was a good correlation between the measures of HPA function and the clinical outcome. These findings encourage further study of HPA function measures as outcome criteria for depressed patients receiving ECT.
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PMID:Neuroendocrine measures in psychiatric patients: course and outcome with ECT. 678 39

To determine whether patients with hypothalamo-pituitary Cushing's disease (HPC-D) can be distinguished on psychological grounds from these presenting with adrenal Cushing's syndrome (AC-S) or with ectopic ACTH syndrome, an in-depth psychological study including full personal, family and socio-professional history and a psychological interview was carried out in 50 patients with endogenous hypercortisolism. The results showed that psychiatric symptoms, such as anxiety and depression, are virtually constant in patients with either HPC-D or AC-S. They are, however, more pronounced in patients with HPC-D, and the latter condition is more likely to develop in subjects with either "psychosomatic" or pre-morbid depressive neurotic personality.
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PMID:[Psychic symptoms and personality of 50 patients with Cushing's syndrome (author's transl)]. 727 33

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.
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PMID:Cushing's syndrome: problems in diagnosis. 745 63

Alterations in the hypothalamic-pituitary-adrenal (HPA) system are well documented in affective disorders. In depression these include increased secretion of cortisol, an insufficient suppressibility of cortisol by dexamethasone, a blunted corticotropin (ACTH) response to corticotropin-releasing hormone (CRH) and a dysfunction of the glucocorticoid receptor. Patients with atopic eczema, a common chronic skin disease, show seasonal variations in disease activity, symptoms of minor depression and immunological disturbances similar to those seen in patients with depression. To explore the integrity of the HPA system integrity in individuals with atopic eczema we studied the 24-h cortisol secretion and the cortisol, ACTH and beta-endorphin responses to CRH in such individuals and in healthy controls matched for sex and age. The 24-h secretion of cortisol did not differ between the patients with atopic eczema and the controls. The net response to CRH administered as a 100 micrograms i.v. bolus was significantly attenuated for both cortisol (24,235 +/- 12,443 vs. 47,019 +/- 34,515 nmol.min/dl; p < .03) and for ACTH (546 +/- 205 vs. 727 +/- 310 pmol.min/l; p < .05) in the patient group, whereas the beta-endorphin response did not differ between the groups (1072 +/- 448 vs. 1603 +/- 421 nmol.min/l). The blunted response of cortisol and ACTH cannot be explained by hypercortisolism as it is the case in major depression. Rather, it may be related to a prolonged underexposure to hypothalamic CRH or to an increased sensitivity of glucocorticoid feedback inhibition.
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PMID:Cortisol, corticotropin, and beta-endorphin responses to corticotropin-releasing hormone in patients with atopic eczema. 767 38


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