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)

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

For the purpose of studying the relation of diversities of basic lesion as well as clinical manifestation to hormonal abnormality in Cushing's syndrome, 12 kinds of steroid hormones was simultaneously measured in plasma by using 2 types of Sephadex LH-20 column chromatography in a total of 30 patients comprosing 28 cases of Cushing's syndrome and 2 cases of adrenocortical carcinoma which had abnormal plasma steroid hormone levels without sign or symptom of Cushing's syndrome. In the group of Cushing's syndrome were included cases of pituitary ACTH-dependent hyperplasia (Hp.), adrenocortical adenoma(Ad.), bilateral nodular hyperplasia, ectopic ACTH syndrome as well as recurrent Cushing's syndrome following subtotal adrenalectomy. Twelve steroids measured in plasma were pregnenolone(Preg)., 17-OH pregnenolone(17Preg.), progesterone(Prog.), 17-OH progesterone(17Prog.), 11-deoxycorticosterone (DOC), corticosterone(B), aldosterone(Ald.), 11-deoxycortisol(S), cortisol(F), dehydroepiandrosterone(DHA), androstendione(A-dione) and testosterone(T), including precursors (Prec.: Preg., 17-preg., Prog., 17-prog.) as well as hormones belonging to the 3 systems in the biosynthetic pathways of steroid; i.e., glucocorticoids(Glu.C.'s: S,F), mineralocorticoids(Min.C.'s: DOC, B, Ald.) and sex steroids(And.'s: DHA, A-dione, T). In addition, steroidogenesis in isolated adrenal cells obtained surgically from patients with Cushing's syndrome due to Hp. and Ad, was observed. The results were as follows: (1) In cases due to Hp., plasma levels of Glu.C's and And.'s were slightly elevated, while levels of Min.C.'s were within the normal range. On the whole, however, the 3 systems were well balanced. (2) In cases due to Ad., elevated secretion of Glu.C.'s and Min.C.'s was observed, while secretion of And.'s was depressed. Among the 3 fractions of And.'s, depression of DHA and A-dione was characteristic of Ad.. (3) Elevation of And.'s in Hp. and Min.C.'s in Ad. in addition to elevation of Glu.C.'s was in fair correlation with moderate virilism in Hp. and with hypertension and hypokalemia in Ad. respectively. (4) In vitro experiments revealed that Ad. produces not only F but all 12 steroids hormones and that increased DOC and depressed DHA secretion reflected in their plasma levels were the characteristics of Ad. in steroidogenesis. Furthermore, isolated adenoma cells were found to produce Ald. at a higher rate than normal or hyperplasia adrenal cells. This finding may suggest that an intermediate type between Cushing's syndrome and primary hyperaldosteronism can exist in cases of adenoma. (5) In ectopic ACTH syndrome, plasma levels of Glu.C.'s, Min.C.'s and And.'s were equally but more markedly elevated as compared with Hp.. The increase of B was characteristic of this disorder and, coupled with a marked increase of F, seems to be the main cause of hypokalemic alkalosis frequently associated with this syndrome. (6) Nodular hyperplasia was accompanied by elevated Min.C...
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PMID:[Plasma steroid hormones in Cushing's syndrome: their relation to cause and clinical manifestations (author's transl)]. 728 45

Among a consecutive unselected series of 29 patients with Cushing's syndrome 21 had bilateral adrenal hyperplasia and 8 had tumours. Twenty-five (86 per cent) were significantly depressed; three of the tumour patients, but only one of the hyperplasia group were free of symptoms so that if there are no psychiatric symptoms there is a three in four chance that the patient has a tumour. There was a family history of depression or suicide or a history of early bereavement or separation in half the cases. In six of the hyperplasia patients a major emotional disturbance had preceded the onset, and in five this was a loss. The severity of the depression was not related to the level of circulating cortisol. The depression was rapidly relieved when the tumour or hyperplastic glands were removed. Depression in Cushing's syndrome might result from a substance other than cortisol produced by the adrenal under excessive pituitary and/or hypothalamic stimulation, which could play a part in the aetiology of depressive illness in general.
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PMID:Cushing's syndrome: a psychiatric study of 29 patients. 737 Apr 77

Fifteen patients with active Cushing's syndrome have been compared with 15 other patients who had been treated successfully for Cushing's syndrome and with 13 patients with other pituitary tumours. Depression was the main psychiatric diagnosis made by the CATEGO programme after Present State Examinations. Patients with active Cushing's syndrome were significantly more depressed (Hamilton Rating Scores), than were the other patients. Compared with the control patients, those with active Cushing's syndrome had slightly lower plasma concentrations of total tryptophan, though the concentrations of freely diffusible tryptophan were not significantly changed.
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PMID:Cushing's syndrome, tryptophan and depression. 737 Apr 78

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

In an attempt to study "manic-depressive" affairs associated with endocrine and mental disorders, our clinical data are analyzed before and after appropriate treatment in Cushing's disease, Cushing's syndrome, hyperthyroid Graves' disease and primary hypothyroidism. Although our data do not provide definite findings on manic-depressive affairs associated with Cushing's disease and syndrome, review data by others indicated a high incidence of depression under untreated condition and its disappearance after appropriate treatment. In contrast, patients with adrenocortical insufficiency did have a depression but this was cleared after supplemental therapy. In hyperthyroid Graves' disease, a number of emotional and mental instability and irritability were noticed before the treatment, but these abnormalities all disappeared after appropriate treatment for 3-6 months. In contrast, patients with primary hypothyroidism did show lethargy and apathy, and these abnormalities disappeared after appropriate treatment. From the data accumulated, it is concluded that adrenal steroid and thyroid hormone do affect the functions of nervous system and, as a result, cause a number of clinical symptoms. The exact biochemical processes underlying these abnormalities are not known and remains for further investigations.
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PMID:[Manic-depressive symptom associated with endocrine and metabolic disorders]. 800 7

A group of pulmonologists from different sites of Argentina convened to establish consensus guidelines for treatment of acute and chronic bronchial asthma. General acceptance that in fatal asthma diagnosis and hospital admission are usually too late and treatment insufficient prompted the need for this meeting. The purpose of treatment was devised to keep the patient symptomless, decrease frequency of exacerbations and the risk of severe attacks. Peak expiratory flow rate (PEFR) measurement in all patients was decided. inhalation of anti-inflammatory drugs (corticosteroids, CE, and/or disodium cromoglycate, DSG, in those younger than 20 years) was established as first line of treatment. Inhaled CE (even in high doses such as 2 mg/day) do not provoke significant adverse systemic effects (immune depression, Cushing syndrome, hyperglycemia in diabetics or osteopenia). Secondary local adverse effects are however frequent: oral and pharyngeal candidiasis and dysphonia. It is advisable considering present evidence, that bronchodilators (Bd) be used preferentially on demand. On account of small bronchodilator effect and frequent secondary adverse effects, use of theophylline should be limited to patients not adequately responsive to anti-inflammatory drugs in high dosage. Immunotherapy is not useful in asthma. Four clinical levels were defined in chronic asthma considering severity of dyspnea, frequency of nocturnal bronchial obstruction, levels of PEFR and amount of required Bd. Guidelines of treatment were established for each clinical level considering increasing dosage of CGS, inhaled CE (up to 2 mg/day) and regular administration of Bd. Indications for systemic CE administration were also established. Three levels of acute asthma (sudden worsening of symptoms) were accepted based on clinical evidence and PEFR values. Treatment was quantitatively adjusted to severity. Criteria for hospital admission either in emergency or intensive care areas and treatment procedures were established.
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PMID:[Standards established by consensus for the treatment of bronchial asthma and its exacerbations]. 811 34

Depression in a common, life-threatening complication of Cushing's syndrome and may occur in several other endocrine disorders. It is not clear, however, whether distinct features pertain to hypercortisolism. We studied depression in Cushing's syndrome differentiating pituitary-dependent and pituitary-independent forms, its incidence compared to Graves' disease, and its appearance in the prodromal phase of both conditions. To 66 consecutive patients with Cushing's syndrome and 70 with Graves' disease, after treatment, a semistructured interview for depressive symptoms based on Paykel's clinical interview for depression was administered. In Cushing's syndrome, the response of depression to normalization of urinary cortisol levels was evaluated by Kellner's global rating method. There was a significant difference in the occurrence of depression (p < 0.001) between Cushing's syndrome (62%) and Graves' disease (23%). Depression appeared in the prodromal phase in 27% of patients with Cushing's syndrome and in 14% of those with Graves' disease, but the difference was not significant. In Cushing's syndrome, there were no significant differences in depression between patients with pituitary-dependent (n = 41) and pituitary-independent (n = 20) forms, or in their response to treatment. About 70% of patients fully recovered from their depression, whereas there was no substantial change in the others and even worsening in 2. Our findings in Cushing's syndrome and Graves' disease are in agreement with previous investigations using specific diagnostic criteria for depression. We found a tendency for this symptom to manifest in the prodromal phase of both illnesses. An endocrine etiology should be, therefore, considered in depressed patients not responding to standard psychiatric treatment.
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PMID:Course of depression in Cushing's syndrome: response to treatment and comparison with Graves' disease. 831 4

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression. Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression. In a series of studies, commencing in patients with Cushing's disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide. In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.
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PMID:Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. 859 44

Cognitive theory ascribes nonendogenous depression to latent dysfunctional beliefs activated by stressors impinging upon core values (e.g., rejection for a sociotropic person). To address ambiguities in past tests of the theory, this study measured personality (Sociotropy-Autonomy Scale) and recent stressors (Life Experience Survey and Hassles Scale) among 14 Cushing syndrome patients and 12 controls. Patients scored nonsignificantly higher in sociotropy, and sociotropy correlated positively with depression among patients. Because depression in Cushing syndrome presumably results from biological dysfunction rather than from the interaction of personality and relevant stressors, these results imply that sociotropy may be a consequence of depression as opposed to a contributory cause. There was no congruence between personality and types of stressors reported, which suggest that mood-dependent recall does not account for past evidence of congruence.
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PMID:Sociotropy, autonomy, stress, and depression in Cushing syndrome. 864 86


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