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

Hypothalamo-pituitary-adrenal (HPA) axis is a very complicated control system playing an important role in stress reaction, where glucocorticoids suppress the autonomic (vegetative), endocrine, immunologic and psychic responses to stressful stimuli. We described the marked clinical, physiological, and biochemical connection between osteoporosis and major depressive disorder (MDD). Both conditions are associated with a hyperactive HPA axis and LC/NE system, and hence with increased CRH, cortisol, and catecholamine secretion. There are numerous states or diseases associated with osteoporosis and we were looking for a hypercorticism value as a one of these. Some recent studies demonstrated that earlier history of MDD was associated with marked osteoporosis. In MDD there are two well-documented biochemical abnormalities: hypercortisolism and its resistance to dexamethasone suppression. The present study included 31 MDD patients (19 males and 12 females, mean age 37 +/- 1.3, age range 29-41 years), and 17 healthy male volunteers (mean age 39 +/- 1.6, age range 34-45 years). In each of our patients 24-hour urinary free cortisol, serum cortisol level at 8 a.m. and 5 p.m., cortisol in dexamethasone suppression test and bone mineral density were measured. We have, therefore, analyzed a group of young men and women with normal menstrual cycles, who were without signs of osteoporosis in the beginning, and who received anti-depressive therapy for many years. Analysis showed that increased levels of cortisol and the occurrence of osteoporosis, that developed as the result of elevated cortisol level. For our workshop we used nonparametric rang-correlation with Spearman's rho = -0.805, with statistic significant at the 0.01 level (2-tailed). Patients under long-term history of depression could develop a very stronger type of osteoporosis i.e. it is before known that the patients with untreated Cushing syndrome developed hard osteoporosis.
 ...
PMID:Depressive disorder as possible risk factor of osteoporosis. 1181 Dec 78

The purposes of this study were to examine the level of improvement of cognitive function 12 months posttreatment in adult patients with Cushing syndrome (CS), the relationships of cognitive function to duration of CS or recovery of the hypothalamic pituitary adrenal (HPA) axis, and depression and improved cognitive functioning. Thirty-three patients with CS and a matched comparison group were enrolled. IQ, depression, and endocrine factors were measured during the active phase of CS and at 12 months posttreatment for CS. Results show no group differences in cognitive function across time but a trend for CS patients to have lower IQ scores at baseline. Individual differences in performance were striking. For some subscales of IQ there was a positive relationship with recovery of the HPA axis and a negative relationship with duration of CS as well as an improvement if depression had decreased. Limitations of the study are cited along with clinical implications and directions for future research.
 ...
PMID:Cognitive function in patients with Cushing syndrome: a longitudinal perspective. 1188 98

Hypercortisolism and altered serotonergic function may account for the pathological symptoms seen in depression. This study examines the impact of 4 days continuous corticosterone treatment on 5-HT agonist-induced behaviour to delineate changes in 5-HT receptor function in the adult rat. The flat body posture, reciprocal forepaw treading, elevated corticosterone, hyperglycaemia, hypothermia and reduced hippocampal 5-HT induced by the 5-HT(1A) agonist 8-OHDPAT (0.3 mg/kg ip) were all significantly attenuated by the corticosterone implant. The elevation in plasma corticosterone and back muscle contractions evoked by the 5-HT(2A) agonist DOI (1 mg/kg ip) were attenuated, whilst wet-dog shakes were enhanced by corticosterone treatment. 5-HT(2B) agonist-induced behaviour and the hypolocomotion and hypophagia induced by the 5-HT(2C) agonist m-CPP (2.5 mg/kg ip) were unaltered but the mCPP-induced elevation in corticosterone was abolished by corticosterone treatment. Hypothalamic 5-HT receptors mediating corticosterone- and 5-HT(1A) receptors, whether on serotonergic nerve terminals or postsynaptic neurones, were downregulated by corticosterone treatment. In contrast, 5-HT(2A) receptors may be up- or downregulated dependent on whether they are on supraspinal or spinal neurones, respectively. A comparison of the brain region-dependent alteration in serotonergic function produced by hypercorticosterone in the rat with that seen in depression is discussed.
 ...
PMID:Alteration in 5-hydroxytryptamine agonist-induced behaviour following a corticosterone implant in adult rats. 1188 72

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.
 ...
PMID:Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. 1205 88

Cushing's syndrome is due to chronic glucocorticoid excess that may have various etiologies. The most common endogenous form is pituitary-dependent bilateral adrenal hyperplasia, which is termed Cushing's disease. Major depression occurs in more than half of the cases. The presence of depressive symptoms connotes severity of clinical presentation and, in patients with hypothalamic-pituitary forms, entails prognostic value. Medical treatment may be used while awaiting more definitive solutions for the illness by surgery. The inhibitors of steroid production (e.g., ketoconazole, metyrapone and aminoglutethimide), rather than antidepressant drugs, are generally successful in lifting depression as well as other disabling symptoms. Since central serotonergic regulation could have a role in the course of Cushing's disease, serotonin antagonists (e.g., cyproheptadine, ritanserin and ketanserin) have been employed. Findings related to the pharmacological response of depression in Cushing's disease were found to have implications for the pathophysiology of depression and the potential involvement of the hypothalamic-pituitary-adrenal axis (HPA axis) in resistance and tolerance to antidepressant drugs. The use of serotonergic drugs in Cushing's disease may yield important insights in the understanding of serotonergic regulation both in Cushing's disease and in the HPA axis in nonendocrine major depression.
 ...
PMID:Residual symptoms in depression an emerging therapeutic concept. 1236 51

Clinical features such as weight gain, depression, hypertension, and menstrual irregularities, although common in the general population, may raise the possibility of Cushing's syndrome. Up to 30% of urine cortisol and dexamethasone suppression screening tests may return an incorrect result, suggesting that better tests are needed. This study evaluated the utility of nighttime salivary cortisol measurement as a screening test for Cushing's syndrome. We evaluated 139 inpatients and 4 outpatients with possible Cushing's syndrome, 16 inpatients and 7 outpatients with other nonadrenal disorders, and 34 healthy outpatients. Using cut points that excluded all subjects without Cushing's syndrome, we compared the sensitivity for the detection of Cushing's syndrome of nighttime salivary cortisol levels (2330 and 2400 h for inpatients and bedtime for outpatients), simultaneous inpatient serum cortisol levels, and urine glucocorticoid excretion. An assay- specific inpatient 2400-h salivary cortisol or an outpatient bedtime salivary cortisol greater than 550 ng/dl (15.2 nmol/liter) identified 93% of patients with Cushing's syndrome (confidence interval, 89-98%) and excluded all individuals without the disorder. Salivary cortisol measurements worked as well as plasma measurements and better than urine glucocorticoid excretion. We concluded that bedtime salivary cortisol measurement is a practical and accurate screening test for the diagnosis of Cushing's syndrome.
 ...
PMID:Nighttime salivary cortisol: a useful test for the diagnosis of Cushing's syndrome. 1236 28

Cushing's syndrome is due to chronic glucocorticoid excess that may have various etiologies. The most common endogenous form is pituitary-dependent bilateral adrenal hyperplasia, which is termed Cushing's disease. Major depression occurs in more than half of the cases. The presence of depressive symptoms connotes severity of clinical presentation and, in patients with hypothalamic-pituitary forms, entails prognostic value. Medical treatment may be used while awaiting more definitive solutions for the illness by surgery. The inhibitors of steroid production (e.g., ketoconazole, metyrapone and aminoglutethimide), rather than antidepressant drugs, are generally successful in lifting depression as well as other disabling symptoms. Since central serotonergic regulation could have a role in the course of Cushing's disease, serotonin antagonists (e.g., cyproheptadine, ritanserin and ketanserin) have been employed. Findings related to the pharmacological response of depression in Cushing's disease were found to have implications for the pathophysiology of depression and the potential involvement of the hypothalamic-pituitary-adrenal axis (HPA axis) in resistance and tolerance to antidepressant drugs. The use of serotonergic drugs in Cushing's disease may yield important insights in the understanding of serotonergic regulation both in Cushing's disease and in the HPA axis in nonendocrine major depression.
 ...
PMID:Erratum to "CNS drugs in Cushing's disease: pathophysiological and therapeutic implications for mood disorders" [Prog. Neuro-Psycol. Biol. Psychiatry, 26, 763 (2002)]. 1218 8

The diagnosis of Cushing's syndrome rests on the demonstration of clinical features and biochemical abnormalities that reflect hypercortisolism. If a patient presents with typical clinical features such as weight gain with truncal obesity and supraclavicular fat deposition, wide purple striae, and proximal muscle weakness, the diagnosis is clear-cut and is nearly always substantiated by a 24-hour urine free cortisol excretion value more than four times the normal level. However, many patients present with signs and symptoms that are common in the general population, such as hypertension, generalized weight gain, reproductive abnormalities, and depression. Many of these patients have normal cortisol excretion and do not have Cushing's syndrome. Others have mild hypercortisolism caused by psychiatric disorders, obligate exercise, morbid obesity, sleep apnea, or uncontrolled diabetes mellitus. These patients may be confused with those with the true Cushing's syndrome, and thus are considered to have a "pseudo-Cushing" state. Additional observation over time, and testing with midnight cortisol measurements, the 2-day-2-mg dexamethasone suppression test, or the dexamethasone suppression-CRH stimulation test may be useful to identify true Cushing's syndrome in these patients.
 ...
PMID:Diagnostic tests for Cushing's syndrome. 1238 46

We report a case of a virilized 59-yr-old woman with elevated serum testosterone levels and bilateral macronodular adrenal hyperplasia. The patient underwent laparoscopic right adrenalectomy, after which the elevated testosterone level transiently normalized. The immediate postoperative depression of the testosterone level suggested that the process was driven by gonadotropins that were suppressed by the stress of surgery. The excised right adrenal mass contained testosterone by immunohistochemistry and LH receptor mRNA by in situ hybridization. The recurrence of hyperandrogenemia suggested that the enlarged left adrenal was also secreting testosterone. The serum testosterone level increased in response to im injection of human chorionic gonadotropin, suggesting control by aberrant LH receptors. Injection of leuprolide acetate (7.5 mg im) to suppress LH levels resulted in normalization of the testosterone level 12 d later that persisted for several weeks. Ectopic receptors mediating Cushing's syndrome have been described in several cases of bilateral adrenal hyperplasia and adrenal adenoma. This is the first case to our knowledge in which pure androgen overproduction in adrenal hyperplasia has been shown to be controlled by LH receptors. In our patient, the control of androgen secretion by LH may explain the postmenopausal onset of virilization and the transient postoperative normalization of the serum testosterone level.
 ...
PMID:Virilization in bilateral macronodular adrenal hyperplasia controlled by luteinizing hormone. 1251 32

Hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis is the main biochemical change, besides disturbed monoaminergic neurotransmission, observed in the patients suffering from a major depression. High incidence of depression in Cushing's syndrome as well as antidepressant effects of adrenocortical enzyme inhibitors in major depression support hypothesis that hyperactivity of HPA axis may be involved in pathogenesis of depression.
 ...
PMID:Effect of antidepressant drugs on the hypothalamic-pituitary-adrenal axis activity and glucocorticoid receptor function. 1252 87


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>