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)

Numerous studies show that most depressed patients show abnormal pituitary responses to challenge by intravenous injection of thyrotropin releasing hormone (TRH). Some patients show after TRH diminished thyroid stimulating hormone (TSH) release, some show unexpected growth hormone release; prolactin release may be increased or decreased. The diminished TSH release is the most widely reported finding. It cannot be accounted for by primary changes in the pituitary or thyroid glands. Interference with TRH-induced TSH release by elevated cortisol may account for some observations, but this possibility has not been studied. The present data provide additional evidence that in depression there is often a disruption of hypothalamic regulatory function.
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PMID:Pituitary responses to thyrotropin releasing hormone in depressed patients: a review. 82 51

Levels of acute phase and other plasma proteins were measured in 21 men with major depression, 28 men with alcohol dependence, and 12 men who acted as controls. The depressed men had significantly elevated levels of the acute phase proteins, haptoglobin and alpha-1-antichymotrypsin, and of immunoglobulin G. The elevations in haptoglobin and alpha-1-antichymotrypsin were highly correlated with each other, and were correlated with the severity of depression and negatively correlated with the thyroid stimulating hormone response to thyrotropin. The alcoholic men had elevated haptoglobin levels, but significantly decreased levels of immunoglobulin G. These findings provide further evidence for an inflammatory response during depression.
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PMID:Elevated levels of acute phase plasma proteins in major depression. 128 77

The serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), human chorionic gonadotropin (hCG), estradiol, progesterone, androstenedione, testosterone (total and free) and dehydroepiandrosterone sulphate (DHEAS) were investigated prior to surgery in 24 postmenopausal women with benign and 28 postmenopausal women with malignant epithelial ovarian tumors. The serum concentrations of hormones were compared with those of 28 healthy, postmenopausal, age-matched controls. Significantly lower serum FSH levels were demonstrated in women with malignant tumors. No significant differences were found between the groups regarding the serum LH levels. The hCG levels were low in all groups. Regarding progesterone and estradiol levels, low postmenopausal steroid levels were found in all groups examined and no significant differences were demonstrated within the groups. No significant correlations between the levels of estradiol and FSH or progesterone and LH were demonstrated. To exclude a central depression of gonadotropin release mediated by the dopaminergic system we examined the thyroid stimulating hormone (TSH) and prolactin. No differences were found between the groups regarding TSH and prolactin levels. A possible relationship between other hormones/factors produced by the tumor and exerting a negative feedback, either centrally or directly, on the gonadotropin release remains to be investigated. A change in biological activity in the gonadotropins might explain the present findings.
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PMID:The pituitary-gonadal axis in women with benign or malignant ovarian tumors. 138 13

Twelve depressed adolescents and 12 controls matched for age, sex, Tanner stage, time of menstrual cycle (females), weight, and time of year assessed were studied over 3 nights. Measurements for cortisol, thyroid stimulating hormone, and growth hormone were made on serum collected at 10 P.M., 12 midnight, 1 A.M., 2 A.M., 3 A.M., 4 A.M., and 6 A.M. in eight pairs and every 20 minutes from 8 P.M. to 7 A.M. in four pairs. Cortisol secretion did not significantly differentiate the groups. Thyroid stimulating hormone secretion was significantly elevated in the depressed group at one time point. Growth hormone secretion significantly differentiated the two groups at most time points, and the depressed adolescents significantly hypersecreted growth hormone (area under the curve). Implications for the diagnosis, etiology, and treatment of adolescent depression are discussed.
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PMID:Nocturnal cortisol, thyroid stimulating hormone, and growth hormone secretory profiles in depressed adolescents. 178 55

The dexamethasone suppression test (DST), the thyrotropin releasing hormone (TRH) test, and the ratio of plasma L-tryptophan to competing amino acids (L-TRP/CAA) were studied in relation to the 21 items of the Hamilton Depression Rating Scale (HDRS) in 123 depressed patients categorized according to DSM-III. The relationships between the biological data and the items or item clusters of the HDRS were assessed by multivariate analyses. The psychopathological correlates of increased post-dexamethasone cortisol and decreased thyroid stimulating hormone (TSH) responsivity to TRH were middle and delayed insomnia and weight loss. The symptom correlates of decreased availability of L-TRP to the brain were psychic anxiety, depersonalization, obsessions and paranoid symptoms. Core depressive symptoms, i.e. depression, loss of interest, feelings of guilt and suicidal thoughts, were not related to the biological markers.
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PMID:Symptom profiles of biological markers in depression: a multivariate study. 211 48

Thirty drug-free patients fulfilling the DSM-III criteria for major depression serially underwent the dexamethasone suppression test (DST), thyroid stimulating hormone (TSH) test and a growth hormone (GH) challenge test with oral desipramine. Fifty-three per cent of the sample showed a blunted GH response, 47% were DST non-suppressors while 26% had a blunted TSH response. Eighty per cent of patients showed some biological abnormality. There was no clear association between any of these abnormalities. Neither was there any association between the neuroendocrine parameters studied and the severity of depression or patient gender. There was a trend for increasing GH blunting and DST non-suppression with increasing age.
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PMID:Neuroendocrine challenge tests in depression: a study of growth hormone, TRH and cortisol release. 214 Mar 74

Nine patients with psoriasis vulgaris were treated for 12 weeks with somatostatin analog, octreotide acetate (SMS 201-995) 50 or 100 micrograms by subcutaneous injection every 12 hours. The purposes of the study were to determine: (1) levels of insulin, glucose, glucagon, pancreatic polypeptide (PP), and SMS 201-995 after a subcutaneous injection of SMS 201-995 and ingestion of a standardized meal; (2) nocturnal (0200 h) thyroid stimulating hormone (TSH) levels before, during, and after treatment; and (3) the pharmacokinetics of SMS 201-995. Insulin peaks at 30 minutes were blunted from 65.8 +/- 11.0 mu U/mL without treatment to 26.7 +/- 8.6 mu U/mL and 7.7 +/- 2.0 mu U/mL after the 50- and 100-micrograms doses, respectively. Glucagon levels remained constant during the meal and were not affected by the 50-micrograms dose. Mean glucose levels were significantly elevated during insulin suppression. PP was also rapidly suppressed by SMS 201-995 and remained so for 4 hours after the injection. Nocturnal TSH was blunted after 12 weeks of treatment (P less than or equal to .05). T4 and T3 resin uptake showed no depression, and patients remained clinically euthyroid. The plasma peak of SMS 210-995 occurred 30 minutes postinjection and half-life was longer than 2 hours. After chronic administration of SMS 201-995, insulin was suppressed with resultant mild carbohydrate intolerance that persisted throughout the treatment course.
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PMID:Treatment of psoriasis with chronic subcutaneous administration of somatostatin analog 201-995 (sandostatin). II. Effect on pancreatic and thyroid hormone. 240 89

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

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

Serum melatonin was determined over 24 hours in 35 patients with breast cancer with either a fresh primary tumor (n = 23) or a secondary tumor (n = 12) and in 28 patients with untreated benign breast disease (controls) having a fibroadenoma (n = 10), fibrocystic mastopathy (n = 14), or other breast diseases (n = 4). Circadian rhythms existed in all groups with acrophases at 2 a.m. A 50% depression of peak and amplitude occurred in the group of patients with primary breast cancer compared with age-matched controls (P less than 0.001, P less than 0.01). The peak declined with increasing tumor size: 27% at Stage T1, 53% at T2 (P less than 0.001), and 73% at T3 (P less than 0.05). In contrast, patients with secondary breast cancer, particularly those receiving antiestrogen therapy, had a melatonin peak similar to controls. These results demonstrated a transient depression of pineal melatonin secretion in primary breast cancer and indicated a dynamic role of the pineal gland in malignancy. To investigate some endocrine effects of a depressed melatonin peak, the 24-hour rhythms of prolactin (PRL) and thyroid stimulating hormone (TSH) were determined in patients with primary breast cancer and compared with patients with secondary breast cancer. The PRL had significant circadian rhythms in both groups; but acrophases occurred at midnight in patients with secondary breast cancer, and there were unusually high concentrations at noon in patients with primary breast cancer. Circadian rhythms were not seen for TSH, but the 24-hour average secretion was depressed by 45% (P less than 0.01) in patients with primary breast cancer. The abnormal concentrations of PRL and TSH in these patients could be due to a depressed melatonin peak normally serving as a central circadian synchronizer and modulator of the secretion of adenohypophysial hormones. Additionally, a positive correlation existed between the nocturnal melatonin peak and progesterone and androgen receptor concentrations in primary tumors indicating a direct involvement of melatonin in the growth control of breast cancer.
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PMID:Stage-dependent depression of melatonin in patients with primary breast cancer. Correlation with prolactin, thyroid stimulating hormone, and steroid receptors. 273 89


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