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)

Chronic pain has been considered as a variant of depression or as a masked depression. In an attempt to unravel the complex relationship between chronic pain and depression, we administered the TRH stimulation test to a uniform group of chronic pain patients classified into those with and without major depression using DSM-III criteria. Eighteen percent showed blunting of TSH response to TRH. There was no significant difference between the two groups.
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PMID:Preliminary study of thyrotrophin releasing hormone stimulation test in chronic low back pain patients. 294 31

Both clinical diabetes and chemically-induced diabetes have been reported to alter control processes of the hypothalamic-pituitary-thyroid axis. One of the sites of alteration appears to be depression of thyrotrophin releasing hormone (TRH) stimulated thyrotrophin (TSH) release. The present study examined the influence of sequential administration of streptozotocin and the goitrogen thiouracil to male mice for 4 weeks in view of their possibly opposing effects on TSH release. The drugs produced the expected results when administered singly, with streptozotocin producing hyperglycemia and thiouracil causing hypothyroxinemia and goitrogenesis. Additionally, thiouracil administration produced hyperinsulinemia. Sequential administration of the drugs appeared to ameliorate the thyroid status and glycemic condition caused by individual exposure. Streptozotocin reduced the goitrogenic influence of thiouracil and thiouracil reduced the hyperglycemia of streptozotocin, but not to control levels. Thus, sequential administration resulted in mice with simultaneously elevated circulating glucose and insulin levels, and depressed thyroxine levels. Similar effects on glucose, insulin, and the thyroxine levels have been reported clinically in patients with non-insulin-dependent diabetes mellitus.
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PMID:Consequences of sequential induction of diabetes mellitus by streptozotocin and hypothyroidism by thiouracil in mice. 294 14

Despite a lack of documented efficacy in controlled trials, triiodothyronine (T3) is frequently administered as an adjunctive therapy for tricyclic resistant depressions. In this study, we tested the efficacy of T3 as an adjunctive treatment using a double-blind, placebo-controlled crossover design. Sixteen depressed patients who were unresponsive to 4 weeks of imipramine therapy (mean dose = 206 +/- 54 mg daily, mean combined blood level = 220 +/- 132 ng/dl) received T3 25 micrograms and placebo for 2 weeks each. There was no evidence of a T3 effect using both Hamilton depression scores and global improvement. No subgroup of responders using baseline TRH stimulation tests could be identified. T3 treatment lowered plasma free T4 (P = 0.001) and TSH (P greater than 0.02) while raising plasma T3 levels (P less than 0.01), indicating the physiological effect of the drug.
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PMID:Failure of T3 to potentiate tricyclic antidepressant response. 296 Jul 19

A patient with Cushing's syndrome due to ectopic ACTH secretion was treated successfully with the new glucocorticoid antagonist RU 486 [17 beta-hydroxy-11 beta-(4-dimethylamino phenyl) 17 alpha-(1-propynyl)estra-4,9-dien-3-one]. This compound is a 19-nor steroid with substitutions at positions C11 and C17 which antagonizes cortisol action competitively at the receptor level. Oral RU 486 was given in increasing doses of 5, 10, 15, and 20 mg/kg . day for a 9-week period. Treatment efficacy was monitored by assessment of clinical status and by measuring several glucocorticoid-sensitive variables, including fasting blood sugar, blood sugar 120 min after oral glucose administration, and plasma concentrations of TSH, corticosteroid-binding globulin, LH, testosterone-estradiol-binding globulin, and total and free testosterone. With therapy, the somatic features of Cushing's syndrome (buffalo hump, central obesity, and moon facies) ameliorated, mean arterial blood pressure normalized, suicidal depression resolved, and libido returned. All biochemical glucocorticoid-sensitive parameters normalized. No side-effects of drug toxicity were observed. We conclude that RU 486 may provide a safe, well tolerated, and effective medical treatment for hypercortisolism.
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PMID:Successful treatment of Cushing's syndrome with the glucocorticoid antagonist RU 486. 299 27

Exposure of FRTL-5 cells to iodide (I-) in excess of 3 microM suppresses the concentrative uptake of I-. The depression of I- uptake measured at the steady state is due to decrease in the rate of I- influx and not to an effect on I- efflux. Exposure to NaI is associated with decreased T4 secretion and also depressed Na+-dependent amino acid accumulation. The depression in I- and amino acid transports increases proportionately with the duration of exposure and concentration of I- used but is not associated with alterations in FRTL-5 cell cAMP levels. The I- suppression effect is blocked, however, when methimazole is present during the incubation with NaI. In agreement with studies in vivo, I- suppression in FRTL-5 cells appears to depend on an intermediate in the organification process and to be independent of a TSH-induced cAMP-mediated action.
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PMID:Iodine suppression of iodide uptake in FRTL-5 thyroid cells. 300 60

Treatment of rats with endotoxin immediately after birth caused destruction of the cell membrane, resulting in depression of the thyroxin level and of the response to thyrotropin in adulthood. The thyroid gland of the rats treated neonatally with endotoxin failed to differentiate TSH from gonadotropin. Neonatal treatment (imprinting) with thyrotropin or gonadotropin after preexposure to the endotoxin improved the adult response to the exogenous hormone presented for imprinting after endotoxin. It appears that during the reconstruction stage following upon membrane perturbation in the critical period of receptor maturation, the adequate hormone or a related molecule can equally adapt the receptor for itself, but neither can fully compensate the perinatal membrane injury, nor the consequent diminution of receptor activity.
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PMID:Can neonatal treatment with a related hormone adapt the receptor for itself? 301 Jun 37

Twenty-two subjects (11 patients with major endogenous depression and 11 controls) received an intravenous test dose of 100 micrograms human corticotropin-releasing hormone (h-CRH). Corticotropin (ACTH), but not cortisol, responses were blunted in depressives. Basal cortisol secretion was higher in depressives than in controls and was negatively correlated to the corticotropin response following h-CRH. This finding indicates the integrity of the glucocorticoid-dependent negative feedback regulation in depression and supports the view that hypercortisolism in depression is primarily due to a suprapituitary disturbance. Comparison of ACTH responses after h-CRH with thyrotropin (TSH) output following thyrotropin-releasing hormone (TRH) revealed a positive correlation (r = 0.65, p less than 0.001). The concordance between ACTH and TSH responses after specific challenges suggests that regulation of both systems is at least in part under a common control.
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PMID:Human corticotropin-releasing hormone in depression--correlation with thyrotropin secretion following thyrotropin-releasing hormone. 301 Nov 29

The effect of adenohypophysial hormones on rat pineal melatonin content and release was examined in vitro. Medium concentration of radioimmunoassayable melatonin decreased after a 6 h exposure to 1-100 ng/ml FSH; pineal levels of melatonin were only decreased by 100 ng/ml FSH. LH (1-100 ng/ml) augmented significantly medium melatonin concentration, tissue levels being increased at 10 ng/ml LH. Parallel increases of explant and medium melatonin content were found after exposure to 1-100 ng/ml TSH. At the smallest concentration employed (1 ng/ml) prolactin increased melatonin content and release while at 100 ng/ml a significant depression of both parameters was found. Growth hormone (1-10 ng/ml) augmented melatonin levels in medium but failed to modify them at 100 ng/ml, although at this concentration tissue melatonin levels increased. ACTH did not modify pineal melatonin synthesis in vitro.
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PMID:In vitro effects of adenohypophysial hormones on rat pineal melatonin content and release. 303 98

Several investigators have reported a paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in depressed patients, but other studies have failed to confirm this. In the present study, the GH response to TRH was studied in depressed patients and normal subjects. The rate of paradoxical GH response to TRH in depression was no different than that observed in control subjects. This was the case whether the data was examined using mean values or using frequency of abnormal responses. Patients with blunted thyrotropin (TSH) responses did not differ in GH release from patients with normal TSH response. A variety of factors may have contributed to the earlier reports of a positive GH response to TRH, including the definition of paradoxical GH release and the fact that depressed patients exhibit more frequent spontaneous diurnal GH release than do normal subjects.
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PMID:Is there paradoxical growth hormone response to thyrotropin-releasing hormone in depression? 308 39

We studied the prolactin response to TRH in 53 unmedicated psychiatric inpatients. The prolactin response of females was significantly greater than the response of male subjects. There was no significant difference in the prolactin response to TRH between depressed patients and those with other psychiatric diagnoses. There was no significant relationship between the prolactin response to TRH and the severity of depression, the TSH response to TRH or the resistance to suppression of cortisol secretion by dexamethasone.
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PMID:Prolactin response to TRH in depression. 308 43


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