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)

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.
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PMID:Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH. 23

TRH and LHRH were simultaneously infused into a group of five male patients with primary unipolar depression and four male secondary depressed patients. Blood samples were measured for LH and TSH just before and two hours following infusion. Six healthy male subjects matched for age were similarly studied. Our results showed: 1) that basal levels of TSH and LH were not different in any of the three groups of subjects, 2) TSH responses in the three groups were not significantly different, and 3) the LH response was significantly greater in the secondary depressed patients than the primary unipolar depression and normal controls at all time intervals after infusion. Our results add to the existing evidence for an abnormality in the hypothalamo-pituitary regulation of pituitary hormones-in particular LH. Such an abnormalit has not been reported in the literature to our knowledge. Our results tend to suggest a biological difference in the two subtypes of depression studied. Neuroendocrine studies would appear to be a useful diagnostic procedure in the differentiation of these subtypes of depression.
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PMID:TSH and LH responses in subtypes of depression. 38 24

Basal hypothalamic deafferentation extending from the posterior border of the optic chiasm to the mid-mammillary bodies resulted in depression of plasma TSH, thyroxine (T4), and triiodothyronine (T3) concentration to 50% of normal controls within 7 days. Administration of 0.15% propylthiouracil (PTU) in the diet form postoperative day 26 caused a pronounced drop in the plasma T3 level and a rise in plasma TSH level within two days in the control animals, but had little effect during this interval in the deafferented animals. After 12 days of PTU, plasma T3 and T4 concentrations had dropped to undetectable concentrations in the control animals but both were still detectable in the deafferented animals. After 25 days of PTU, plasms T4 and T3 levels were undetectable and plasma TSH levels were significantly elevated above normal in all animals. Thyroid hypertrophy at that time was as great in the deafferented as in the control rats, although plasma TSH concentration was 50% lower in the former. Administration of 0.1 mug/100 g BW TRH iv on postoperative day 37, when plasma T4 and T3 were undetectable in the controls but still present in the deafferented animals, produced an equally high concentration of plasma TSH in all animals. We interpret these data to support the concepts that: 1) a major source of neural drive of that TRH which stimulates the secretion of TSH by the adenohypophysis lies outside the medial basal hypothalamus, 2) a decrease in TRH reaching the adenohypophysis causes a lower setting of the "thyrostat" sensitive to the concentration of circulating thyroid hormone, and 3) increased TSH secretion and resultant goitrogenesis is delayed in animals with impaired TRH secretion because of the slower rate of secretion of thyroid hormone than in intact controls and the longer time thus required to markedly reduce the concentration of circulating thyroid hormone.
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PMID:The effect of basal hypothalamic isolation on pituitary-thyroid activity and the response to propylthiouracil. 40 61

The antidepressive efficacy of TRH was investigated in 15 endogenous depressive patients in a double-blind cross-over design. The Hamilton depression scale, the AMP (PAS) system, v. Zerssen scale and thermometer scales were used. No therapeutic effect could be demonstrated. The blunted TSH-response to TRH, which has been described by other investigators, was confirmed. There was suggestive evidence of a psychoendocrinological relationship in the sense that the more severe the "somatic depressive" syndrome as calculated from the AMP system, and the more marked the diurnal variation of the endogenous type is, the lower are the basal TSH-values and the smaller the response to TRH. Thus, TRH may become a useful tool to identify subgroups of depressive patient populations.
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PMID:Psychoendocrinological and therapeutic effects of TRH in depression. 40 1

Nineteen out of 51 depressed patients showed abnormal TSH response to TRH in terms of exaggerated, diminished and delayed responses. The basal value of T3 and its response to TRH were significantly lower in patients with delayed or diminished response than in the normal subjects. These results indicate that the dysfunction of the hypothalamo-pituitary thyroid axis plays an important role in the pathogenesis of depression.
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PMID:Function of hypothalamo-pituitary thyroid axis in depressed patients. 40 54

In 183 out patients of our department FSH, LH, prolactin and testosterone were measured in one single serum sample. In 43 of these, measurements were done prior and 30 min after injection of LH-RH and TRH. An analysis of the ejaculate was performed in each case. If prolactin levels are grouped according to sperm count or testosterone levels, means of prolactin do not differ significantly between these groups. Some individual levels exceed the normal range. The TRN stimulated prolactin levels are lowered when related to high testosterone levels. Significantly statistical correlations do not exist. Mean FSH levels show a clear depression related to high sperm counts and high testosterone levels. A significantly statistical correlation is found between FSH, LH and prolactin levels each. Determination of prolactin in patients with fertility disturbances may be helpful to detect a hyperprolactinemia, which possibly causes inhibition of the spermatognesis.
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PMID:[Prolaction level in the serum of patients with disorders of spermatogenesis]. 63 89

Changes in thyroid activity and variations in the hypthalamo-pituitary-thyroid hormone levels were examined in rats exposed to heat (34 degrees C)for3 weeks. Thyroid activity evaluated histologically (epithelium/colloid ratio, nuclear size) by radioiodine exploration (24 hrs 125 I uptake, ratio of mono- to di-125 iodotyrosines - MIT/DIT, ratio of tri- to tetra-125 iodothyronines-T3/T4, and plasma 125I-T4 and assay of plasma T4, evolves in a triphasic manner. 1.a depression phase between day 0 and day 2.5. 2. a rebound of thyroid activity between day 2.5 and day 9.3 a stabilization of thyroid parameters from day 9 to day 24. These results indicate adaptation of thyroid function to heat after 3 weeks. In phase i, plasma TSH )MeKenzie bioassay) fell to undectable levels concurrent with a 50% decrease in hypothalamic TRH (in vitro assay). Plasma TSH peaked on day 4.5, fell on day 9.5 and returned progressively to initial levels. Hypothalamic TRH returned to initial levels after 6.5 days. The rapid and simultaneous decrease in hypothalamic TRH, plasma TSH, plasma T4 and thyroid activity by the 36th hour of heat exposure (34 degrees C) suggests initiation at the hypothalamic level. In the secound phase, the rebound in thyroid activity is presumably due to the peak in circulating TSH in ralation to the marked decrease in plasma T4. The oscillations of phase 2 and the stabilization of all the thyroid parameters in phase 3 may be the reflection of an apparent discrepancy remains between a low plasma T4 and a normal or subnormal plasma TSH. A modification in the "set point" for the control of TSH secretion is discussed.
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PMID:Variations of rat thyroid activity during exposure to high environmental temperature (34 degrees C). Relation between hypothalamic pituitary and thyroid hormone levels. 80 54

The repeated systemic infusion of TRH (200 mug, twice daily) was effective in repeatedly elevating plasma T4 levels (20-40 min postinfusion) for the 3 experimental days. The post-TRH treatment (saline infusion) exhibited a depression of plasma thyroxine levels, possibly explained by previous high thyroxine levels exerting a suppressive effect on the hypothalamic-pituitary-thyroid axis. A depression of plasma glucocorticoid levels was shown within 1 hr in both experiments after TRH administration. The results indicate that TRH administration (systemic) is effective in temporarily elevating thyroxine levels and simultaneously lowering plasma glucocorticoids in cattle.
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PMID:Effect of thyrotropin-releasing hormone (TRH) on plasma glucocorticoids and thyroxine in cattle. 80 23

Both oral and intravenous TRH produce systematic alterations in brain function of depressive patients as determined by scalp-recorded computerized cerebral biopotentials (computer EEG). The computer EEG (CEEG) profiles of both formulations are not only very similar to each other, but also resemble the CEEG profiles of psychostimulant compounds (Bio-availability). As in CEEG findings, TSH plasma levels also indicate that oral TRH is indeed an active compound. Although some "antidepressive" effects were observed after both formulations, they were not present in every patient, and it was not always the case after repetitive TRH administration, nor were the effects on depressed mood too impressive. On the other hand, in almost all patients certain behavioral effects of TRH were seen which related to "life instincts" and "life performance". The increase of interest, desire and drive for work, food and sex was one of the most striking findings, particularly after intravenous TRH. This may be responsible for the "antidepressive" effects of TRH in patients in whom depression may be the result of an inhibition of "instinctive" functions.
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PMID:Clinical and CNS effects of oral and I.V. Thyrotropin-releasing hormone in depressed patients. 80 53

Twenty-five depressed patients were examined as to their growth hormone responses to TRH. An enhanced pituitary growth hormone response to intravenous injection of 500 mug TRH was observed in eight depressed patients, while TRH administration did not raise growth hormone levels in nine of 10 normal subjects examined. Occurrence of enhanced response of growth hormone was not related to the thyrotropin values after TRH administration. Bipolar patients exhibited enhanced growth-hormone response more frequently than unipolar patients. Five patients with involutional depression and neurotic depression who showed the most insufficient thyrotropin release to TRH administration together with lowered thyroid function revealed to be non-responders of growth hormone.
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PMID:Enhanced growth hormone responses to TRH injection in bipolar depressed patients. 81 72


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