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

The hormonal response of the anterior pituitary was studied in 10 normal males undergoing treadmill exercise testing, in 5 male patients undergoing diagnostic gastroscopy, and in 8 male patients undergoing elective surgery under general anaesthesia. Serum TSH was depressed below the baseline value at 2 and 3 h post-treadmill exercise, at 1, 2 and 3 h post-gastroscopy and from 10 min through 2 h post-surgery. Serum triiodothyronine was depressed below the baseline value at 10 min through 2 h post-surgery. Serum prolactin, growth hormone and cortisol were elevated by all three stressful procedures. Both gastroscopy and surgery resulted in an elevation of serum luteinizing hormone levels. There was no significant change in serum FSH levels in any of the three procedures. The post-stress depression in TSH levels could result from the suppressive effect at the hypothalamic-pituitary level of high serum levels of cortisol generated by the stress of the procedures.
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PMID:The effect of stressful diagnostic studies and surgery on anterior pituitary hormone release in man. 57 11

Coexistence of an autonomous thyroid adenoma (ATA) with chronic thyroiditis suggests a complex pathogeny pointing to the autonomous character of the nodule and to the presence of immunitary disorders. The rarity of this association and the paucity of data prompted us to present 4 cases of a series of 71 thyroidectomized ATA cases. The rarity of ATA associated with chronic thyroiditis, accumulation of radioiodine under the conditions of euthyroidism only at the adenoma level as well as the possibility for the disease to occur in hypopituitarism, all support the hypothesis of an initial thyreotropic deficiency, with subsequent hyperplasia "of necessity". Later on there is an autonomous hyperfunction increasing pituitary depression, with total extinction of the thyroid tissue outside the adenoma. When the two lesions are associated, we consider that initially there was the TSH-dependent thyroiditis that developed during which, by accidental depression of TSH secretion a local hyperplasia occurs which later becomes autonomous.
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PMID:Association of autonomous thyroid adenoma with chronic thyroiditis. 59 31

The relationship between the degree of depression and the circadian variation of serum TSH, T3 and T4 was investigated in 19 endogenously depressed patients. The difference between the hormone concentrations at 2 p.m. and at 12 p.m. was taken as an estimate of the magnitude of circadian variation. It was found that the circadian variation in serum TSH was inversely related to the degree of endogenous depression. This was mainly due to a diminution or absence of the night increase of TSH in severely depressed patients. A circadian variation of serum free T3 was found in the less depressed patients whereas no diurnal change was found in serum free T4. In severely depressed patients there were no significant diurnal changes in free thyroid hormone concentrations. The results indicate a hypothalamic dysfunction in manic-depressive psychosis.
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PMID:Disturbed circadian variation of serum thyrotropin in patients with endogenous depression. 66 84

The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) were investigated in patients with depression. Intravenous injection of synthetic TRH (500 mug) caused a significant increase in plasma GH (peak value: 7.7 minus 35.0 ng/ml) in 8 of 13 patients with mental depression. After clinical recovery these patients had no response of plasma GH to TRH. TRH administration did not raise plasma GH in normal subjects examined. Plasma PRL responses to TRH were significantly enchanced (P smaller than 0.05) in depressed patients compared with control subjects. Plasma TSH responses to TRH were significantly blunted in patients with depression (P smaller than 0.05). These results suggest disorders in the hypothalamo-pituitary function in depression.
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PMID:Growth hormone and prolactin release after injection of thyrotropin-releasing hormone in patients with depression. 80 76

Rats (200-260 g) were exposed in sealed, recycling chambers continuously for 2-30 days to gas mixtures designed to maintain the same alveolar PO2 in the presence or absence of inert gas. Mixtures with inert gas (N2, He, or Ne) were at ground level; those without inert gas (100 percent O2) were in an altitude chamber. The O2 categories were: I-100 percent O2 at 747 torr; II-74 percent O2 + 26 percent inert and 566 torr 100 percent O2; III-47 percent O2 + 53 percent inert and 381 torr 100 percent O2; IV-21 percent O2 + 79 percent inert and 197 torr 100 percent O2. One of the two room-air controls was "restricted-fed" to the level of the lowest intake group. Measurements included body, pituitary, and thyroid weight, food and water intake, plasma volume and hematocrit, pituitary and plasma TSH, and plasma PBI. Severe depression in all variables and over 50 percent mortality was seen in I by day 4. All variables were depressed in II, but there was no mortality to 20 days. Pituitary-thyroid function appeared to be particularly sensitive to depression by hyperoxia, with plasma TSH levels reduced between 42 and 60 percent in II and III. No effect was attributable to the inert gas, whether it was N2, He, or Ne, nor was any specific effect traceable to the presence or absence of inert gas.
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PMID:Pituitary-thyroid function of rats in hypobaric oxygen-inert gas environments. 80 43


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