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)

Thyrotropin-releasing hormone tartrate (TRH-T) was administered in 17 cases of organic brain lesions and 2 cases of disturbed mental activity (psychical depression), and its effect, mainly on the level of consciousness and electroencephalogram, was examined. Ten consecutive administrations of 0.5--1.0 mg/day TRH-T, as TRH, resulted in improvement of disturbance of consciousness in 8 of 16 cases. This effect was not necessarily correlated with the degree of disturbance or the site of the lesion. Improvement was seen even in those cases where disturbance of consciousness had been fixed over a long period. The effect on the electroencephalogram was small and did not parallel the degree of improvement of the level of consciousness. Abnormal TSH and thyroid hormone values were not seen despite the continued administration of TRH-T. These results would appear to indicate that the continuous administration of TRH-T has a mild activating effect directly on the central nervous system, and not through the endocrine mechanism, and exerts no damage on the internal environment in vivo.
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PMID:Clinical studies of thyrotropin-releasing hormone tartrate (TRH-T) as a direct stimulant to the central nervous system. 3 57

Antithyroid activity of orally administered goitrin was assessed by parallel-line assay in chicks using four indices. The relative potency of goitrin in chicks was estimated to be approximately 0.31 times the potency of PTU in causing enlargement of thyroid gland, 0.06 times in effect on depression in plasma thyroid hormone, and 0.08 times in inhibitory effects on biosynthesis of thyroid hormone in the gland. It might be concluded that thyroid hormone synthesis is not so much suppressed to the degree expected from the enlargement of thyroid gland when goitrin is administered orally to the chick.
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PMID:Antithyroid activity of goitrin in chicks. 5 53

The report at issue discusses the relationship between laryngeal papillomatosis and the endocrine system. It is referred to the clinical course of a 19-years-old patient suffering infantil laryngeal papillomatosis and antuitary insufficiency since childhood. The cause of hormonal insufficiency was the destruction of the hypophysis by a craniopharyngeoma. As a result of this insufficiency the total metabolic process of the patient was reduced to a "vita-minima"-function for years. Despite this metabolic depression the laryngeal papillomas have grown excessively. The number of recurrent papillomas could not even be reduced by exstirpation of the craniopharyngeom although the secundary insufficiency of the adrenal cortex and the secundary hypothyreosis have been compensated by cortisone and thyroxine. A hormonal influence on the laryngeal papillomas by the adrenocorticotrophic hormone and the thyroid hormone could be excluded. An inhibitory effect on the papillomas by the somatotrophic hormone seems unlikely. Furthermore the effect of the sexual hormones remains doubtful. The regression of laryngeal papillomas frequently observed by the end of puberty supports a hormonal influence by gonadotrophic hormone.
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PMID:[Recurrent infantile laryngeal papillomas and antuitary insufficiency (author's transl)]. 13 12

Experiments were conducted on male albino rats (298); a study was made of the effect of experimental thyrotoxicosis of various severity on the state of the hypothalamo-hypophyseal-adrenal system. It was found that the hypothalamo-hypophyseal-adrenal system responded differently to the excess of thyroid hormone, depending on the strength and duration of action. Mild thyrotoxicosis was accompanied by its activation expressed in increased CRF of the hypothalamic extracts, a reduction of the ACTH in the hypophysis and a fall of ascorbic acid content in the adrenal glands. Severe and prolonged thyrotoxicosis was accompanied by a depression of the hypothalamo-hypophysio-adrenal system function. It was concluded that the action of thyroid hormones on the CRF secretion served as the leading mechanism of the mentioned reactions.
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PMID:[The effect of experimental thyrotoxicosis on the state of the hypothalamo-hypophyseo-adrenal system in rats]. 17 50

In order to determine the role of thyroid hormone in prolactin (PRL) secretion in patients with amenorrhea-galactorrhae, PRL response to 500 mug of iv thyrotropin-releasing hormone (TRH) was studied before and after the administration of triiodothyronine (T3) in 10 patients with amenorrhea-galactorrhea. Seven of these patients were euthyroid and the other 3 had hypothyroidism. The patients in the euthyroid group received 50 mug of T3 daily for 7 days and 75 mug q.d. for the ensuing 14 days. The hypothyroid patients received T3 at progressively increasing doses from 10 mug q.d. to 75 mug q.d. during 34 to 68 days. In the initial test, the elevated basal levels of PRL, 61.9 +/- 9.8 ng/ml (Mean +/- SE) exhibited a slight but insignificant net increase (7.7 +/- 2.1 ng/ml) after TRH injection in the euthyroid group. However, a marked response to TRH with a net increase of 147.2 +/- 26.3 ng/ml from the basal level of 47.3 +/- 11.2 ng/ml was observed in the hypothyroid patients. After treatment with T3, both the basal level (56.9 +/- 8.3 ng/ml) and the net increase (9.9 +/- 3.6 ng/ml) of PRL following TRH stimulation remained virtually unchanged in the euthyroid group. The hypothyroid group, in contrast, displayed a significant depression of both the basal level (26.1 +/- 13.0 ng/ml) and the net increase (33.8 +/- 6.5 ng/ml) of PRL to TRH stimulation. The diminution of the basal levels and responses of thyroid-stimulating hormone (TSH) to TRH stimulation was observed in all cases of both groups. These results suggest that the level of thyroid hormone has little pathogenic role in PRL secretion in euthyroid patients with amenorrhea-galactorrhea, in contrast to its marked effect in hypothyroid patients with amenorrhea-galactorrhea.
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PMID:Effect of triiodothyronine treatment on prolactin secretion in patients with amenorrhea-galactorrhea. 40 25

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 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

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 effect of long-term diphenylhydantoin (DPH) treatment on thyroid hormone concentrations and protein binding was determined in a randomized controlled trial. As has been demonstrated previously, total thyroxine (T4) concentrations were significantly depressed in patients on DPH. There was no significant effect on indirect indices of protein binding of thyroid hormones, and the free thyroxine index (FTI) was also significantly depressed. Triiodothyronine (T3) and thyrotrophin (TSH) concentrations were either unaffected, or only very slightly affected by DPH. Significant effects on the FTI were still apparent 4 weeks after discontinuing treatment. It is concluded that the depression of total T4 levels observed in vivo is not due solely to diminished protein binding, but may instead be largely explained by reports suggesting enhanced degradation of T4 following DPH therapy.
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PMID:Thyroid hormone levels and protein binding in patients on long-term diphenylhydantoin treatment. 87 45

Alveolar hypoventilation is known to occur in myxedema. To clarify the role of hypoxic ventilatory drive and hypercapnic ventilatory drive in thyroid hormone insufficiency states, 10 patients with myxedema and seven with hypothyroidism (thyroid ablation) were studied before and after thyroid replacement. An index developed for hypoxic ventilatory drive was markedly reduced in myxedema: 17 plus or minus 4.7 (S.E.M.) (normal, 126 plus or minus 8.7) (P smaller than 0.01) and increased to 78 plus or minus 12.6 (p = 0.02) with thyroid hormone replacement. In the hypothyroid group this index was also depressed as compared to normal at 67 plus or minus 20 (p smaller than 0.01) and increased to 114 plus or minus 19 (p smaller than 0.02) with replacement. An index for hypercapnic ventilatory drive was depressed in myxedema, 0.69 plus or minus 0.01), but was not significantly depressed in hypothyroidism. With thyroid hormone replacement this index did not significantly increase in either group. We conclude that both myxedema and hypothyroid states produce depression of hypoxic ventilatory drive that is responsive to replacement therapy. This alteration in ventilatory control may contribute to the hypoventilation seen in myxedema.
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PMID:Ventilatory control in myxedema and hypothyroidism. 111 61


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