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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients who met Research Diagnostic Criteria for a history of bipolar affective disorder gave informed consent for open discontinuation of lithium therapy for 3 weeks. There was no significant change after lithium discontinuation in the number of depressive or manic symptoms, in mood score, in total Zung Depression score, or in any of the 20 items found in the Zung Depression scale. There were significant reductions in total severity of side effects, and improvement in the three side effects reflecting renal function: polydipsia, polyuria, and nocturia. These changes were reflected in the significant increase in urine specific gravity. Significant changes in side effects did not take place until at least 2 weeks after lithium was discontinued. Other significant relationships were found between increases in serum thyroid hormone levels and in urine specific gravity, and decreases in Vmax of platelet serotonin uptake and increases in degree of clonidine-induced hypotension.
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PMID:Clinical and laboratory effects of discontinuation of lithium prophylaxis. 402 76

Postmenopausal patients with metastatic breast cancer were treated with medroxyprogesterone acetate (MPA) (Clinovir) in dosages between 500 and 1500 mg orally per day. The relation of MPA plasma concentrations and endocrine effects were studied in a longitudinal fashion. MPA exerted suppressive effects on the basal and gonadotropin-releasing hormone (GnRH) stimulated gonadotropin secretion, cortisol, dehydroepiandrosterone (DHEA), and estradiol (E2) in a dose-dependent manner leading to a complete suppression with 1500 mg orally per day. The depression of thyroid hormones (T3 and T4) coincided with a depression of the thyroxine-binding index (TBI). MPA did not affect human growth hormone (hGH), basal and thyrotropin-releasing hormone (TRH) stimulated thyroid-stimulating hormone (TSH) and aldosterone. Basal and TRH-stimulated prolactin (PRL) secretion showed a slight but distinct elevation. From these data it is concluded that in postmenopausal patients MPA exerts its antitumor activity by an interference with the hypothalamo-pituitary adrenal axis in the sense of a selective pharmacologic hypophysectomy leading to complete suppression of adrenal steroid secretion. Additionally, MPA inhibits tumor cell growth through the progesterone receptor. A dual mechanism for the antitumor activity of high dose is postulated MPA: ablative through suppression of the hypothalamo-pituitary-adrenal axis and subsequent estrogen deprivation, and additive via the progesterone receptor directly on the tumor cell. The significance of gonadotropin suppression in the postmenopause for breast cancer growth is unclear. The depression of T3 and T4 is due to a depression of thyroid hormone-binding proteins. The elevation of PRL secretion may be explained by a slight estrogenic activity of MPA metabolites.
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PMID:Pharmacokinetic and pharmacodynamic basis for the treatment of metastatic breast cancer with high-dose medroxyprogesterone acetate. 608 20

1. Effects of thyroid hormone on the development of neuromuscular junctions (n.m.j.s.) were investigated electrophysiologically in the diaphragms (sternal region) of normal, hypo- and hyperthyroid rats from the age of birth (day 0) to day 35.2. Hypothyroidism in new-born rats was induced either by daily administration of propylthiouracil to mothers or by subcutaneous injection of 150 muCi (131)I on day 1. Hyperthyroidism was induced by daily injection of thyroxine.3. In normal rats up to day 10, muscle fibres were innervated polyneuronally. By day 20, multiple innervation was eliminated and muscle fibres received only a single input. In hypothyroid rats elimination of polyneuronal innervation was retarded by 5-8 days, while in hyperthyroid rats the elimination was accelerated by 2-3 days.4. The frequency of miniature end-plate potentials (m.e.p.p.s) in normal rats increased from one per 40 sec on days 0-5 to 1/sec on days 25-35. The m.e.p.p. frequency in hypothyroid rats was 25-65% of that in normal rats of the same age. In hyperthyroid rats the m.e.p.p. frequency was normal up to day 18 but subnormal afterwards. The duration of m.e.p.p. measured on day 22-23 was slower in hypothyroid rats and faster in hyperthyroid rats, relative to m.e.p.ps in normal rats.5. The sensitivity to acetylcholine (ACh) at extrajunctional regions in normal rats was about 100 mV/nC at birth and declined to 1 mV/nC by day 26. In hypothyroid rats, the ACh sensitivity was as high as 30 mV/nC on day 26; in hyperthyroid rats, ACh sensitivity on day 26 was undetectable.6. With pairs of nerve stimuli (applied at a 50 msec interval), the second end-plate potential was facilitated until day 10 and depressed after day 16 in normal rats. This shift from facilitation to depression during development was not altered in either hypo-or hyperthyroid rats.7. It is concluded that the lack and excess of thyroid hormone retards and facilitates the development of n.m.j.s. respectively. Possible mechanisms for this altered development are discussed.
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PMID:Altered developmental changes of neuromuscular junction in hypo- and hyperthyroid rats. 612 7

The effects of insulin and thyroid hormone treatments on cardiac sarcoplasmic reticular function were investigated in chronic streptozotocin-induced diabetes in rats. ATP-dependent Ca2+ transport and Ca2+-stimulated ATPase activities were depressed significantly in microsomal samples from diabetic rats in comparison with control (P less than 0.05). This defect was seen at various times of incubation (1-20 min) and different concentrations of free Ca2+ (10(-7) to 10(-5) M Ca2+) and was accompanied by changes in the protein composition and phospholipid contents of the microsomal fraction. The defect in calcium transport in microsomal vesicles was not evident until 28 days after streptozotocin (65 mg/kg iv) injection, whereas increases in plasma glucose levels due to insulin-deficiency occurred within 3 days. All changes in function and composition of the sarcoplasmic reticulum were reversed by insulin administration to the diabetic rats. Although the plasma level of thyroid hormone was decreased in the diabetic rat, thyroid hormone treatment did not restore microsomal calcium transport in the diabetic animals. The results of this study provide some evidence that the depression in cardiac sarcoplasmic reticular calcium accumulation during diabetes is a consequence of insulin deficiency and associated chronic metabolic changes but the hypothyroid condition that accompanies experimental diabetes does not appear to play any role in this defect.
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PMID:Defective sarcoplasmic reticular calcium transport in diabetic cardiomyopathy. 613 70

Nineteen patients with overt hypothyroidism were examined for the prevalence of myocardial disfunction, respiratory disturbances, peripheral neuropathy, and visual failure due to pituitary enlargement. Prevalences of pericardial effusion and myocardial disfunction (decrease PEP/LVET) were 50% and 75%, respectively. The degree of decreased myocardial function did not parallel with the grade of pericardial effusion. Arterial blood analysis indicated a frequent incidence of hypoxia in hypothyroidism. The incidence of hypoxia was 69%. The hypoxia was improved by thyroxine replacement therapy. In 6 patients examined for the ventilatory control, all had the index for hypercapnic ventilatory drive lower than normal control. It was suggested that the hypoxia in hypothyroidism was caused by a depression of the respiratory center in the brain and by anemia. Sensory nerve conduction was diminished in 6 of 11 hypothyroid patients and motor conduction in 6 of 15 was studied. In distal segments of sensory nerves, the abnormality frequently appeared before clinical symptoms of polyneuropathy. Visual field defect was detected in 71% of patients suffering of primary hypothyroidism. The most common characteristic change was the defect in the central visual field. All cases of visual field defect were cured by thyroid hormone replacement therapy. Two cases with deteriorated visual failure who did not improve during physiological replacement, were successively treated with over dosage of thyroid hormone.
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PMID:Unusual manifestations in primary hypothyroidism. 622 84

Studies of erythrocyte (RBC) cation fluxes and concentrations in hyperthyroid subjects have recently been reported with the suggestion that Na-K ATPase activity was decreased. We have studied tha kinetics of total and ouabain-sensitive K+ uptake utilizing 86Rb as a tracer in the intact erythrocytes of 7 hyperthyroid subjects and compared the results of those of a healthy control population. We find total K+ transport is depressed in the RBC of hyperthyroid subjects. The Vmax for K+ transport for hyperthyroid subjects is 1.8 +/- 0.17 x 10(-4) mM K+/10(9) RBC/hour versus a control of 2.3 +/- 0.14 x 10(-4) mM K+/10(9) RBC/hour. This depression in Vmax is evident in spite of no significant differences in the Km for the system when hyperthyroid subjects (2.7 +/- 0.19 mM) are compared to controls (2.38 +/- 0.21 mM). Further, the depressed K+ transport appears to be the result of depressed ouabain--insensitive K+ transport. Although the percent of the ouabain-sensitive K+ transport is greater in the hyperthyroid subject (82.5%) versus controls (72.5%), this simply reflects a relative change in a system where total transport is dropping but the ouabain-sensitive component is remaining unchanged. None of these findings can be directly or indirectly related to thyroid hormone and it is suggested that the ion transport changes reflect factors independent of thyroid hormone.
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PMID:Cation transport in intact erythrocytes of hyperthyroid patients: role of the NaK-ATPase pump. 627 79

This review of thyroid influence on body growth in poultry is organized around the following parameters of growth: increase in body weight and skeletal size, muscle growth, and growth of cartilage and bone. The greatest effect of goitrogens on growth of embryos occurs during late embryogenesis at a time when normal thyroid hormone levels are increasing. Posthatching growth is reduced in severely hypothyroid animals, and body weight gain is affected more than bone growth. Thyroid hormone replacement restores body growth of thyroidectomized chickens, but supplemental hormone in normal animals has no beneficial effect on growth. Excessive T3 (fed at 1 ppm) is detrimental to growth and feed efficiency. No clear correlation between thyroid hormone concentration and growth rate of normal chickens has been identified. Growth depression in sex-linked dwarf birds is at least partially reversed by supplemental T3. Muscle growth is reduced in goitrogen-treated chickens and the growth reduction is reversed by supplemental thyroxine. Total DNA accumulation is reduced in hypothyroid chickens, but muscle mass relative to DNA content is normal following long-term treatment; this suggests some regulation of muscle mass relative to DNA content. T3 increases the number of muscle fiber nuclei in hypothyroid chickens and the uptake of 3H-thymidine into nuclei within the basal lamina. T3 directly stimulates growth and maturation of embryonic chick cartilage and enhances the in vitro action of somatomedins on cartilage growth. There is little information concerning the role of the thyroid in posthatching cartilage and bone growth in poultry.
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PMID:Thyroidal influence on body growth. 639 92

It has been generally accepted that increased thyroid function facilitates treatment response in depression. Recent data show that response to several antidepressant treatments, particularly lithium and carbamazepine, are associated with decreased thyroid hormone levels. An alternative hypothesis that decreased thyroid indices are related to antidepressant response is proposed and clinical and research implications are discussed.
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PMID:Thyroid function and affective illness: a reappraisal. 644 Jun

Transient hypothyroidism was observed in two young women a few months following childbirth. It is suggested that throughout their pregnancy they had already suffered from auto-immune thyroiditis, the symptoms of which were suppressed at that time, as found in many other auto-immune diseases. Being transient, post-partum hypothyroidism is an exception to the rule that treatment by thyroid hormone replacement should never be stopped in hypothyroidism. Post-partum hypothyroidism has to be considered in every suspected case of post-partum depression, because of the possible similarity in the clinical presentation.
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PMID:Transient post-partum hypothyroidism. 668 61

Alterations in circulating thyroid hormone concentrations occur in a variety of nonthyroidal disease states. In the present study, thyroid hormone levels were measured every 8 to 12 hours in 19 otherwise healthy individuals suffering acute severe trauma necessitating admission to the Maryland Institute for Emergency Medical Services Systems. Four fatalities occurred within 48 hours of admission. The mean total T3 level fell rapidly after the onset of trauma and remained low throughout the observation period. Reverse T3 rose concurrent with the fall in T3 but gradually returned to normal in the survivors. Total and free T4 levels remained normal in the survivors but fell below normal in the fatalities on the samples obtained preceding death. Changes in free T4 were consistent in three separate radioimmunoassay systems. Pharmacologic doses of glucocorticoids administered to seven of the 15 survivors and to the four fatalities did not result in an acute depression in total and free T4 levels in the survivors. Post-mortem examination of three fatalities did not reveal evidence of significant thyroid or pituitary disease. These results suggest that in acutely traumatized patients: 1) T3 declines rapidly and remains depressed throughout the illness; 2) continued fall of T4 to subnormal levels is associated with a poor prognosis; and 3) steroid therapy alone cannot explain the acute changes observed in hormone levels.
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PMID:Circulating thyroid hormone changes in acute trauma: prognostic implications for clinical outcome. 669 35


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