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

In order to find the correlation between dexamethasone suppression test (DST) and TSH response to TRH in the differential diagnosis of subtypes of depression, and to evaluate the possible relationship between Hypothalamic-Pituitary-Adreno-cortisol axis, Hypothalamic-Pituitary-Thyroid axis function, psychopathological symptoms, and the possible influence of age and sex, 107 depressed patients were studied. The relationship between both tests (DST and THS response to TRH) and the subtypes of depression was unspecific. The results did not show psychopathologic differences between depression subgroups. DST appeared to be a good marker for the "state" of illness, whereas TSH was better as a predictor for the outcome.
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PMID:[Usefulness of neuroendocrine function tests in the differential diagnosis of depression]. 251 35

A neuroendocrine study was conducted in eight children and adolescents with dysthymic disorders (three females and five males) and in eight age- and sex-matched psychologically normal controls. The dexamethasone suppression test (DST), TSH and GH responses to TRH stimulation and GH response to clonidine stimulation were studied in parallel in each patient. Depressive symptomatology was monitored with the Poznanski Rating Scale. The DST, TRH and clonidine tests revealed normal responses in each patient. TRH induced abnormal GH rises in five of the eight patients. There were no correlations between neuroendocrine parameters and degree of depression, age, sex or weight of the patients, age of onset, duration and family history of the disease.
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PMID:Neuroendocrine investigation in children and adolescents with dysthymic disorders: the DST, TRH and clonidine tests. 252 97

Several endocrine parameters were assessed in 35 alcoholic inpatients after admission to hospital, and 17 of the 35 were retested after several weeks of sobriety. No difference was found in clonidine-stimulated growth hormone (GH) secretion between male alcoholics and male healthy controls, but significant positive correlations of GH secretion and alcohol content in expired breath on admission and gamma-GT values after abstinence were observed. Nonsuppression in the dexamethasone suppression test was found in 17% of the patients on admission, which seemed to be due to alcohol withdrawal. Postdexamethasone cortisol levels were significantly positively correlated with the "apathic syndrome" (r = 0.40; p less than or equal to 0.05). About one-third of the patients showed a blunted response in the TRH-test both on admission and after abstinence. No significant influence of alcohol intake, withdrawal or familial disposition on prolactin values could be detected. The results of the TRH test and the DST point to similar endocrinological patterns in alcoholics as in depressive patients and thus support the hypothesis of a link between alcoholism and depression.
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PMID:Endocrinological studies in alcoholics during withdrawal and after abstinence. 254 97

Current theories of affective disorders do not account for many of the biological markers replicated in patient studies. We link many biological findings in a reasonable physiological relationship, compatible with mechanisms of action of pharmacological and electroshock therapies for depression. We propose that excessive phospholipase-A2 (PLA2) activity disrupts membrane fluidity, composition, and therefore, the activity, of membrane-dependent proteins. Similar disruptions in these proteins are documented in depressed patients and can be accounted for by excessive PLA2 activity. This paradigm accounts for disturbances in the activity of Na-K-ATPase, beta2- and alpha2-adrenergic receptors, MAO, norepinephrine and serotonin uptake, and imipramine binding. Disturbances in other membrane-dependent proteins, tyrosine and tryptophan hydroxylase, can explain the biogenic amine hypothesis. Inhibition of glucocorticoid receptor and TRH receptor binding to their respective ligands by PLA2 may explain patient nonsuppression in the Dexamethasone Suppression Test and poor response in the TRH stimulation test. Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Thus, postpartum depression and premenstrual tension syndrome may be described in the paradigm. The mechanisms of action of tricyclic antidepressants, lithium, electroconvulsive shock, and some novel antimanic agents can be described in terms of alterations of PLA2 activity. Interestingly, ethanol perturbs membrane fluidity and membrane-bound enzymes in a manner similar to excessive PLA2 activity. A hereditary factor predisposing patients to affective disorders may be a gene defect at either PLA2 or in its regulation.
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PMID:Are disturbances in lipid-protein interactions by phospholipase-A2 a predisposing factor in affective illness? 256 35

The results of 11 experiments in a total of 571 rats (initial body weight of 150-250 g) are reported and some findings differing from those by others are discussed. It was repeatedly found that the animals after bilateral or even unilateral superior cervical sympathetic gangliectomy (GX) did not gain body weight during the first week after surgery. Though they started to grow later, for several weeks their body weight remained significantly less than that of sham operated controls (SH). Though such phenomenon has not yet been described, it may well explain the increase of thyroid weight (as expressed per body weight) after gangliectomy alone or combined with antithyroid drug treatment or hypophysectomy as described by others. It was suggested that such changes may depend on general metabolic changes resulting in a striking inhibition of body weight gain rather than on some specific effect of GX on the thyroid. This view was supported by evaluating the data on absolute and relative thyroid weight from 4 experiments in a total of 265 animals. The level of thyroxine (T4) and thyrotropic hormone (TSG) was repeatedly found to be significantly decreased after GX for until about 72 h and 24 h after surgery, respectively, which was in agreement with the data reported by others. However, the onset of such decrease was repeatedly found to appear at 6 or 8 h after surgery (in one experiment even at 3 h after surgery) which is also contrasting to the onset of T4 decrease at 14 h after surgery as found by others who suggested a correlation of such thyroid depression with a depletion of noradrenaline from the thyroid and may be even from median eminence. In these experiments, however, a decrease of T4 level was found several hours before the depletion of noradrenaline from the thyroid which appeared at 12 h after surgery and remained at similar level until 40 days, while no remarkable changes of that were found in SH animals (with the excretion of slight increase after 24 h). Between about 4 and 40 days after surgery no significant changes in T4 and TSH levels after GX were found as compared with SH animals is in agreement with others.4+n one experiment the increase of T4 at 2 h after TRH injection, resulting apparently from the effect of endogenous TSH, was significantly inhibited in GX animals at 8 days after surgery, while in other experiments (at 8 and 40 days after surgery) no difference in T4 level increase was found in GX animals as compared with SH ones. In general, it may be suggested that superior cervical sympathetic gangliectomy may result in some temporary and perhaps transient changes in pituitary-thyroid function in rats.
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PMID:Studies and reevaluations of some aspects on thyroid function after superior cervical sympathetic gangliectomy in rats. 280 86

TRH and naloxone influence on the clinical hormonal manifestations of the alcohol withdrawal syndrome (AWS) was studied. The results obtained were suggestive of the association of the pathogenesis of symptoms like frustration, skin hyperemia, tachycardia, and raised BP with function of the peptidergic system. It should be noted that symptoms like depression, sleep disturbances and headaches happened to be more sensitive to TRH while sweating is more sensitive to naloxone. A positive therapeutic effect of naloxone in the early period of AWS was likely to result from lowered function of the opiate system. The data obtained led to a preliminary conclusion of a close interrelationship and involvement of the hormonal, peptidergic and opiate systems in AWS pathogenesis, this being an important factor for the understanding of alcohol-induced abnormalities and for the choice of pathogenetically founded therapeutic methods.
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PMID:[Participation of the peptidergic and endogenous opiate systems in the pathogenesis of early manifestations of the alcohol abstinence syndrome]. 283 19

Twelve patients suffering from mental anorexia were examined on clinical and biological grounds, based on the hypothesis of the functional depression of the noradrenergic track. The initial values of MHPG and of catecholamines were below normal. The quantitative results for depression and retardation were lessened significantly under beta-stimulant treatment. Only glucuro-conjugate MHPG excretion increased significantly, but the MHPG values were much lower than normal at the end of the treatment. The correlations between biochemical and behavioural parameters were worth noticing as far as the retardation scale was concerned. The present study shows the advantage of the dexamethasone suppression test and of the response of TSH under TRH.
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PMID:[Disorders of noradrenergic pathways in anorexia nervosa. Results]. 285 80

We investigated the ameliorating effects of DN-1417 (a TRH analog) on the changes of behavior, EEG, neurochemical parameters and regional cerebral blood flow (rCBF) in rats with global cerebral ischemia. Global cerebral ischemia was produced by 10-min occlusion of both common carotid arteries 24 hr after the permanent electrocauterization of bilateral vertebral arteries. DN-1417 was administered intraperitoneally as soon as possible, following recirculation of carotid blood flow. DN-1417 shortened significantly the recovery times of righting reflex (RR) and spontaneous movement (SM) at 2.5 mg/kg and higher doses, and it recovered effectively the EEG activity at 10 mg/kg during recirculation after 10-min cerebral ischemia. In addition, DN-1417 (10 mg/kg) recovered the various changes such as decrease of 5-hydroxytryptamine (5-HT) levels, increase of cyclic AMP (cAMP) levels, inhibition of [3H]-choline uptake, depression of choline acetyltransferase (CAT) and acetylcholine esterase (AChE) activities, and shortened the durations of hyperperfusion and hypoperfusion of rCBF. As a result, it is identified that DN-1417 ameliorates the disturbance of consciousness supposedly caused by behavioral and EEG abnormalities during recirculation following the temporary cerebral ischemia, and the effect of DN-1417 seems to be mediated by normalizing of alterations in the brain monoaminergic and cholinergic systems, as well as rCBF, and the effectiveness for disturbance of consciousness in clinical situations would be expected.
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PMID:[Pharmacological study of the temporary cerebral ischemic rats produced by bilateral vertebral and carotid artery occlusion. Effects of DN-1417]. 286 Nov 49

The finding of a diminished TSH response to exogenously administered TRH in a significant proportion of depressed patients has now been established as one of the most reproducible findings in biological psychiatry. More than 50 reports, in which more than 1000 patients have been studied, reveal that the TSH response is blunted in approximately 25% of patients with major depression. TSH blunting is clearly not specific for depression, because it also has been observed in mania, alcoholism, and borderline personality disorder. It is doubtful that TSH blunting represents a non-specific response to mental stress: it was found only rarely in schizophrenic patients, and the TSH response to in vivo flooding therapy in phobic patients was normal. In both depression and alcoholism, TSH blunting has been reported to be sometimes a state marker and sometimes a trait marker, i.e. the fault was found to persist into remission in more than half the patients. In both conditions, TSH blunting was unrelated to the patients' age, body weight, height, body surface, thyroid status, and serum cortisol concentrations. It also is unlikely that TSH blunting was due to increased dopaminergic inhibition of thyrotroph cells: serum prolactin concentrations in TSH blunters were found to be normal, and pretreatment with haloperidol had no effect on either basal TSH levels or TSH blunting. In depression, TSH blunting was not associated with previous drug intake, dexamethasone suppression test abnormalities, or variables of biogenic amine metabolism, nor did it usefully segregate between primary and secondary depression or between unipolar and bipolar subgroups. Preliminary evidence suggests that TSH blunting in depression may be related to duration of illness, history of violent suicide attempts, and a reduced 24 h TSH secretion. In alcoholism, TSH blunting was unrelated to family or personal history of depression and duration of abstinence. With reference to clinical utility, TSH blunting may aid in assessing the response to antidepressant treatment, predicting outcome to such treatment, assessing the risk for violent suicide attempts, and describing relationships between different psychiatric populations (e.g. depression and alcoholism).
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PMID:The TRH-induced TSH response in psychiatric patients: a possible neuroendocrine marker. 286 65

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.
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PMID:The nature of neuroendocrine abnormalities in depression: a controversial issue in contemporary psychiatry. 288 Mar 46


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