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

Numerous endocrine abnormalities are found in depressive illness and, among these, several have been proposed as useful markers in diagnosis, prediction of treatment response, monitoring treatment outcome or in understanding of etiology. This paper reviews five endocrine systems--the hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-thyroid axis, growth hormone regulation, prolactin regulation and pineal function, in which such abnormalities have been reported. The dexamethasone suppression test (DST) results are affected by a variety of other diseases and confounding conditions. Furthermore, variability in dexamethasone availability has recently been shown to be an important factor, influencing post-DST cortisol levels. Refined tests, taking into account all these factors, or alternative tests of hypothalamic-pituitary-adrenal function may lead to improved clinical utility. Pineal function is now the focus of considerable investigation. Low nocturnal output of melatonin is found in unipolar and bipolar affective disorder and is normalized by treatment with antidepressant drugs which block re-uptake of noradrenaline. These findings support the hypothesis of noradrenergic abnormality in depression. In seasonal affective disorder there is evidence for a phase delay in the melatonin rhythm which may be a key factor in the seasonal disorder. Effective light therapy causes a phase advance in the abnormal melatonin rhythm. Whether the normalization of the melatonin rhythm is instrumental in producing the antidepressant effect is yet to be determined. There are wide spread neuroendocrine abnormalities in depressive illness. These abnormalities encompass many different pituitary hormones, as well as the pineal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine probes as biological markers of affective disorders: new directions. 268 81

This study was undertaken to assess the value of growth hormone (GH) response to clonidine as a tool in the differential diagnosis between depression and dementia. This response is known to be blunted in depression, and neurochemical changes observed in senile dementia of the Alzheimer type (SDAT) could lead to an up-regulation of GH secretion. No difference was observed between GH response in depressed and demented patients. Together with studies on GH basal secretion in Alzheimer's disease, this finding suggests that the final consequence of SDAT-related changes in an accentuation of the effects of aging on GH reactivity.
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PMID:Clonidine-induced growth hormone secretion in elderly patients with senile dementia of the Alzheimer type and major depressive disorder. 271 Aug 69

The dexamethasone suppression test (DST) was performed in 38 patients satisfying the Research Diagnostic Criteria (RDC) for cortisol, human growth hormone (hGH), prolactin, triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH) were determined at 4:00 p.m. before the administration of dexamethasone, whereas cortisol, hGH and TSH were determined at 4:00 p.m. the day after. Among hormonal variables, only cortisol index (the ratio of the pre-DST cortisol to the post-DST cortisol) was barely useful for discriminating depression. The cortisol index was also correlated with RDC incapacitating subcategory and with symptoms of affect such as depressed mood and psychic anxiety.
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PMID:Hormonal changes in major depressive disorder. 271 17

Abnormalities in several hypothalamic-pituitary-target organ axes in depression may reflect alterations in central neurotransmitter receptor function. As the alpha 2-adrenergic receptor has been implicated in a variety of neuroendocrine abnormalities in depression, we assessed the role of alpha 2-adrenoceptor dysfunction in mediating response abnormalities of growth hormone, cortisol, and prolactin after intravenous clonidine administration (an alpha 2-adrenergic receptor agonist) in 18 patients with major depression (12 with melancholic features, 6 without melancholic symptoms) and 9 healthy volunteers. In particular, we examined the hypothesis that these abnormalities might be more evident in patients with DSM-III melancholic depression. After clonidine, the mean growth hormone response was significantly lower in melancholic depressives compared to controls (p = 0.02), and the shape of the growth hormone response profile was also significantly different in melancholic patients (p = 0.04). There was an overall decrease in the mean cortisol concentration after clonidine in melancholic patients and control subjects (p = 0.02), as well as a larger cumulative prolactin response in melancholic patients compared to those without melancholic features (p = 0.02). The present results confirm prior observations of a blunted growth hormone response after clonidine and suggest that alterations in alpha 2-adrenergic receptor activity might also contribute to several neuroendocrine abnormalities in patients with melancholic depression.
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PMID:Multiple hormone responses to clonidine administration in depressed patients and healthy volunteers. 274 43

Studies of the mode of action of antidepressant treatments and the biological basis of depression have recently concentrated on monoamine neurotransmitter receptors. This paper reviews the studies relating to alpha 2-adrenoceptors. Chronic administration of some but not all antidepressant treatments to animals alters the number and function of brain alpha 2-adrenoceptors. In man, platelet alpha 2-adrenoceptors have been widely studied as a quantifiable peripheral model of central alpha 2-adrenoceptors. The majority of studies have not identified clear differences in platelet alpha 2-adrenoceptors between drug-free depressed patients and control subjects, nor have they identified unequivocal effects of antidepressant treatments. Methodological problems and choice of radioligand may contribute to discrepancies between studies. Central alpha 2-adrenoceptor function in man has been assessed by measuring neuroendocrine and physiological responses to clonidine. Despite considerable variation in procedure, in diagnostic criteria, and in the interval since previous treatment, most studies find the growth hormone response attenuated in depressed patients. This provides the strongest evidence to date of an abnormality of alpha 2-adrenoceptors in depression. However, it seems likely that none of the measures to date adequately mirrors the function of the cortical and limbic receptors implicated in the pathophysiology of depression. It is also likely that no single neurotransmitter abnormality is common to all depressed subjects and that future studies should be aimed at the inter-relationship and dysregulation of several neurotransmitter systems.
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PMID:Alpha 2-adrenoceptors in depression. 281 61

Responses to intravenous clonidine, a possible central noradrenergic probe, were examined in patients with depression before and after treatment with clorgiline, a selective monoamine oxidase type A inhibitor. Pulse rate, mean arterial blood pressure, plasma norepinephrine, 3-methoxy-4-hydroxyphenylglycol, and growth hormone were measured. Clorgiline treatment (2.5 to 10 mg/day) produced a variable reduction in the hypotensive response to clonidine but did not influence heart rate or plasma norepinephrine responses. Clorgiline markedly reduced the urinary output of norepinephrine and metabolites, indicating a reduced turnover of norepinephrine. None of the measured parameters corresponded with clinical effect. These data suggest that any clorgiline-induced alterations in alpha 2-receptor function as measured by responses to clonidine are modest and highly variable. Furthermore, since the variable and inconsistent changes in alpha 2-receptor function are dissociated from the massive changes in norepinephrine metabolism, regulation of presynaptic alpha 2-receptors appears unlikely to mediate the effects of clorgiline in patients with depression.
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PMID:Dissociation of norepinephrine turnover from alpha-2 responses after clorgiline. 282 65

The authors administered the growth hormone-releasing factor (GRF) stimulation test to 19 patients with major depression and 19 age- and sex-matched control subjects to test the hypothesis that a blunted growth hormone (GH) response to clonidine reflects a central alpha 2-adrenergic receptor subsensitivity in depression. GH response to GRF was significantly higher in patients with depression than in control subjects. This group difference was mainly attributable to three of the 19 depressed patients who exhibited markedly high GH responses to GRF. These results suggest that the blunted GH response to clonidine seen in patients with depression is not due to a pituitary defect in GH secretion.
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PMID:Growth hormone-releasing factor stimulation test in depression. 282 32

Eighteen patients with major depressive disorder of the endogenous subtype (8 unipolars and 10 bipolars) were submitted to blood sampling at 15 min interval for 24 h with polygraphic sleep recording during an acute episode of depression. Plasma growth hormone (GH), adrenocorticotrophin (ACTH) and cortisol were measured in each sample. The depressed patients hypersecreted GH during the daytime and had hypercortisolism which was evident throughout the 24 h span. The nadir of ACTH and cortisol rhythms was advanced by an average of 3 h as compared to the timing observed in normal subjects. These abnormalities were more pronounced and more consistent in patients with unipolar rather than bipolar depression. These results are consistent with the hypothesis that disorders of circadian time-keeping may characterize major endogenous depression.
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PMID:[Neuroendocrine rhythms in uni- and bipolar depressions]. 283 36

Analgesic concentrations of nitrous oxide were administered to 6 healthy male subjects, and blood samples were assayed for prolactin, ACTH, follicle stimulating hormone, luteinising hormone, growth hormone, cortisol and thyroid hormones. Analgesic nitrous oxide (mean concentration = 48.8%) produced statistically significant elevation of prolactin and depression of cortisol whilst not producing statistically significant changes in the other hormones assayed. The increase in prolactin and decrease in cortisol levels are similar to the hormonal changes associated with administration of opioids in man. We have also confirmed the findings of other workers that cortisol levels may not always be correlated with ACTH levels.
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PMID:Hormonal responses to analgesic nitrous oxide in man. 285 16

A blunted growth hormone (GH) response to clonidine and other pharmacologic stimuli has been reported in patients with depression. This blunted growth hormone response to clonidine has led to the speculation that there is a central alpha-2 adrenergic receptor subsensitivity in depression. This hypothesis is based on the assumption that the pituitary somatotroph response to growth hormone-releasing factor (GHRF) is not altered in depression. In the present preliminary study, the somatotroph response to GHRF in depressed patients and normal controls has been evaluated in four depressed patients and four age- and sex-matched controls. The GH response to GRF is highly variable both in normal individuals and in the depressed patients studied. Larger numbers of patients and controls must be studied before any definitive conclusions can be drawn about GH responses to GRF in depressed patients.
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PMID:Growth hormone response to growth hormone-releasing factor in depression. 285 37


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