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)

Fifty-six patients with acromegaly were treated with external irradiation, 50 Gy, after unsuccessful pituitary surgery. A 50% reduction of pre-irradiation growth hormone levels was obtained in 51/56 patients. This level was reached after 26 +/- 14 months in 33 patients with prolactin levels less than 25 micrograms/l at diagnosis, after 21 +/- 17 months in 18 patients with prolactin greater than or equal to 25 micrograms/l, and after 20 +/- 21 months in 12 patients with prolactin greater than 40 micrograms/l at diagnosis. A further 50% decrease of growth hormone levels was obtained in 40/51 patients 42 +/- 22 months after radiotherapy, indicating that in clearly responsive patients, the growth hormone depression after radiotherapy follows a first order reaction. Four patients did not reach a 50% reduction of growth hormone levels 48-80 months after radiotherapy. During 10 years of follow-up, the growth hormone depression tended to be more pronounced in patients with mixed secretion of growth hormone and prolactin. The reduction of growth hormone levels was not correlated with the irradiated volume or the cumulative radiation effect. Within the first year, prolactin increased within the normal range in normoprolactinemic patients and remained so during follow-up. In hyperprolactinemic patients, prolactin decreased successively but to a lesser extent than growth hormone. Pituitary insufficiencies increased over time and three patients developed GH-insufficiency. Hypothalamic damage as indicated by prolactin changes was a regular phenomenon after radiotherapy.
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PMID:External irradiation of growth hormone producing pituitary adenomas: prolactin as a marker of hypothalamic and pituitary effects. 200 40

Twelve depressed adolescents and 12 controls matched for age, sex, Tanner stage, time of menstrual cycle (females), weight, and time of year assessed were studied over 3 nights. Measurements for cortisol, thyroid stimulating hormone, and growth hormone were made on serum collected at 10 P.M., 12 midnight, 1 A.M., 2 A.M., 3 A.M., 4 A.M., and 6 A.M. in eight pairs and every 20 minutes from 8 P.M. to 7 A.M. in four pairs. Cortisol secretion did not significantly differentiate the groups. Thyroid stimulating hormone secretion was significantly elevated in the depressed group at one time point. Growth hormone secretion significantly differentiated the two groups at most time points, and the depressed adolescents significantly hypersecreted growth hormone (area under the curve). Implications for the diagnosis, etiology, and treatment of adolescent depression are discussed.
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PMID:Nocturnal cortisol, thyroid stimulating hormone, and growth hormone secretory profiles in depressed adolescents. 178 55

Because of its neuroendocrine effects, amphetamine infusion has been used as a probe to investigate neurobiological correlates of depressive illness. In two separate studies, a total of 72 adolescents with major depressive disorder and 66 normal adolescents were given dextroamphetamine, 0.15 mg/kg, intravenously. Their cortisol, growth hormone, and prolactin responses were measured. These endocrine responses did not reliably distinguish adolescents with major depressive disorder from those without it, nor did they reliably delineate any specific depressive subgroup. These findings are compared with those from similar studies of adult depression.
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PMID:Hormonal responses to dextroamphetamine in depressed and normal adolescents. 205 77

There is circumstantial evidence that increases in prolactin secretion evoked by L-tryptophan infusion involve 5-HT1 receptors, whereas growth hormone responses do not. Propranolol is a beta-adrenoceptor antagonist that also possesses antagonist properties at 5-HT1 receptors. Propranolol (80 mg, PO) failed to attenuate the prolactin response to L-tryptophan infusion (100 mg/kg, IV) in seven volunteers; the role of 5-HT1 receptors in this response remains uncertain. The growth hormone response to tryptophan was enhanced by propranolol, consistent with previous reports of an inhibitory beta-adrenoceptor influence on GH secretion. Excessive beta-adrenoceptor function might explain the blunted growth hormone response to tryptophan in depression.
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PMID:Hormonal response to L-tryptophan infusion: effect of propranolol. 208 37

Plasma noradrenaline (NA), adrenaline (A), dopamine (DA), platelet serotonin (pS), free serotonin (fS), cortisol (CRT), growth hormone (GH), peripheral blood lymphocytes (lymph), lymphocyte subpopulations (LSS) and CD4/CD8 ratio were serially assessed in 50 non-medicated, advanced cancer patients (spontaneous evolution) and in age- and sex-paired controls. Clonidine tests and psychiatric evaluations were also serially performed. Patients showing long symptomless periods had all normal values except for raised pS, whereas those who remained free of symptoms for only a short time had raised NA, A and CRT, plus lowered pS values. Further increases in NA, A and CRT, plus additional increases in DA and fS, occurred during exacerbation periods, during which times reductions in lymph, LSS and NK also were observed. Patients in terminal stages showed maximal decreases of all neurotransmitters and immunological parameters; only DA and fS remained raised. Psychiatric interviews performed simultaneously with the clonidine tests revealed a low incidence of moderate depression during symptomless periods and no depression during exacerbation periods. Several significant positive and negative correlations between neurotransmitters and immunological parameters were found during exacerbation periods. Pain, although not intense, and other symptoms required occasional administration of low doses of non-opiate analgesics.
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PMID:Psychoneuroendocrinological and immunological parameters in cancer patients: involvement of stress and depression. 210 65

To determine the extent of dysregulation of growth hormone (GH) secretion in endogenous depression, we measured nocturnal serum GH concentrations and GH responses to thyrotropin-releasing hormone (TRH, gonadotropin-releasing hormone (LHRH), and dexamethasone administration in 40 Research Diagnostic Criteria primary, definite endogenous depressives and 40 individually matched normal control subjects. Compared with their controls, the patients showed no difference in basal nocturnal GH concentrations or in GH responses to TRH or LHRH. The GH measures were not significantly related to the other endocrine measures reported previously, including dexamethasone suppression test status. None of the diagnostic schemes for endogenous/melancholic depression which we studied was significantly related to the GH measures in the patients. Of the other subject and symptom variables, the mood depression factor of the Hamilton depression scale and the performance difficulty factor of the Beck depression inventory were moderately negatively correlated with the nocturnal GH measures. These findings suggest that, in contrast to the previously reported hypothalamopituitary-adrenal cortical and thyroid axis abnormalities in our patients, GH secretion was relatively normal. Patients with more severe depressed mood and greater difficulty accomplishing tasks did have moderately lower nocturnal GH values.
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PMID:Neuroendocrine aspects of primary endogenous depression. X: Serum growth hormone measures in patients and matched control subjects. 211 Nov 83

In a recent report, we confirmed the role of dopamine in the pathophysiology of depression by demonstrating a blunted response of growth hormone (GH) to apomorphine, a selective dopaminergic agonist, in endogenous depressive patients. Few data are available on the possible psychopathological correlates of disturbances in the apomorphine test. In this study, we assessed the relationship between GH response to apomorphine and the Minnesota multiphasic personality inventory (MMPI) scales in a sample of 20 major depressive inpatients. The GH response (area under the curve) after apomorphine injection was positively correlated with the social introversion scale scores (r = 0.56, df = 19, p less than 0.01) and the anxiety scale scores (r = 0.45, df = 19, p = 0.04). These results suggest dopaminergic overactivity in anxious psychopathology rather than in depressive psychopathology. The relationship between the social introversion scale score and the apomorphine test is in agreement with the dopaminergic hypothesis of schizophrenic disorders.
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PMID:Psychopathological correlates of dopaminergic disturbances in major depression. 213 7

Thirty drug-free patients fulfilling the DSM-III criteria for major depression serially underwent the dexamethasone suppression test (DST), thyroid stimulating hormone (TSH) test and a growth hormone (GH) challenge test with oral desipramine. Fifty-three per cent of the sample showed a blunted GH response, 47% were DST non-suppressors while 26% had a blunted TSH response. Eighty per cent of patients showed some biological abnormality. There was no clear association between any of these abnormalities. Neither was there any association between the neuroendocrine parameters studied and the severity of depression or patient gender. There was a trend for increasing GH blunting and DST non-suppression with increasing age.
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PMID:Neuroendocrine challenge tests in depression: a study of growth hormone, TRH and cortisol release. 214 Mar 74

Incubation of cultured goldfish pituitary cells with 10 nM to 1 microM apomorphine (APO), a non-selective dopamine agonist, increased growth hormone (GH) release in a dose-dependent manner. GH release was also stimulated in a dose-dependent manner by 0.1 nM to 1 microM salmon gonadotropin (GTH)-releasing hormone (sGnRH), sGnRH analog, and chicken GnRH-II (cGnRH-II). The magnitude of GH responses to 1 microM GnRHs were less than that to 1 microM APO. GH responses to 10 nM to 1 microM APO were not significantly increased by the addition of GnRHs. Static incubations with 0.1 nM to 1 microM of the dopamine D1 agonist SKF38393 did not alter basal GTH release, or the GTH responses to 10 nM sGnRH and cGnRH-II. In contrast, the D1 agonist SKF38393 significantly increased basal GH secretion with maximal stimulation achieved at 100 nM concentration, and GH responses to 10 nM sGnRH and 10 nM cGnRH-II were enhanced by simultaneous applications of SKF38393. Incubation with 1 microM of the D2 agonist LY171555 decreased basal GTH release. Additions of 0.1 nM to 1 microM LY171555 caused dose-dependent decreases in the GTH secretion induced by 10 nM sGnRH and cGnRH-II. In contrast, basal and GnRH-stimulated GH release were not affected by coincubations with LY171555. The D1 antagonist SKF83566 and the D2 antagonist domperidone, at 1 microM concentrations, specifically blocked the D1 agonist SKF38393-stimulated increase in GH release and the D2 agonist LY171555-induced depression of GTH secretion, respectively. In cell column perifusion studies, the D1 agonist SKF38393 at 0.1 nM to 1 microM had no effects on GTH release, but significantly elevated GH secretion rates when applied at 0.1-1 microM concentrations. The GH release induced by 1 microM SKF38393 was significantly reduced by simultaneous perifusion with 1 microM of the D1 antagonist SKF83566. Treatments with SKF38393 and/or SKF83566 did not affect net GTH and GH responses to sGnRH challenges. In contrast, perifusion with 0.1 and 1 microM of the D2 agonist LY171555 depressed basal as well as sGnRH-induced GTH responses. These effects of 1 microM LY171555 were completely blocked by simultaneous applications of 1 microM domperidone, a D2 antagonist. Treatments with these D2 selective drugs did not affect basal and sGnRH-stimulated GH release. These results indicate that in cultured goldfish pituitary cells, activation of dopamine D1- and D2-like receptors specifically stimulates GH release and inhibits both basal and stimulated GTH secretion, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differential actions of dopamine receptor subtypes on gonadotropin and growth hormone release in vitro in goldfish. 214 20

The growth hormone (GH) response to desipramine was measured in ten patients meeting criteria for post-stroke depression (PSD), eight age-matched post-stroke (PS) non-depressed patients and eight healthy controls. Responses were significantly blunted in patients with PSD. These findings suggest diminished alpha-2 adrenoceptor function may be an important marker for PSD.
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PMID:Alpha-2 adrenergic receptor function in post-stroke depression. 216 47


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