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)

Certain metabolic effects were investigated in post-menopausal women undergoing oral estrogen replacement therapy for 6 months using various substances. The increases in serum concentration of the estrogen-sensitive proteins, pregnancy zone protein (PZP), and sex hormone binding globulin (SHBG) had very similar and dose-dependent patterns. Ethinyl-estradiol was found to be much more potent than the "natural" estrogens. Estriol in various doses did not increase the protein level. Gonadotropin inhibition occurred in a dose-dependent manner. In terms of FSH suppression ethinyl-estradiol was approximately 120 times as potent as the "natural" estrogens. There was a striking resemblance between the "estrogenicity" of four different estrogens when expressed both in inhibition of gonadotropins and in induction of the two serum proteins SHBG and ceruloplasmin. Estriol caused a significant depression of FSH when given orally in a dose of 2 mg three times daily. Prolactin was found to decrease during treatment with low doses of estrogens. Estrogen therapy was found to have only moderate effects on adrenal androgens. Tamoxifen, and anti-estrogen, was found to exert distinctly estrogenic effects during treatment of post-menopausal women. In post-menopausal women with low amounts of circulating estrogens the tamoxifen-receptor complex itself may produce a net estrogenic response. Serum samples from post-menopausal women treated with ethinyl estradiol 0.05 mg and estrone sulphate 2.5 mg daily were found to reduce the lymphocyte reactivity in mixed lymphocyte cultures.
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PMID:Estrogen replacement therapy after the menopause. Estrogenicity and metabolic effects. 628 33

Neuroendocrine strategies in affective disorders have explored both resting values of hormones and hormonal responses to stimuli such as hypoglycemia, TRH, LHRH, dexamethasone, methadone and morphine. The abnormalities established to date have involved growth hormone, cortisol and TSH responses in particular. Prolactin has not been investigated to the same extent. We therefore describe several prolactin studies exemplifying selected neuroendocrine strategies. Our studies of prolactin responses included acute cases of either primary or secondary depression, stabilized bipolar patients, and healthy controls both off and on lithium. We found prolactin response to hypoglycemia significantly reduced in primary but not secondary depressions. Lithium administration led to flattened prolactin responses to hypoglycemia in stabilized bipolar patients but not in healthy controls. The flattened response in patients was observed already after 3 weeks of lithium, and remained flattened after years of treatment. The findings suggest a greater degree of prolactin response reduction in those patients showing most pronounced stability on lithium treatment.
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PMID:Neuroendocrine strategies in affective disorders. 642 Aug 43

1. We tested a group of acutely depressed patients with a neuroendocrine battery and confirmed the alterations of growth hormone response to hypoglycemia and TSH response to TRH reported by others. 2. In addition, in the same patient sample we found markedly reduced response of prolactin to hypoglycemia. 3. Prolactin response remained low when the patients were retested during depression, however, normalization took place on recovery. 4. An attempt is made to explain these findings by underlying neurotransmitter abnormalities.
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PMID:Prolactin response to hypoglycemia in acute depression. 681 97

Prolactin and somatotropin secretory rhythmicity was studied in 7 inhibited depression male patients, evaluated by the Hamilton Rating Scale for depression, before and after trazodone (400 mg i.v. once daily) treatment. The mean 24-hour hormone levels of the patients were comparable to the controls. Trazodone enhances the prolactin value, increasing chiefly the titres during sleep which were lower in respect to controls before treatment. The drug decreases the mean 24-hour somatotropin levels, mainly the values during sleep. A serotoninergic effect is possibly involved. An improvement of mood has been observed in all cases.
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PMID:Neuroendocrinological and clinical data upon trazodone treatment in depressed patients. 713 75

Prolactin concentrations of 30 unmedicated psychiatric inpatients and 11 normal controls were measured at baseline and at 30 and 60 minutes after the administration of 10 mg of intramuscular methadone hydrochloride. Methadone raised the prolactin level at 60 minutes to more than twice the mean baseline level for the full subject sample. Patients with depressive disorders had lower mean basal prolactin levels than did the other subjects, and also manifested attenuated prolactin responses to methadone. Eight of 16 depressives had markedly blunted prolactin responses, a finding consistent with other studies reporting deficient responses in depression. These data are consistent with the hypothesis that the pathophysiology of depressive disorders involves dysfunctions in the anterior pituitary itself or in the hypothalamic neurotransmitter and neuromodulator systems (eg, endorphins) that regulate the secretion of prolactin and other neurohormones.
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PMID:Blunted prolactin response. A neuroendocrine abnormality manifested by depressed patients. 714 2

Evidence exists that oversecretion of cortisol may be responsible for the clinical manifestations and serotonergic abnormality in depressive illness. Using the cortisol synthesis inhibitor ketoconazole, we investigated the effects of directly lowering cortisol on the symptoms and the response of prolactin (PRL) to d-fenfluramine in eight patients suffering from major depression. Prolactin responses to d-fenfluramine were measured, and patients were treated with 400-600 mg of ketoconazole for 4 weeks, after which they were retested. Five patients treated with ketoconazole recovered from their depression, while the other three had decreases in their Hamilton Depression Rating Scale (HAMD) scores of < or = 50% and were deemed partial responders. Posttreatment prolactin responses to d-fenfluramine were higher than pretreatment values. Ketoconazole normalizes the blunted prolactin responses to d-fenfluramine and may be an effective method by which to treat depression. This implies that hypercortisolemia may be responsible for the clinical features and serotonergic subsensitivity observed in depression.
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PMID:Cortisol synthesis inhibition: a new treatment strategy for the clinical and endocrine manifestations of depression. 777 44

Prolactin and cortisol responses to dl-fenfluramine challenge were examined in 11 patients with chronic fatigue syndrome and in 11 healthy controls who were age and gender matched. After obtaining two baseline samples, each subject was given 60 mg of dl-fenfluramine orally and further blood samples were drawn hourly during the following five hours in order to measure prolactin and cortisol levels. There was no difference in either baseline or fenfluramine-induced hormonal responses between patients with chronic fatigue syndrome and controls. There was also no correlation between depression scores on HAM-D and hormonal responses in patients with chronic fatigue syndrome. The findings of this study do not support a role for 5-HT in chronic fatigue syndrome.
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PMID:Neuroendocrine assessment of serotonin (5-HT) function in chronic fatigue syndrome. 870 60

Fifteen inpatients (nine women, six men) aged 50-86 years with DSM-IIIR major depression were treated with electroconvulsive therapy (ECT). Electrode placement (unilateral versus bilateral) and total number of treatments were determined by the patients' own psychiatrists according to clinical indications. Prolactin (PRL) was determined after the 1st, 6th, 7th, 9th, 11th, and final ECT treatments. Subjects were rated with the Hamilton Depression Rating Scale (HDRS) at baseline, after the sixth ECT treatment, and upon completion of ECT. PRL response to unilateral ECT was consistent across treatment for each subject. Percentage PRL increase was significantly higher for bilateral than unilateral ECT (alpha = 0.05). Subjects with final HDRS of < 12 tended to have greater peak, increase, and percentage increase PRL at the first unilateral treatment than subjects with final HDRS of at least 12; these trends approached statistical significance (Kruskal-Wallis one-way analysis of variance; peak: p = 0.059, chi = 3.556, df = 1; increase: p = 0.099, chi = 2.722, df = 1; percentage increase: p = 0.099, chi = 2.722, df = 1). Decrease in HDRS after the sixth treatment failed to show a statistically significant relationship to any PRL parameter at the initial unilateral treatment. Further studies are needed to characterize the relationship between PRL response, seizure activity, and stimulus dosing.
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PMID:Prolactin release and clinical response to electroconvulsive therapy in depressed geriatric inpatients: a preliminary report. 779 64

We found a 38% lower maximal prolactin response to an oral challenge dose of 60 mg of dl-fenfluramine relative to placebo in younger (< 30 years) depressed inpatients compared with the response in age-matched healthy controls (p < .03). Severity of depression did not correlate with prolactin response. Prolactin responses in older depressed patients (> or = 30 years) did not differ from older controls. Younger depressed patients differed from older depressed patients in terms of earlier age of onset of first lifetime episode of major depression, greater degree of suicidal intent during a recent suicide attempt, double the level of hopelessness on admission to hospital, and a higher rate of comorbid borderline personality disorder. A blunted prolactin response to fenfluramine may be interpreted as evidence for reduced serotonergic function in younger depressed patients and may underlie their observed greater suicidality and hopelessness.
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PMID:Blunted serotonergic responsivity in depressed inpatients. 852 71

Hypothalamic-pituitary-adrenal (HPA) axis and central 5-HT function were compared in chronic fatigue syndrome (CFS), depression and healthy states. 10 patients with CFS and 15 patients with major depression were matched for age, weight, sex and menstrual cycle with 25 healthy controls. Baseline-circulating cortisol levels were highest in the depressed, lowest in the CFS and intermediate between the two in the control group (P = 0.01). Prolactin responses to the selective 5-HT-releasing agent d-fenfluramine were lowest in the depressed, highest in the CFS and intermediate between both in the healthy group (P = 0.01). Matched pair analysis confirmed higher prolactin responses in CFS patients than controls (P = 0.05) and lower responses in depressed patients than controls (P = 0.003). There were strong inverse correlations between prolactin and cortisol responses and baseline cortisol values. These data confirm that depression is associated with hypercotisolaemia and reduced central 5-HT neurotransmission and suggest that CFS may be associated with hypocortisolaemia and increased 5-HT function. The opposing responses in CFS and depression may be related to reversed patterns of behavioural dysfunction seen in these conditions. These findings attest to biological distinctions between these disorders.
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PMID:Contrasting neuroendocrine responses in depression and chronic fatigue syndrome. 855 Sep 54


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