Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three hundred thirteen patients with first-episode psychosis were assessed using the Royal Park Multidiagnostic Instrument for Psychosis (RPMIP) to determine differences among seven DSM-III-R diagnoses in the comparative frequencies and diagnostic efficiencies of DSM-III-R schizophrenia prodromal symptoms. Patients with a diagnosis of schizophrenia and schizophreniform disorder were significantly more likely to evince prodromal symptoms. A multinomial logit model suggested that individual prodromal symptoms were relatively poor at distinguishing between diagnoses. This was confirmed when sensitivity, specificity, and positive (PPP) and negative (NPP) predictive power of individual prodromal symptoms were examined. Although DSM-III-R schizophrenia prodromal symptoms do occur more commonly in schizophrenia, they are by no means pathognomonic of that disorder.
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PMID:Prodromal symptoms of schizophrenia in first-episode psychosis: prevalence and specificity. 755 67

The aim of this study is to obtain CRF (Corticotropin Releasing Factor) stimulation at a suprahypothalamic level with a psychological stressor and to evaluate its response in anorexia nervosa. CRF plays a major role in the mechanisms underlying the hypothalamo-pituitary-adrenal (HPA) system's response to stress. Animal studies clearly showed that CRF is involved both in the adaptation to a novel environment and the regulation of eating behaviour. CRF's staietogenic effect is mediated via the paraventricular nucleus. Three groups of age matched young women were studied: 8 patients meeting the DSM III-R criteria for anorexia nervosa, 8 underweight healthy volunteers and 10 normal weight volunteers. All subjects were submitted to an auditory stimulation test ("psychosocial stress test") consisting of an intellectual task in which maximal performance is impossible to achieve, the subjects being permanently disturbed by various meaningful noises. Subjects were asked to answer self-rating scales for anxiety and tension prior to and after the test. CRF reactivity was measured by salivary cortisol (RIA). After the test, anorexia nervosa patients exhibit a significantly higher salivary cortisol response compared to the normal weight volunteers. In most of cases, salivary cortisol response was not correlated with the psychological variables. The range of the response is very explosive in two anorectic patients. Our data are consistent with the hyperactivity of the corticotropic axis stress response in anorexia nervosa, but request further investigations to prove that.
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PMID:[Corticotropin-releasing factor and anorexia nervosa: reactions of the hypothalamus-pituitary-adrenal axis to neurotropic stress]. 786 77

1. Forty six women presenting with symptoms of premenstrual syndrome (PMS) were studied. Ages ranged from 21 to 32. All women answered a questionnaire based on DSM-III-R criteria. They then had serum beta-endorphin levels drawn on day 1 and day 20 of their menstrual Cycle. 2. Beta-endorphin levels were compared with symptom presentation. Such symptoms as anxiety, food cravings and physical discomfort were associated with significant decline in beta-endorphin. Other symptoms were found equally distributed in both groups. The existence or absence of beta-endorphin decline in specific PMS subgroup was postulated.
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PMID:Symptoms of premenstrual syndrome as a function of beta-endorphin: two subtypes. 820 81

To further explore whether the hypercortisolism of anorexia nervosa reflects an alteration in the set point for corticotropin-releasing hormone (CRH) secretion or is a manifestation of glucocorticoid resistance, we examined plasma ACTH and cortisol responses to the competitive glucocorticoid antagonist RU 486 (10 mg/kg, p.o. at 8.00 h) versus placebo (PBO) in 7 healthy female volunteers and 8 patients with DSM-III-R anorexia nervosa, all of whom were studied while underweight [64.3 +/- 2.1% average body weight (ABW), mean +/- SE] and 5 of whom were restudied longitudinally following refeeding (> or = 85% ABW, mean 87.4 +/- 0.4% ABW). Blood samples were obtained from 16.00 to 16.30 h and from 4.00 to 8.00 h following dosing. Underweight anorexics were significantly hypercortisolemic by 24 h urinary free cortisol excretion compared with controls (239 +/- 37 vs. 119 +/- 12 nmol/day, p < 0.01). Both controls and underweight anorexics had robust early morning (4.00-8.00 h) plasma cortisol responses to RU 486 (465 +/- 61 and 719 +/- 49 nmol/l) compared with PBO (370 +/- 52 and 451 +/- 31 nmol/l; p < 0.02 and p < 0.01, respectively). The underweight anorexics showed a significant mean early morning plasma ACTH response to RU compared with placebo (3.28 +/- 0.63 vs. 2.01 +/- 0.24 pmol/l, p < 0.05), while the controls showed a trend toward an increase in mean plasma ACTH after RU (3.11 +/- 0.36 pmol/l) compared with PBO (2.31 +/- 0.41 pmol/l, p < 0.13); plasma ACTH means were greater on the RU day than the placebo day at 20 of 25 sampling points (p < 0.001). However, the increment in ACTH on the RU day compared to the placebo day was greater in the underweight anorexics at the first 20 of 25 consecutive time points of the early morning sampling period (p < 0.001). Moreover, underweight anorexics showed a significant plasma ACTH and cortisol response to RU 486 at 16.00-16.30 h (8-8.5 h following administration), while the controls showed no significant response of plasma ACTH or cortisol at this time. When restudied following weight recovery, anorexic patients showed reductions in 24-hour urinary free cortisol excretion (to 191 +/- 40 nmol/day) which were no longer significantly elevated compared with control values.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of the glucocorticoid antagonist RU 486 on pituitary-adrenal function in patients with anorexia nervosa and healthy volunteers: enhancement of plasma ACTH and cortisol secretion in underweight patients. 823 66

The neuroendocrine responses to subcutaneous (SC) administration of the dopamine (DA) agonist apomorphine (APO) hydrochloride (0.75 mg) were studied in a large group of subjects: 110 drug-free inpatients with either DSM-III-R schizophrenia (SCZ, n = 46), schizoaffective disorder (SAD, n = 14), or major depressive episode (MDE, n = 50), plus 18 hospitalized controls. Compared to a saline test, APO induced a significant increase of growth hormone (GH), adrenocorticotropin (ACTH), and cortisol (COR) release and a decrease in prolactin (PRL) secretion. No change in thyrotropin (TSH) levels was observed. In the total sample the extents of ACTH, COR and GH responses were correlated, but in the group of 88 subjects who exhibit a normal GH stimulation this correlation disappeared. This discrepancy suggests that APO-induced ACTH and COR stimulation may be mediated by pathways different from those mediating GH stimulation. According to diagnostical categories, we found significant lower ACTH and COR stimulation in the schizophrenic group and in patients with SAD, compared with that among controls or depressed patients. We found also a significant difference between subgroups of schizophrenic patients. These results agree with the hypothesis that different aspects of psychosis might involve different subtypes of DA-receptors with different localizations and sensitivities.
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PMID:Multihormonal responses to apomorphine in mental illness. 853 20

The emerging concept of opioid peptides as a new class of chemical messengers of the neuroimmune axis and the presence of a number of immunological abnormalities in infantile autism prompted us to correlate biological (hormonal and immunological) determinations and behavioural performances during treatment with the potent opiate antagonist, naltrexone (NAL). Twelve autistic patients ranging from 7 to 15 years, diagnosed according to DSM-III-R, entered a double-blind crossover study with NAL at the doses of 0.5, 1.0 and 1.5 mg/kg every 48 hours. The behavioural evaluation was conducted using the specific BSE and CARS rating scales NAL treatment produced a significant reduction of the autistic symptomatology in seven ("responders") out of 12 children. The behavioural improvement was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase of the T-helper-inducers (CD4+CD8-) and a significant reduction of the T-cytotoxic-suppressor (CD4-CD8+) resulting in a normalization of the CD4/CD8 ratio. Changes in natural killer cells and activity were inversely related to plasma beta-endorphin levels. It is suggested that the mechanisms underlying opioid-immune interactions are altered in this population of autistic children and that an immunological screening may have prognostic value for the pharmacological therapy with opiate antagonists.
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PMID:Opioid-immune interactions in autism: behavioural and immunological assessment during a double-blind treatment with naltrexone. 902 57

To determine the relationship of pretreatment hypothalamic-pituitary-adrenal cortical (HPA) axis measures in major depressives to the occurrence of relapse following discontinuation of successful treatment, we compared pretreatment demographic, clinical, and HPA axis measures in 35 patients with DSM-III-R primary major depression divided into two groups. One group (n = 26) required continuing treatment to hold their symptoms in abeyance, and the other group (n = 9) had been successfully tapered off medication, remained in remission, and had been medication-free for at least 1 month. The major features that differentiated the 26 patients who required continuing medication to abate their symptoms from the 9 patients who were successfully discontinued from treatment were trends toward a longer duration of episode prior to initial study and increased baseline corticotropin (ACTH) 1-39, and significantly higher baseline cortisol and cortisol response to ACTH 1-24, in the former group. These results suggest that measures of HPA axis hyperactivity, along with longer duration of the index depressive episode, may predict the need for continuing medication for patients to remain in remission.
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PMID:Pituitary-adrenal cortical axis measures as predictors of sustained remission in major depression. 920 24

The influence of clonidine pretreatment on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide (CCK-4) was characterized. Patients with panic disorder (DSM-III-R) were given 50 micrograms CCK-4 i.v. at 1100 hours on 2 separate study days. In a randomized double-blind design they were additionally infused with 150 micrograms clonidine or placebo from 1040 to 1110 hours. After CCK-4 all patients experienced symptom attacks. No effects of clonidine on panic psychopathology or blood gas parameters were observed. After CCK-4, in the clonidine condition the pituitary release of adrenocorticotropin (ACTH) and prolactin was seemingly enhanced compared to placebo. Our results suggest that CCK-4-induced panic attacks are not suppressible by presynaptic alpha-2 receptor stimulation. Moreover, they point to a synergistic postsynaptic action of clonidine to CCK-4 upon pituitary hormone secretion. The diverging sites of action might possibly explain the discrepancies of psychopathological alterations and stress hormone secretion.
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PMID:Influence of clonidine on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide in patients with panic disorder. 933 81

Recent studies in depression have reported alterations in both hypothalamic-pituitary-thyroid (HPT) axis activity and serotonin (5-HT) function; however, the functional relationships between the two systems have not been well defined in patients with major depressive episode. Thyrotropin (TSH) response to 0800 and 2300 h protirelin (TRH) challenges, and adrenocorticotropic hormone (ACTH), cortisol, and prolactin (PRL) responses to D-fenfluramine (D-FEN), a specific 5-HT releasing/uptake-inhibiting agent, were examined in 60 drug-free DSM-IV major depressed inpatients and 20 hospitalized controls. Compared with controls, patients showed lower basal serum 2300 h TSH, 2300 h maximum increment in serum TSH above baseline (delta TSH) and difference between 2300 h delta TSH and 0800 h delta TSH (delta delta TSH) levels. The hormonal responses to D-FEN (i.e. delta ACTH, delta cortisol and delta PRL) were interrelated. No significant difference in basal and post-D-FEN ACTH, cortisol or PRL values were found between controls and patients. A negative relationship between hormonal responses to D-FEN and 2300 h delta TSH and delta delta TSH values was observed in the depressed group. When patients were classified on the basis of their delta TSH test status, patients with reduced delta delta TSH values (i.e. with HPT axis abnormality) had hormonal D-FEN responses comparable to those of controls. Patients with normal delta delta TSH values (i.e. without HPT axis abnormality) showed lower ACTH, cortisol and PRL responses to D-FEN than controls and patients with abnormal delta delta TSH values. These results suggest that: (1) pathophysiological mechanisms other than 5-HT dysregulation may be involved in TSH blunting in major depressed patients; (2) 5-HT function is reduced in some depressed patients, especially those without HPT axis abnormality; and (3) HPT dysregulation may be regarded as a compensatory mechanism for diminished central 5-HT activity.
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PMID:Thyroid axis activity and serotonin function in major depressive episode. 1045 6

1. It has been hypothesized that psychotic symptoms in depression may be due to increased dopamine activity secondary to hypothalamic-pituitary-adrenal (HPA) axis overactivity. 2. To test this hypothesis, the authors examined the cortisol response to dexamethasone suppression test (DST, 1 mg orally) and multihormonal responses to apomorphine (APO, 0.75 mg s.c.)--a dopamine agonist--in 150 drug-free hospitalized patients with DSM-IV major depressive episode with psychotic features (MDEP, n=35), major depressive episode without psychotic features (MDE, n=74), or schizophrenia paranoid type (SCZ, n=41), and 27 hospitalized healthy controls (HCs). 3. MDEPs showed increased activity of the HPA system (i.e. higher post-DST cortisol levels) than HCs, SCZs and MDEs. However, there were no differences in adrenocorticotropic hormone (ACTH), cortisol, prolactin and growth hormone (GH) responses to APO between MDEPs and MDEs and HCs. On the other hand, SCZs showed lower APO-induced ACTH stimulation and a higher rate of blunted GH than HCs, MDEs and MDEPs, suggesting a functional alteration of the hypothalamic dopamine receptors in SCZs. 4. In the total sample and in each diagnostic group, DST suppressors and non-suppressors showed no differences in hormonal responses to APO. 5. These results suggest a lack of causal link between HPA axis hyperactivity and dopamine dysregulation. In contrast to schizophrenia, psychotic symptoms in depression seem not to be related to dopamine function dysregulation.
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PMID:Dopaminergic function and the cortisol response to dexamethasone in psychotic depression. 1080 Jul 44


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