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)

A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.
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PMID:A case of histiocytosis X associated with panhypopituitarism and hyperimmunoglobulinemia G and E. 22 67

The possibility that the fetal brain or pituitary either initiates parturition or influences the course of labour was studied in human and rat. The results when corticotropin or neurohypophysial hormones were injected directly into human anencephalic fetuses in utero, and data obtained from 147 clinical records of such fetuses, seemed to show that the fetal brain does not trigger the onset of parturition. On the other hand, the course of labour was seriously protracted in anencephalic fetuses. Gestation length of brain-aspirated rat fetuses was not significantly longer than in sham-operated controls. However, the course of labour was protracted in the brain-aspirated fetuses. A similarly protracted expulsion pattern was observed in Brattleboro rats homozygous for a hypothalamic form of diabetes insipidus. These data all pointed to the likelihood that fetal neurohypophysial hormones stimulate the course of labour. Neither oxytocin nor vasopressin could be demonstrated in the rat fetus on the last day of pregnancy, when specific immunofluorescence was used. However, a closely related compound was found that was identified as most probably being vasotocin. The hypothesis is put forward that this fetal hormone normally stimulates the course of labour.
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PMID:The influence of the fetal hypothalamus and pituitary on the onset and course of parturition. 24 94

After brain death, 32 potential organ donors were studied to determine serum and plasma concentrations of hypothalamic-pituitary hormones, thyroid hormones, and cortisol over a period of up to 80 hr. Diagnosis of brain death was established either on the basis of clinical criteria (n = 16) or by angiography (n = 16). While 78% of the organ donors developed diabetes insipidus, none of the circulating hormones of the anterior pituitary gland showed a progressive decline in concentration according to their plasma half-lives. With the exception of arginine vasopressin (AVP), no hormone concentration was found to be subnormal due to the onset of brain death. The subnormal free triiodothyronine (FT3) values in 62% of cases (median FT3 of 2.2 pmol/L within the first 24 hr) and the cortisol concentration of 6.9 micrograms/dl correlate with the frequency of similar findings in patients with severe head injuries. While the adrenocorticotropic hormone (ACTH) concentrations of 10-53 pg/ml remained constant during the study period, thyroid-stimulating hormone (TSH) and human growth hormone (hGH) concentrations showed a 12- and 35-fold increase from baseline values after 30-40 hr. These results suggest that, despite the now generally accepted criteria of brain death, there is still some residual function, and thus also perfusion of the hypothalamic-pituitary neuroendocrine system. This residual function appears to be sufficient to maintain hormonal plasma levels at least in the low reference range in most donors. Hormonal depletion in organ donors subsequent to brain death, as suggested repeatedly in the literature, could not be confirmed. The analysis of serum or plasma concentration patterns of a number of hormonal parameters following brain death does not support the rationale for a routine replacement therapy of total triiodothyronine (TT3) or cortisol to maintain endocrine homeostasis prior to organ harvest. However, dexamethasone therapy may be followed by suppression of the adrenal cortex of the organ donor. In these cases, cortisol substitution may be indicated.
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PMID:Acute endocrine failure after brain death? 133 23

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.
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PMID:Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog. 284 1

Anti-neurophysin serum was applied in the immunohistochemical technique to anterior pituitary tissues obtained from normal and chronically dehydrated rats and also from rats with chronic diabetes insipidus (Brattleboro strain). In all cases there was a positive staining in the corticotrophs, which also stained for either beta-endorphin (beta-END) or adrenocorticotrophin hormone (ACTH). It was concluded that corticotroph-neurophysin may be synthesized independently of either ACTH or beta-END.
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PMID:Non-coordinate localization of corticotroph-neurophysin and beta-endorphin in the anterior pituitary gland of the rat. 301 38

The development of an acute hemorrhagic shock in rats with hereditary diabetes insipidus (DI), lacking vasopressin, is very dramatic, compared to rats of the parent strain Long Evans (LE). After removal of 50% of the circulating blood for LE, and 30% for DI, the mortality for both LE and DI groups was 50%, the shock index being 0.049 and 0.028, respectively. Infusion of either vasopressin (107 mU/100 g) or naloxone (0.2 mg/100 g) in DI rats, prevented the progression of hemorrhagic shock into irreversible stage, and augmented survival up to 66% and 57%, respectively. The specific opioid antagonist naloxone exerted a therapeutic effect on rats with hemorrhagic shock by antagonism of opioid receptors, without influencing ACTH and aldosterone secretion in DI rats. This is another evidence for the role of beta-endorphin in the pathogenesis of hemorrhagic shock.
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PMID:Effect of specific opioid-receptor antagonist naloxone on rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) during acute hemorrhagic shock. 301 80

The frequency of detection of serum antibodies against pituitary cells was determined in 32 patients with the primary empty sella syndrome. Antibodies reacting with corticotropin-secreting mouse AtT20 and PRL-secreting rat GH3 cells were found in 24 (75%) and 15 (47%), respectively, of the 32 patients; 14 patients (44%) had antibodies reacting with both cell lines. In patients with pituitary adenomas, the prevalence of antipituitary antibodies was significantly lower than in those with the empty sella syndrome; 1 of 9 acromegalic patients had antibodies reacting with GH3 cells, and 2 of 9 prolactinoma patients and 1 of 7 patients with nonfunctioning adenomas had antibodies reacting with both AtT20 and GH3 cells. Among 6 patients with idiopathic diabetes insipidus, 1 patient had antibodies reacting with AtT20 and GH3 cells, and 2 patients had antibodies reacting with either AtT20 or GH3 cells. None of 5 patients with established autoimmune diseases (3 with systemic lupus erythematosus and 2 with autoimmune adrenal failure) had antipituitary antibodies in their serum. These results suggest that pituitary antibodies may be related to the development of pituitary atrophy and the primary empty sella syndrome, and that the test may be clinically useful as a screening test for the empty sella syndrome.
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PMID:Antipituitary antibodies in patients with the primary empty sella syndrome. 341 43

In the normal Wistar rat, the plasma alpha-MSH level was raised by hypertonic saline injection (as compared with control rats injected with isotonic saline). No such rise in alpha-MSH followed hypertonic saline administration in the Brattleboro (hereditary diabetes insipidus) animal (compared to isotonic saline injected controls). It is suggested that, in the rat, endogenous antidiuretic hormone is involved in the secretory response of the pars intermedia to osmotic stimuli.
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PMID:Antidiuretic hormone involvement in the release of alpha-melanocyte-stimulating hormone by hyperosmotic stimuli. 404 29

Based on drug release by microporous hollow fibers and the recent introduction of microporous polymers, a new technique was developed for controlled delivery of peptides. Small-diameter microporous polypropylene tubing, lumen-loaded with microgram quantities of vasopressin, and coated with collodion, releases vasopressin after in vitro immersion slowly (1-100 ng/d) and constantly for months. The mechanism of pseudo-zero-order delivery is based on high adsorption of vasopressin, keeping the void volume concentration of dissolved vasopressin constant, which is consequently a constant driving force of outward diffusion. The collodion coating prevents the entry of proteinaceous compounds which would result in rapid desorption of vasopressin. The present delivery module provides a lasting release for other peptides as well (lysine-vasopressin, oxytocin, alpha-melanocyte-stimulating hormone and, to a lesser extent, Met-enkephalin). The microporous polymer-collodion device is biocompatible and, loaded with vasopressin, successfully alleviates the diabetes insipidus of Brattleboro rats deficient for vasopressin. Subcutaneous implantation normalized diuresis for a period of 60 d and constant urine vasopressin excretion is observed. When the commercially available osmotic minipump is too large for implantation, the small size of the present controlled-delivery system allows peptide treatment of young and immature laboratory rats, even if located in utero.
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PMID:Controlled long-term release of small peptide hormones using a new microporous polypropylene polymer: its application for vasopressin in the Brattleboro rat and potential perinatal use. 652 41


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