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)

Human ACTH-producing tumor and plasma have been examined by gel filtration and ion exchange chromatography to detect the possible presence of reported multiple forms of immunoreactive beta-endorphin (I-EP) Ion exchange chromatography of I-EP obtained from gel filtration showed four components of I-EP [two major peaks in the positions of EP-(1-31) and EP-(1-27) and two minor peaks in the positions of N-acetyl EP-(1-31) and N-acetyl EP-(1-27)] in two ectopic ACTH-producing lung cancers, and two components of I-EP [the major peak in the position of EP-(1-31) and minor peak in the position of N-acetyl EP-(1-31) in an ectopic ACTH-producing thyroid cancer. Only a single peak in the position of EP-(1-31) was present in plasma from a patient with Nelson's sindrome and a patient with Addison's disease, in the pituitary adenomas from six patients with Cushing's disease, and in the nontumorous pituitary tissues from a patient with Cushing's disease and a patient with acromegaly. These data suggest that the posttranslational processing of EP in human pituitary is different from that in the ectopic ACTH-producing tumor.
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PMID:Multiple forms of immunoreactive beta-endorphin are present in an ectopic adrenocorticotropin-producing tumor but not in normal pituitary or pituitary adenomas. 627 95

Dopamine regulates the secretion of pituitary hormones: it inhibits permanently the production of prolactin and blocks the gonadotrophins and the thyroid-stimulating hormone. It stimulates inconstantly the secretion of growth hormone and it does not control corticotropin. Dopamine agonists and antagonists are currently used in the investigation and the treatment of hyper-prolactinemia and acromegaly.
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PMID:[Dopamine and pituitary hormones. Physiology and pathology (author's transl)]. 628 97

Advances in CT scanning and digital subtraction angiography have improved the accuracy of preoperative diagnosis of pituitary disease. Modern radioimmunoassay techniques are able to evaluate "subdivisions" and "relatives" of the classic pituitary hormones, including monomeric and oligomeric growth hormones, somatomedin C, beta-lipotropin, and beta-endorphin, as well as the alpha subunit of follicle-stimulating hormone. Pituitary pathologic states can now be identified immunologically in patients in whom results of radiologic studies are normal. Bromocriptine, a centrally active dopamine antagonist and ergot derivative, is effective in the treatment of prolactinomas, but it is not effective in the treatment of acromegaly. Transsphenoidal surgery remains the treatment of choice in adults with pituitary-dependent Cushing's disease. The surgical advantages of the sublabial, transseptal, transsphenoidal approach include wide-field pituitary accessibility via a midline exposure.
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PMID:Pituitary surgery: current status, including transsphenoidal surgery. 638 85

This report describes the histologic, immunocytochemical, and ultrastructural study of a multihormonal carcinoid tumor of the pancreas, secreting a growth hormone releasing factor (GRF) which provoked acromegaly. The patient presented a nonfamilial multiple endocrine neoplasia, type 1. The absence of radiologic signs of a pituitary adenoma in conjunction with elevated plasma levels of pancreatic polypeptide, glucagon, somatostatin, as well as growth hormone (GH), led to the discovery of the tumor. Its surgical excision produced a rapid disappearance of most of the clinical and biologic disorders. No immunoreactive GH was found in the tumor using radioimmunoassay and immunocytochemistry. In contrast, three peptides with GH-releasing activity were extracted and characterized. Immunocytochemistry showed that the GRF-reactive cells, together with rare somatostatin-storing cells, made up areas which demonstrated a medullary pattern of growth with extracellular amyloid deposits. Under electron microscopic examination, actively secreting cells were observed which carried endocrine granules of 100 to 150 nm in diameter. The other regions of the tumor presented a different type of growth and were composed of pancreatic polypeptide-, glucagon-, or somatostatin-reacting cells. Cells immunostained with antisera raised against beta-endorphin were also noted. These data suggest that GRF may be a new biologic marker for pancreatic endocrine tumors.
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PMID:Multihormonal carcinoid tumor of the pancreas. Secreting growth hormone-releasing factor as a cause of acromegaly. 643 52

A patient with mild acromegaly had recurrence of symptoms and signs of a chiasmal-area lesion seventeen years after radiation therapy for a presumed pituitary adenoma. A mass was found anterior to the pituitary gland. Abnormal tissue removed from the sphenoid sinus and sella turcica consisted of a predominantly ganglion-cell lesion. A few ganglion cells were immunoreactive for somatostatin. There were some small cysts lined by cells with immunostaining for glial fibrillary acidic protein, growth hormone or prolactin. Some cells with vacuoles and eosinophilic granules showed immunostaining for growth hormone, prolactin, ACTH, and beta-endorphin and, thus, appeared to be of adenohypophyseal origin. Cases of intrasellar ganglion-cell lesions have been reported, most of them associated with pituitary adenomas and acromegaly. The findings in this case are discussed in relation to the hypothesis that displaced, hypothalamic-type ganglion cells may produce a growth hormone-releasing factor that stimulates the development of a growth hormone-secreting pituitary adenoma. An alternative hypothesis is suggested that includes this concept, but also allows for the influence of non-neuronal cells on neuronal differentiation and for the possible influence of adenohypophyseal hormones on the replication of hypothalamic-type neurons in the lesion.
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PMID:Intrasellar neural-adenohypophyseal choristoma. A morphological and immunocytochemical study. 704 19

Local expansion of pituitary tumors causes nonspecific symptoms, including hormone insufficiency, that may exist for years before diagnosis. Although they are more specific, symptoms of pituitary hormone oversecretion may also remain unrecognized and give rise to difficult diagnostic problems. Gonadotropic tumors do not elicit specific endocrine symptoms, whether they secrete complete gonadotropins or their biologically inactive free subunits. Hyperprolactinemia is not due to tumor secretion in the majority of cases, including some with a tumor in the pituitary (compressive hyperprolactinemia). When acromegaly is suspected, the unequivocal proof of excess growth hormone secretion is not easy to obtain, due to intermittent growth hormone secretion, both in normals and in acromegalics. The large variety of tests available for the etiological diagnosis of hypercorticism indicates the diagnostic difficulties that can be encountered. Corticotrope pituitary adenomas may be minute, and ectopic corticotropin secretion may remain occult. But on the other hand, the quality of the diagnostic tools available improves constantly. This includes new hormone measurements, such as insulin-like growth factor 1 and its binding proteins, dynamic tests, selective pituitary blood drawing by inferior petrosal sinus catheterism, pituitary nuclear magnetic resonance imaging and somatostatin-analogue scintiscan. In addition to the improving techniques of transphenoidal neurosurgery and pituitary radiotherapy, medical management of pituitary tumors remains a distinct possibility. Tumor hormone secretion can be controlled in some cases by drugs such as dopaminergic agents, somatostatin analogues and gonadoliberin analogues, which may also exert an antitumoral mass effect. Within the next few years we will be confronted with an increasing number of incidentally discovered pituitary tumors, due to the frequent use of high-resolution intracranial imaging.
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PMID:[Endocrinological aspects of hypophyseal tumors]. 759 64

Diagnostic advances have resulted in earlier and more frequent recognition of pituitary tumors. Pituitary tumors cause problems owing to the hormones they secrete or the effects of an expanding sellar mass--hypopituitarism, visual field abnormalities, and neurologic deficits. Prolactin-secreting tumors (prolactinomas), which cause amenorrhea, galactorrhea, and hypogonadism, constitute the most common type of primary pituitary tumors, followed by growth hormone-secreting tumors, which cause acromegaly, and corticotropin-secreting tumors, which cause Cushing's syndrome. Hypersecretion of thyroid-stimulating hormone, the gonadotrophins, or alpha-subunits is unusual. Nonfunctional tumors currently represent only 10% of all clinically diagnosed pituitary adenomas, and some of these are alpha-subunit-secreting adenomas. Insights into the pathogenesis and biologic behavior of these usually benign tumors have been gained from genetic studies. We review some of the recent advances and salient features of the diagnosis and management of pituitary tumors, including biochemical and radiologic diagnosis, transsphenoidal surgery, radiation therapy, and medical therapy. Each type of lesion requires a comprehensive but individualized treatment approach, and regardless of the mode of therapy, careful follow-up is essential.
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PMID:Pituitary tumors. Current concepts in diagnosis and management. 774

Three cases of a composite sellar tumour composed of a gangliocytoma and an adenoma are presented. Two patients who showed acromegaly and hyperprolactinaemia had a gangliocytoma and a growth hormone (GH)-prolactin cell adenoma in close proximity. The gangliocytoma contained growth hormone-releasing hormone (GHRH) by immunohistochemistry. At the electron microscopical level, the gangliocytoma was characterized by numerous synaptic vesicles. The third patient, a child with Cushing's disease, presented a corticotropin-releasing hormone (CRH)-positive gangliocytoma in close contact with an adrenocorticotropic hormone (ACTH) secreting adenoma, the latter a typical densely granulated ACTH cell adenoma. Ultrastructurally, the gangliocytoma revealed synaptic vesicles and sparse secretory granules. The results suggest that gangliocytomas may promote the development of pituitary adenomas by hypersecretion of releasing hormones. Whereas 20 cases of sellar GHRH producing gangliocytomas in acromegaly are reported in the literature, the combination of a CRH-positive gangliocytoma and an ACTH cell adenoma in Cushing's disease is apparently the first case.
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PMID:Combined sellar gangliocytoma and pituitary adenoma in acromegaly or Cushing's disease. A report of 3 cases. 792 20

A 27-yr-old woman was referred for evaluation of acromegaly and hyperprolactinemia. She had undergone left adrenalectomy at 12 and right adrenalectomy at 17 for Cushing's syndrome due to adrenocortical nodular hyperplasia. At this time a pituitary tumor was found by brain computerized tomography, but plasma levels of growth hormone (GH), prolactin (PRL) and adrenocorticotropin (ACTH) were normal. When she was 23, symptoms and signs of acromegaly and subsequently galactorrhea-amenorrhea had developed. Plasma GH and PRL were increased and she was followed up by the administration of bromocriptine (2.5 mg-12.5 mg/day, p.o.). However the plasma GH level had been increasing gradually. On admission, plasma GH and PRL were high (19.5 micrograms/L, 61.0 micrograms/L, respectively) and increased in response to thyrotropin releasing hormone (TRH, 500 micrograms i.v.). An intrasella mass, which had been detected when she was 17, had become enlarged and was removed by Hardy's operation. Microscopically, the resected tumor was an eosinophilic adenoma. Immunohistochemical studies showed GH, PRL and ACTH positive cells localized in the tumor. Immunoultrastructural analysis of the tumor confirmed that GH, PRL and ACTH were present in secretory granules and Golgi apparatus in the tumor cells. The patient was a rare case of acromegaly with hyperprolactinemia developed after bilateral adrenalectomy of Cushing's syndrome due to adrenocortical nodular hyperplasia, all of which manifestations may be caused by a GH, PRL and ACTH secreting pituitary adenoma.
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PMID:Acromegaly with hyperprolactinemia developed after bilateral adrenalectomy in a patient with Cushing's syndrome due to adrenocortical nodular hyperplasia. 795 91

We examined the effect of phorbol ester on growth hormone (GH)-releasing hormone (GRH)-induced GH secretion and cyclic adenosine monophosphate (cAMP) production in three pituitary adenomas and thyrotropin-releasing hormone (TRH)- and corticotropin-releasing hormone (CRH)-induced redistribution of protein kinase C (PKC) from cytosol to membrane in a pituitary adenoma resected from patients with acromegaly. GRH stimulated GH secretion in accordance with cAMP production in three cases, whereas 12-O-tetradecanoyl phorbol-13 acetate (TPA) stimulated GH secretion with cAMP production in one case. Simultaneous addition of GRH and TPA enhanced cAMP production in three pituitary adenomas. Moreover, addition of TPA with GRH resulted in additive secretion of GH in vitro. In one case, we were able to measure PKC activity and prove translocation of PKC stimulated by TRH and CRH in accordance with GH secretion in vitro and in vivo. These results suggest that TPA, an activator of PKC, has a stimulatory effect on GRH-induced cAMP production and that, finally, TRH- and CRH-induced PKC activation may cause greater secretion of GH by enhancement of cAMP production in human GH-hypersecreting adenoma cells.
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PMID:Growth hormone secretion in human acromegalic pituitary adenomas: cyclic adenosine monophosphate and protein kinase C responses. 859 91


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