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)

Electron microscopy of an amphophil pituitary adenoma surgically removed from a 51-year-old woman who had Nelson's syndrome revealed that the tumor was composed of melanocorticotroph cells. This finding is consistent with the view that in the human pituitary gland one single cell type produces both adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (MSH). In contrast to the ultrastructure of pituitary adenomas associated with Cushing's syndrome, no or only very few microfilaments were detected in the cytoplasm of the tumor cells, suggesting that adrenocortical steroids are required for the formation of microfilaments. The presence or absence of microfilaments in the tumor cells may be regarded as a distinguishing ultrastructural feature between Cushing's syndrome and Nelson's syndrome. It appears that changes in the level of circulating corticoids may affect the ultrastructural features of melanocorticotroph cells not only in normal pituitaries but also in adenohypophyseal adenomas.
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PMID:Light and electron microscopic features of a pituitary adenoma in Nelson's syndrome. 17 83

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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PMID:Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances. 19 Feb 56

Cases of seven different types of surgically resected pituitary adenoma are described. Included are tumours secreting prolactin or growth hormone or both, and nonfunctioning tumours--undifferentiated and oncocytic tumours, and one tumour with cells of the adrenocorticotropin-melanocyte-stimulating hormone type. The final interpretation of a case of pituitary adenoma should include an assessment of thorough morphologic studies, using not only routine staining and light microscopy but also immunostaining and electron microscopy, to complement the biochemical, radiologic and clinical evaluation.
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PMID:A new look at pituitary adenomas: structure elucidating function. 20 3

A human pituitary adenoma responsible for a case of Nelson's syndrome was maintained in organ culture and the incubation medium was examined with four different RIAs; human corticotropin (ACTH), beta-MSH, lipotropin (LPH), and beta-endorphin (beta-End). All four immunoreactivites (IRs) were present in the medium obtained after 24 h of incubation. Gel exclusion chromatography under denaturing conditions (6 m guanidine HCl) revealed several immunoreactive components. Two components having both human beta-MSH (beta-hMSH) and human LPH (hLPH) IR coeluted with beta-hLPH and gamma-hLPH; a component with beta-hMSH IR but no hLPH IR coeluted with [125I]beta-hMSH; a component with human ACTH (hACTH) IR eluted at the position of hACTH. Sephadex G-50 gel exclusion chromatography revealed that approximately 80% and 20% of human beta-End (beta-hEnd) IR were accounted for by components coeluting with beta-hLPH and beta-hEnd, respectively. These data demonstrate the presence in this incubation medium of materials similar to if not identical with beta-hLPH, gamma-hLPH, hACTH, beta-hMSH, and beta-hEnd; they suggest that all of these peptides may be secreted in the circulation of patients with Nelson's syndrome.
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PMID:Characterization of lipotropin-, corticotropin-, and beta-endorphin-immunoreactive materials secreted in vitro by a human pituitary adenoma responsible for a case of Nelson's syndrome. 22 44

A patient with a pituitary adenoma secreting adrenocorticotropin hormone manifested panhypopituitarism after an episode of pituitary apoplexy. The previously elevated urinary levels of 17-ketogenic steroids dropped sharply, and plasma cortisol became undetectable. The apoplexy also resulted in a partially empty sella on which the dorsum sellae collapsed. Recurrent Cushing's disease developed and was cured by transsphenoidal resection of a microadenoma.
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PMID:Cushing's disease with pituitary apoplexy leading to hypopituitarism, empty sella, and spontaneous fracture of the dorsum sellae. Case report. 22 16

Using radioimmunoassay of human melanotropic hormone (beta-MSH), were studied in one female patient with Nelson's syndrome the properties of the immunoreactive beta-MSH (beta-MSH-IR) secreted in the circulation in vitro by a pituitary adenoma. With Sephadex G-50 gel, beta-MSH-IR of plasma or from a culture mediium is eluted in greater part in a volume corresponding to a molecular weight of some 6,000 to 10,000. In the radioimmunological systems employed, the dilution curve of beta-MSH-IR in a culture medium is not parallel to that of synthetic human beta-MSH; by contrast, it is parallel to that a lipotropine, purified human beta-LPH.
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PMID:[Secretion of a beta lipotropine type substances by a corticomelanotropic adenoma in Nelson's syndrome (author's transl)]. 59 50

A 57-year-old obese woman with hypertension, diabetes mellitus, osteoporosis, and a 40-year history of secondary amenorrhea was diagnosed with corticotropin-dependent Cushing's syndrome. Dynamic endocrine testing and radiological evaluation did not reveal definitively the source of the excess corticotropin. Bilateral adrenalectomy was performed with resolution of the signs and symptoms of hypercortisolism. Four years later, the patient was noted to have rising serum corticotropin levels and an enlarging pituitary mass; hyperprolactinemia also was documented. A diagnosis of Nelson-Salassa syndrome was made, and she underwent a transsphenoidal adenomectomy. A histological examination of the specimen revealed two distinct, albeit contiguous, adenomas: a corticotroph adenoma and a lactotroph adenoma. Postoperatively, the serum prolactin and corticotropin levels decreased significantly. Although the stalk section effect resulting from compression by a pituitary adenoma can raise serum prolactin levels, a concurrent lactotroph adenoma should be considered in patients with nonfunctional or functional pituitary adenomas of other types associated with significantly elevated prolactin levels. The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed.
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PMID:Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. 131 62

Bilateral simultaneous inferior petrosal sinus sampling, associated with the oCRH stimulation test (100 micrograms i.v. as a bolus) was performed in 22 patients with Cushing's syndrome and no signs of pituitary abnormalities. Catheters were inserted into both femoral veins. More than one site in the superior and inferior vena cava was sampled before reaching the inferior petrosal sinuses. Blood samples for ACTH and beta-endorphin were gently aspirated from both petrosal sinuses and from a peripheral vein simultaneously. Blood was drawn at 0, 5, 10 and 15 min after oCRH injection. Seventeen of 22 patients showed an ipsilateral to peripheral vein ratio higher than 1.5, and 12 patients showed a lateralization of ACTH levels after oCRH stimulation. Seventeen patients underwent transsphenoidal pituitary surgery. Nine patients had a pituitary adenoma at the expected side; 1 at the contralateral side, while in 2 it was central. Three of 4 patients in whom the ipsilateral/peripheral ratio was less than 1.5 had the highest ACTH levels at the superior or inferior vena cava, not responsive to oCRH stimulation. One of these had a mediastinal and one a pulmonary mass. The third one, with an occult ectopic source, is still under investigation. At immunohistochemical and biological in vitro studies, both tumors were shown to secrete ACTH. In 13 patients in whom both beta-endorphin and ACTH measurements were performed, these hormones showed similar patterns of response. In conclusion, simultaneous bilateral petrosal sinus catheterization is a useful tool in the differential diagnosis of Cushing's syndrome as concerning pituitary and ectopic forms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective venous sampling in the differential diagnosis of ACTH-dependent Cushing's syndrome. 132 99

A 19-year-old man with blurred vision, headache, and no signs or symptoms of hormone excess was found to have a pituitary adenoma. The tumor was removed by a transfrontal approach. He had postoperative radiation therapy, but subsequently had three recurrences, all removed surgically. By histology, the tumor was a chromophobic, slightly acidophilic pituitary adenoma. Immunohistochemistry revealed the presence of adrenocorticotropin (ACTH) in all four biopsies, alpha-subunit of glycoprotein hormones, and, to a lesser extent, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in the third and fourth tumor resection specimens. Ultrastructurally, the tumor had typical features of a silent corticotroph adenoma subtype 2. In tissue culture, the second, third, and fourth specimens released ACTH, alpha-subunit, FSH, and LH and responded to corticotropin-releasing hormone with increased release of ACTH, alpha-subunit, FSH, and LH. To our knowledge only one silent corticotroph adenoma has been reported previously which expressed plurihormonality. Change in immunohistochemical profile in malignant tumors is a well-known phenomenon; however, it was not reported previously in benign pituitary adenomas. The factors accounting for changing tumor phenotype are unknown.
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PMID:Changes in hormone production of a recurrent silent corticotroph adenoma of the pituitary: a histologic, immunohistochemical, ultrastructural, and tissue culture study. 164 19

Determining the cause of Cushing's disease and correcting the abnormality presents a continuing challenge to the clinician despite remarkable advances in diagnostic and therapeutic techniques. We present seven cases to illustrate 1) the classic disorder cured by pituitary adenomectomy; 2) persistence of the disease after adenomectomy; 3) Cushing's disease manifesting in the puerperium and remitting with dopamine agonist therapy; 4) a patient whose disease relapsed at least five times during 20 years of treatment by adrenalectomy, pituitary radiation, mitotane, and pituitary adenomectomy; 5) the Nelson syndrome; 6) the ectopic adrenocorticotropic hormone (ACTH) syndrome in a patient with dexamethasone suppressible urinary cortisol who had a pituitary adenoma which stained positively for ACTH but who was not cured by total hypophysectomy; and 7) a patient whose ACTH-secreting tumor proved fatal despite repeated surgical, radiologic and pharmacologic measures.
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PMID:Cushing's disease: dilemmas of diagnosis and management. 164 7


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