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)

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 case report is presented of the need for both bromocriptine and human menopausal gonadotropin (hMG) for induction of ovulation in a patient who developed partial hypopituitarism and persistent hyperprolactinemia even after a transsphenoidal pituitary microadenectomy. The patient, a 27-year old white female, initially presented in 1979 with a history of amenorrhea and galactorrhea after discontinuing oral contraceptives (OCs). Her menstrual cycles had been regular since her menarch at age 13 until she began taking OCs at age 20. Preoperative endocrine evaluation in 1979 revealed serum luteinizing hormone (LH), 9.1 mIU/ml; serum follicle stimulating hormore (FSH), 6.4 mIU/ml; serum thyroid stimulating hormone (TSH), 3.8 mIU/ml; serum prolactine (PRL), 300 ng/ml; serum thyroxine (T4), 6.4 mcg/dl; and an attenuated PRL response to thyrotropin releasing hormone (TRH). Radiographic studies revealed a pituitary tumor of approximately 1 cm in diameter. In July 1979 a transsphenoidal hypophysectomy was performed. Pathologic examination revealed a pituitary adenoma with a monomorphic basophilic cell population with fibrosis and chronic inflammation. The patient required prednisone therapy postoperatively for 3 months secondary to compromised adrenal status. Prednisone therapy was discontinued in October 1979 after a normal cortisol (F) response to induced hypoglycemia was documented. The patient's serum PRL levels remained elevated at 111 ng/ml in August 1979 and 269 ng/ml in October 1979. Her amenorrhea and galactorrhea persisted. Bromocriptine therapy, 2.5 mg 3 times daily, was instituted in October 1979. She became normoprolactinemic, with a serum PRL of 6 ng/ml, and the galactorrhea disappeared but the amenorrhea persisted. In February 1981 she was referred for further consultation on her fertility status. Bromocriptine therapy was discontinued. In April 1981 she underwent a thorough endocrine evaluation. The results indicate that GnRH stimulation was unable to elicit a pituitary gonadotropin response anywhere near normal levels of FSH and LH, thus suggesting pituitary hypogonadotropism. Growth hormone release was subnormal in response to the insulin induced hypoglycemia and L-dopa ingestion. Hyperprolactinemia was obvious but the patient's serum TSH, T4, and adrenocorticotropin (ACTH) levels were normal. A diagnosis of hyperprolactinemia with partial hypopituitarism and gonadotropin deficiency was made. Bromocriptine therapy was reinstituted at 2.5 mg twice daily in June 1981, with good results. In November 1981 her serum PRL was normal, and as she was desirous of pregnancy, ovulation induction with bromocriptine and Pergonal was carried out. The patient is now 6 months pregnant and doing well. This case illustrates the poor functional results for surgery for pituitary microplactinomas.
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PMID:Partial hypopituitarism and hyperprolactinemia: successful induction of ovulation with bromocriptine and human menopausal gonadotropins. 681 37

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

Inferior petrosal sinus sampling (IPSS) for adrenocorticotropic hormone (ACTH) levels in patients with Cushing's syndrome has become a useful method to distinguish ACTH-secreting pituitary tumors (Cushing's disease) from other causes of the syndrome, principally ectopic adrenocorticotropin secretion by an occult tumor. Although the test is generally regarded as highly specific, the authors recently encountered two patients whose IPSS measurements were false-positive for Cushing's disease. The results of IPSS suggested a pituitary origin of ACTH secretion in both patients, but transsphenoidal surgery failed to disclose a pituitary adenoma or to improve postoperative plasma cortisol levels. Both patients subsequently were found to have an ACTH-secreting carcinoid tumor of the lung. The false-positive IPSS studies were due to periodic hormonogenesis. The patients must be hypercortisolemic at the time IPSS is performed for the study to be valid.
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PMID:False-positive inferior petrosal sinus sampling in the diagnosis of Cushing's disease. Report of two cases. 749 Jun 27

There is general agreement that postoperative radiation therapy is beneficial for patients with subtotally resected pituitary adenomas. We have identified 41 such patients treated during a 20-year period who received postoperative irradiation for a pituitary adenoma. The usual dose was 5040 cGy in 28 fractions. The mean follow-up time was 10.3 years. On routine hematoxylin and eosin (H&E) staining, there were thirty-three chromophobe, seven eosinophilic, and one basophilic adenoma. Tissue blocks were stained for growth hormone (GH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), prolactin (PRL), and/or adrenocorticotropin (ACTH) using the peroxidase-antiperoxidase immunohistochemistry (IHC) method. Routine H&E staining was a poor predictor of the IHC stain. While most patients with a known clinical endocrine syndrome stained positive on IHC for the suspected offending hormone, many patients without a clinical syndrome also stained positive indicating the presence of hormonally occult adenomas in this locally invasive group. The IHC stain results were compared to clinical outcome. The presence of positive GH IHC staining decreased the 15-year progression-free survival (PFS) from 100% to 64% compared to GH negative adenomas (p = 0.06). There was a trend toward decreased 15-year PFS in patients who did not stain for LH. Positive staining for prolactin, ACTH, or TSH had no influence on the progression-free survival. We conclude that additional prognostic information can be obtained in this subset of patients (by performing IHC analysis) that is not known by the clinical presentation or appearance on H&E stain.
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PMID:Immunohistochemistry as a predictor of clinical outcome in patients given postoperative radiation for subtotally resected pituitary adenomas. 750 78

The therapeutic efficacy of sustained dopaminergic stimulation in Cushing's disease (CD), was investigated performing a three-month trial with monthly 50-100 mg injections of a bromocriptine depot preparation (Parlodel LAR, Sandoz) in six patients with CD. Dopaminergic treatment did not consistently influence pituitary-adrenal activity, as judged by plasma ACTH, cortisol and urinary free cortisol levels as well as by clinical findings. Interestingly, treatment with bromocriptine was associated with reappearance of menses in the three patients who were amenorrheic. In the five patients submitted to inferior petrosal sinus sampling, a parallelism between ACTH and PRL concentrations could be observed with a PRL rise, ipsilateral to that of ACTH, ensuing in three patients after administration of corticotropin-releasing hormone. In one patient a 55% reduction in the size of the pituitary adenoma was demonstrated by MRI carried out at the end of treatment. Our findings lead to the following conclusions: a) administration of depot injections of bromocriptine to patients with CD appears unable to correct hypercortisolism, although it can induce restoration of menses in amenorrheic patients; b) enhanced PRL concentrations at the pituitary level are probably involved in the amenorrhea often accompanying Cushing's disease.
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PMID:Effect of injectable bromocriptine in patients with Cushing's disease. 758 34

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

A patient was diagnosed with Cushing's syndrome during her first pregnancy. Bilateral simultaneous inferior petrosal sinus corticotropin sampling with corticotropin-releasing hormone stimulation was performed before transphenoidal pituitary adenomectomy, with successful localization of the pituitary adenoma. Her Cushing's syndrome was controlled postoperatively with resolution of hypertension. This case report demonstrates that the procedure of bilateral simultaneous inferior petrosal venous corticotropin sampling can be safely performed during pregnancy.
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PMID:Bilateral inferior petrosal sinus corticotropin sampling with corticotropin-releasing hormone stimulation in a pregnant patient with Cushing's syndrome. 805 45

A 42-year-old man presented with classical symptoms of Cushing's disease. Endocrinological examinations indicated the presence of a adrenocorticotropin-(ACTH) producing pituitary adenoma. Magnetic resonance imaging showed a cystic sellar lesion, which had features of a Rathke's cleft cyst, whereas the adenoma was not depicted. The ratio of blood ACTH concentration between cubital vein, left, and right cavernous sinus was 1: 1.4: 20. During transsphenoidal surgery, in addition to the Rathke's left cyst, a tiny adenoma was detected beneath the left pituitary lobe. Cavernous sinus sampling is a useful auxiliary in the localization of an ACTH-producing adenoma, as in this case.
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PMID:A case of Cushing's disease accompanied by Rathke's cleft cyst: the usefulness of cavernous sinus sampling in the localization of microadenoma. 809 Dec 86

Clinico-pathological correlations in horses with pituitary adenomas are poorly understood. This paper describes the functional and morphological features of five cases of equine pituitary adenoma and of a case of multinodular pituitary hyperplasia. New findings reported include immunoreactivity for beta-lipotropin (beta-LPH), beta-melanocyte-stimulating hormone (beta-MSH), gamma 3-MSH, prolactin (PRL), and follicle-stimulating hormone (FSH) in neoplastic cells of the pituitary adenoma; and, in the multinodular hyperplasia, beta-LPH, beta-endorphin (beta-END), alpha-MSH, beta-MSH, gamma 3-MSH and FSH immunoreactivity. It is suggested that the equine pituitary syndrome does not correspond to human Cushing's disease, as generally accepted, but is related to the overproduction of several pro-opiomelanocortin (POMC)-derived peptides by the cells of the tumour or hyperplastic nodules.
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PMID:Equine pituitary adenoma: a functional and morphological study. 824 32


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