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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report on the morphological features of a pituitary adenoma that produced growth hormone (GH) and adrenocorticotropic hormone (ACTH). This hormone combination produced by a single adenoma is extremely rare; a review of the available literature showed that only one previous case has been published. The tumor, which was removed from a 62-year-old man with acromegaly, was studied by histological and immunocytochemical analyses, transmission electron microscopy, immunoelectron microscopy, and in situ hybridization. When the authors used light microscopy, the tumor appeared to be a bimorphous mixed pituitary adenoma composed of two separate cell types: one cell population synthesized GH and the other ACTH. The cytogenesis of pituitary adenomas that produce more than one hormone is obscure. It may be that two separate cells--one somatotroph and one corticotroph--transformed into neoplastic cells, or that the adenoma arose in a common stem cell that differentiated into two separate cell types. In this case immunoelectron microscopy conclusively demonstrated ACTH in the secretory granules of several somatotrophs. This was associated with a change in the morphological characteristics of secretory granules. Thus it is possible that the tumor was originally a somatotropic adenoma that began to produce ACTH as a result of mutations that occurred during tumor progression.
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PMID:Pituitary adenoma producing growth hormone and adrenocorticotropin: a histological, immunocytochemical, electron microscopic, and in situ hybridization study. Case report. 1006 42

Management of pituitary tumors has improved in the past decade since the introduction of novel therapeutic agents. As a result, several treatment options are now available. Dopamine agonists are the preferred treatment for both symptomatic microprolactinomas and macroprolactinomas; these drugs result in normalization of hormone levels and tumor shrinkage in most treated patients. New formulations (such as cabergoline and parenteral bromocriptine) with prolonged duration of action offer improved compliance with treatment and cure rates. For acromegaly and adrenocorticotropin hormone (ACTH)-secreting, thyroid-stimulating hormone (TSH)-secreting, and nonfunctional adenomas, surgery often results in cure. Octreotide and the long-acting, slow-release somatostatin analogues are effective medical alternatives to or adjuvants for transsphenoidal surgery in patients with growth hormone-secreting and TSH-secreting tumors. No drug treatment is available for symptomatic nonfunctional tumors, and patients with ACTH-secreting adenomas may benefit from cortisol-lowering drugs after surgical failure. Pituitary irradiation may be required after surgery for ACTH-secreting, TSH-secreting, and nonfunctioning tumors; it is less commonly required for acromegaly. Although many pituitary tumors are successfully resected, functional adenomas may not be cured by surgery. As more-effective drugs are introduced for the management of pituitary tumors, more patients with hormone-secreting adenomas are being successfully treated medically.
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PMID:Management of pituitary tumors. 973 86

The present work was aimed at studying the combined effects of somatostatin and corticotropin releasing hormone on the activities of the pituitary-adrenocortical axis and neurohypophysis. Patients with active acromegaly were intravenously injected with a 100 micrograms human corticotropin releasing hormone bolus before and after a 3-month subcutaneous treatment with somatostatin-octreotide (SMS 201 995; Sandostatin; 200 micrograms t. i. d.). When the Sandostatin effect was investigated, corticotropin releasing hormone test was started 2 hrs after its first daily dose. Peripheral venous blood samples were taken before and 20, 60, 90 and 120 min after the corticotropin releasing hormone load. Plasma corticotropin, arginine-8-vasopressin and oxytocin were measured by radioimmunoassay, and serum cortisol by fluorimetry. In healthy subjects, corticotropin releasing hormone stimulus elicited increases of plasma corticotropin, serum cortisol, plasma arginine-8-vasopressin and oxytocin levels by 186, 41, 178 and 58 per cent, respectively. Untreated acromegalics exhibited missing arginine-8-vasopressin, blunted corticotropin, and normal oxytocin and cortisol responses. Sandostatin therapy improved the arginine-8-vasopressin reaction, suppressed the basal levels of corticotropin and cortisol with the maintenance of cortisol stimulability; the peak-reaction of corticotropin became normal in two patients, however, with a shortened duration of response. Diuresis of the patients increased under the treatment. Sandostatin markedly alleviated the clinical symptoms and suppressed the growth hormone secretion, but did not influence the size of the pituitary adenomas. Among other factors, the alterations of growth hormone and cortisol may be hypothesized to take part in the changes of the corticotroph and neurohypophysial functions.
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PMID:[Effect of somatostatin-octreotide on secretion of adrenocorticotropin, cortisol and neuro-hypophyseal hormones in acromegaly]. 991 27

We reviewed the clinical features, essential laboratory data, pituitary imaging findings (computerized tomography and magnetic resonance imaging), management, and outcome of 353 consecutive patients with the presumptive diagnosis of pituitary tumor investigated from January 1984 through December 1997 at University Hospital, Lausanne, Switzerland. In 18 cases primary empty sella turcica was diagnosed, and in 13 cases of pseudacromegaly there were no endocrine abnormalities. The remaining 322 patients disclosed abnormal pituitary masses, including 275 pituitary adenomas, 18 craniopharyngiomas, 6 cases of primary pituitary hyperplasia, 6 intrasellar meningiomas, 6 cases of distant metastases, 4 intrasellar cysts, 2 chordomas, 1 primary lymphoma, and 1 astrocytoma. Biologic data and immunohistochemical analysis of the excised tissues demonstrated that prolactinomas and nonsecreting adenomas (NSAs) were the most frequent pituitary tumors (40% and 39%, respectively), followed by somatotropic adenomas with acromegaly (11%) and Cushing disease (6%). In contrast with the vast majority of NSAs, which significantly expressed glycoprotein hormones in tissue without secreting them, there was a small group of glycoprotein hormone-secreting adenomas (2%), which had a more severe clinical course after surgery. Thirty-eight pituitary masses were incidentally discovered, most of them NSAs. The expansion of pituitary adenomas into the right cavernous sinus was twice as frequent as to the left cavernous sinus. For the differential diagnosis of hyperprolactinemia, basal prolactin (PRL) levels above 85 micrograms/L, in the absence of renal failure and PRL-enhancing drugs, and a PRL increment of less than 30% after thyrotropin-releasing hormone (TRH) accurately ruled out functional hyperprolactinemia due to NSA, and were typical of prolactinomas. For screening and follow-up of acromegaly, basal growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels, as well as the paradoxical GH response to TRH (present in 2/3 acromegalic patients), could be used as convenient tools, but the most accurate test for diagnosis and prediction of outcome after therapy was GH (lack of) suppression during oral glucose tolerance test. In Cushing disease, single evening plasma cortisol was as good as the overnight dexamethasone suppression test for screening, and a combined dexamethasoneovine corticotropin-releasing hormone (oCRH) test was as accurate as the long dexamethasone suppression test to confirm the diagnosis. Bilateral inferior petrosal sinus catheterization coupled with oCRH test confirmed the pituitary origin of excess adrenocorticotropic hormone (ACTH) in all patients, including those with normal pituitary on magnetic resonance imaging (50% of the cases). However, this procedure failed to predict tumor localization correctly within the pituitary in 21% of patients. Pituitary cysts, meningiomas, and craniopharyngiomas with an intrasellar component were correctly diagnosed based on pituitary imaging in 75%, 67%, and 44% of cases, respectively. The remainder, as well as the cases of pituitary hyperplasia, metastases, and other less frequent pathologies, were initially diagnosed as NSAs or as masses of unknown nature. When surgery was indicated, pituitary adenomas and other intrasellar masses were operated on by the transsphenoidal route, with the exception of 100% of meningiomas, 83% of craniopharyngiomas, and 10% of NSAs, which were operated on by the transcranial route. Favorable late surgical outcome of prolactinomas could be predicted by a restored PRL response to TRH. However, dopamine agonist (DA) therapy, usually resulting in satisfactory control of PRL levels and in tumor shrinkage, progressively displaced surgery as primary treatment for prolactinomas throughout the study period. After full-term pregnancy, the size of prolactinoma decreased in 7 of 9 patients, and PRL was normal in 2. Surgery was the first treatment for NSAs, with a tumor rela
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PMID:Diagnosis, treatment, and outcome of pituitary tumors and other abnormal intrasellar masses. Retrospective analysis of 353 patients. 1042 6

Pituitary diseases are relatively common entities in the general population. They include pituitary adenomas and hypopituitarism. Pituitary tumours can cause symptoms of mass effect and hormonal hypersecretion that can be reversed with surgical resection or debulking of the adenoma, radiotherapy, or medical treatment. Transsphenoidal adenomectomy is the treatment of choice for acromegaly, Cushing's disease, gonadotropin-secreting tumours; and thyrotropin (TSH)-secreting adenomas. Pituitary irradiation and medical therapy are secondary options. Conversely, medical treatment is the primary choice for prolactinomas. Dopamine agonists are very effective in the treatment of prolactin (PRL)-secreting tumours, with rates of control as high as 80 to 90% for microprolactinomas (< 10 mm) and 60 to 75% for macroprolactinomas (> or = 10 mm). Somatostatin analogues have also shown efficacy in patients with acromegaly who have not responded to surgery or in patients with TSH-secreting adenomas who have not improved with surgery and radiotherapy. In patients with Cushing's disease, who are not cured surgically or who relapse after pituitary adenomectomy and irradiation, steroidogenic inhibitors can be an efficient method of controlling the hypercortisolism. Pituitary insufficiency is the partial or complete loss of the anterior hypophyseal function, which is due to hypothalamic or pituitary disease. Although the classic sequence of loss of pituitary secretion is growth hormone (GH), gonadotropins, TSH, and corticotropin (ACTH), the order to begin the replacement therapy of the deficient hormone(s) is cortisol, thyroxine, androgens/estrogens and, if necessary, GH. There are multiple preparations that can be used to achieve clinical and biochemical improvement. In general, the hormone replacement therapy is lifelong.
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PMID:Pituitary disorders. Drug treatment options. 1071 1

Pituitary adenomas are a diverse group of benign neoplasms. The hormonally active tumours present with well-recognised syndromes and include acromegaly (growth hormone adenoma), Cushing's disease (corticotropin adenoma), and amenorrhea-galactorrhea (prolactin adenoma or prolactinomas). The hormonally inactive, or clinically non-secreting, adenomas generally come to clinical attention secondary to local mass effect or pituitary deficiency. With the exception of the prolactinomas, transsphenoidal surgery remains the first-line therapy for most pituitary adenomas. The current diagnosis and surgical management of pituitary adenomas is discussed.
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PMID:Surgical management of pituitary adenomas. 1238 Jul 32

Pituitary adenoma with growth hormone (GH) and corticotropin (ACTH) production causing apparent acromegaly and Cushing disease is extremely rare. A 45-year-old woman had a pituitary macroadenoma and severe insulin resistance. Physical examination showed a fully developed acromegaly associated with mild Cushingoid features. Serum GH, insulin-like growth factor-I, ACTH, and cortisol levels were all elevated. Hormonal loading tests resulted in GH levels increasing paradoxically in response to thyrotropin-releasing hormone (TRH), but not corticotropin-releasing hormone (CRH). A similar unexpected increase in ACTH and cortisol levels occurred in response to TRH and GH-releasing hormone. After trans-sphenoidal resection of the pituitary macroadenoma immunohistochemistry revealed the presence of either diffuse but faintly GH-positive cells or sparse but distinct ACTH-stained cells. A marked amelioration of insulin resistance was observed postoperatively. The elevated ACTH and cortisol levels should therefore be investigated by CRH and dexamethasone suppression tests for the coexistence of Cushing disease to exclude the possibility of underlying ACTH-producing tumors.
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PMID:A multihormonal pituitary adenoma with growth hormone and adrenocorticotropic hormone production, causing acromegaly and Cushing disease. 1249

Pituitary tumors, depending on their respective cell type, manifest various endocrinopathies. Prolactinomas may present as hypogonadism and galactorrhea and can be diagnosed by measuring morning prolactin levels. Gonadotropinomas rarely cause gonadal hyperstimulation, and dynamic thyrotropin-releasing hormone stimulation testing is often required to elicit a diagnostic gonadotropin and/or subunit secretory response. Acromegaly is a multisystemic debilitating disease for which early diagnosis and treatment are crucial. Diagnostic criteria include a lack of plasma growth hormone suppression during the oral glucose tolerance test and elevation of age- and sex-matched insulin growth factor-1 levels. Patients harboring corticotropin-secreting adenomas characheristically present with signs and symptoms of hypercortisolism. Inferior petrosal sinus sampling for corticotropin may be required for microadenoma localization. Thyrotropinomas produce inappropriate thyrotropin (TSH) secretion and hyperthyroidism. The new third-generation TSH assay has improved the rate of detection of these lesions at an earlier stage.
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PMID:Pituitary tumor endocrinopathies and their endocrine evaluation. 1269 Sep 78

Medical therapy with a dopamine agonist is the most effective for treatment of a prolactin-producing adenoma and is considered as primary treatment. Surgery and pituitary radiation are reserved for patients who either do not tolerate or do not respond to a dopamine agonist drug. A somatostatin analogue is effective medical therapy for patients with acromegaly, and this is usually administered if there is persistent GH hypersecretion after surgical resection. Medical treatment for patients with Cushing's disease is directed at the adrenal glands to reduce cortisol hypersecretion. Unfortunately, there is no effective medical therapy to reduce pituitary corticotropin production. Medical therapy for a gonadotrope adenoma with a dopamine agonist or somatostatin analogue has limited utility but is employed in patients who are unable to undergo surgery and may delay or prevent additional tumor growth. Many patients with a pituitary adenoma can be successfully treated with one treatment, either a dopamine agonist for a prolactinoma or surgery for other types of tumors. A substantial number of patients require multimodality therapy, however, including medical therapy, surgery, and pituitary radiation. Because the biologic behavior of pituitary adenomas varies considerably, a patient with a pituitary adenoma requires lifelong regular monitoring for hormone hypersecretion, tumor recurrence, and development of new pituitary hormone deficiency. A coordinated plan of care among endocrinologists, neurosurgeons, neuroophthalmologists, and radiation therapists is necessary to provide optimal care for these patients.
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PMID:Medical treatment of functional pituitary tumors. 1269 Sep 80

Tumors vary in how they affect pregnancy depending upon the hormone secreted. Some hormone oversecretion syndromes must be controlled to allow pregnancy to proceed without undue maternal and fetal morbidity (Cushing's disease and hyperthyroidism) whereas treatment during pregnancy for other tumors is not necessary. Surveillance for tumor growth during pregnancy is necessary primarily for prolactinomas. A literature search was conducted to identify the effects of pregnancy on pre-existing pituitary tumors and the effects on the outcome of pregnancy due to hormone oversecretion by pituitary tumors. Results show that hyperprolactinemia and Cushing's disease may interfere with fertility and usually need to be controlled to allow for conception. Cushing's syndrome, acromegaly and hyperthyroidism secondary to hypersecretion of thyroid-stimulating hormone (TSH) may increase maternal morbidity (gestational diabetes, hypertension) and fetal morbidity and mortality. Intervention is warranted to remove a tumor that secretes adrenocorticotropic hormone (ACTH) during pregnancy to reduce the risk of fetal loss and to control hyperthyroidism. In contrast, surgery or medical therapy for adenomas that secrete growth hormone (GH) and for clinically nonfunctioning adenomas is not indicated during pregnancy. Pregnancy may cause an increase in the size of tumors that secrete prolactin (PRL), especially macroadenomas, so close surveillance is indicated and re-institution of bromocriptine therapy may be necessary to treat such an increase in tumor size. An increase in the size of other types of tumors during pregnancy is very rare.
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PMID:Pituitary tumors and pregnancy. 1291 26


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