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)

Two patients developed recurrent Cushing's disease 3 and 7 years after total bilateral adrenalectomy. In the first patient, a 65-year-old man, the adrenal tissue was not localized by radioactive cholesterol scintigraphy. Plain x-ray films of the skull revealed a normal sella turcica. Although clinical improvement resulted from the discontinuation of cortisone replacement therapy, urinary free cortisol levels remained elevated and the patient was treated with pituitary irradiation. Serum and urine cortisol levels gradually returned to normal. Four years after irradiation, the plasma adrenocorticotropic hormone (ACTH) concentration was elevated, but tomography of the sella turcica and urinary cortisol excretion remained normal. The second patient, a 41-year-old man, displayed elevated ACTH levels and x-ray evidence of a pituitary tumor at the time of recurrent Cushing's disease. After trans-sphenoidal hypophysectomy, the hypercortisolism abated and the ACTH concentration returned to normal. Adrenal scintigraphy frequently locates cortisol-secreting tissue in patients with recurrent Cushing's disease, and some investigators suggest treatment by the surgical removal of the adrenal remnant. Although the etiology of Cushing's disease is controversial, current evidence suggests that most cases result from ACTH-producing pituitary tumors. We suggest, therefore, that the anterior pituitary gland may be a more suitable target than the adrenal remnant for the treatment of recurrent Cushing's disease.
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PMID:Recurrent Cushing's disease: successful treatment by pituitary irradiation or trans-sphenoidal hypophysectomy in two cases. 625 6

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic-depletion as the cause of PDH.
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PMID:Hypothalamic catecholamine levels in dogs with spontaneous hyperadrenocorticism. 626 Nov 80

A patient with clinical hypercortisolism and an infiltrating ductal carcinoma of the right mammary gland is presented. Provocative testing of adrenal function demonstrated the pattern of ectopic adrenocorticotropic hormone (ACTH) production. Ultrastructural analysis of the tumor revealed 150-200 nm electron-dense granules that when primarily fixed in OsO4 appeared as membrane-bound, centrally dense cored granules. ACTH was extracted from the tumor tissue and immunocytochemically localized in the tumor cell cytoplasm. A clinically significant level of estrogen receptor protein was present in the tumor tissue (120 fmol/mg protein). This case confirms the ability of mammary carcinoma to produce the ectopic ACTH syndrome.
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PMID:Adrenocorticotropin production by a mammary carcinoma. 626 28

Plasma endogenous adrenocorticotropic hormone (ACTH) concentrations as well as basal and post-ACTH-stimulation plasma cortisol concentrations were measured in 6 dogs ultimately shown to have hyperfunctioning adrenocortical tumors. The basal and post-ACTH-stimulation plasma cortisol concentrations were found to fluctuate in 4 dogs in which repeat studies were done. Three dogs had at least 1 normal and 1 abnormally high plasma cortisol concentration after exogenous ACTH administration. A 4th dog had 1 normal and 1 abnormally high resting cortisol concentration. One dog tested twice 3 days apart had similar test results each time and a 6th dog was tested once. All of the dots had at least 1 plasma endogenous ACTH concentration greater than 2 standard deviations below the normal mean. All endogenous ACTH concentrations were less than those previously reported for dogs with pituitary-dependent hyperadrenocorticism. The results indicated that the diagnosis of adrenocortical tumor cannot reliably be made on the basis of the plasma cortisol response to exogenous ACTH; however, the use of plasma endogenous ACTH determination can be an important diagnostic aid.
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PMID:Effect of functional adrenocortical tumors on plasma cortisol and corticotropin concentrations in dogs. 626 86

A 51-year old man presented with the classical features of Cushing's syndrome which had evolved over the previous 5 yr, and was found to have ACTH secretion from an atypical thymic carcinoid tumor. Tumor extract, assayed under conditions designed to prevent artefactual generation of peptides, was found to contain a wide variety of immunoreactive hormones including ACTH, alpha-MSH, CLIP, beta-endorphin and met-enkephalin. The ACTH-related peptides were probably derived from a common precursor, pro-opiocortin, but the presence of met-enkephalin suggests the production of a separate type of precursor molecule. The tumor was locally invasive and, depsite subtotal excision and radiotherapy, continued to secrete large amounts of ACTH. Hypercortisolism was controlled longterm with pharmacological adrenal blockade and steroid replacement.
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PMID:Ectopic secretion of ACTH and met-enkephalin from a thymic carcinoid. 628 29

Pituitary adenomas were found in 21 (84%) of 25 dogs with spontaneous pituitary-dependent hyperadrenocorticism. Six dogs had pars intermedia adenomas, whereas 15 had tumours of the pars distalis. Diffuse corticotroph cell hyperplasia was found in 1 of the 4 pituitaries without adenoma; in 2 dogs with pituitary adenoma, coexisting hyperplasia of the surrounding corticotrophs was also present. Immunocytochemical staining of the pituitaries revealed positive staining for ACTH, beta-lipotrophin, and beta-endorphin in the majority of both pars distalis and pars intermedia adenomas. The most frequent and intense staining was found with anti-beta-endorphin. In most part intermedia tumours, many cells stained strongly for alpha-MSH; double immunostaining of one pars intermedia adenoma for ACTH and alpha-MSH showed that some tumour cells stained only for ACTH or alpha-MSH whereas others contained both peptides. Only occasional cells stained for alpha-MSH in pars distalis adenomas.
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PMID:Immunocytochemical study of the hypophysis in 25 dogs with pituitary-dependent hyperadrenocorticism. 628 90

Corticotropin-releasing factor, a hypophyseo-tropic hormone that stimulates adrenocorticotropic hormone (ACTH) secretion, has recently been isolated, characterized, and synthesized in the sheep and rat. We report on a patient with metastatic carcinoma of the prostate presenting with anterior and posterior pituitary hormone deficiency together with ACTH-dependent Cushing's syndrome. At postmortem examination, large areas of the median eminence and pituitary stalk were replaced by tumor, but the corticotrophs were markedly hyperplastic. Immunostaining of tumor cells was positive for corticotropin-releasing factor and was negative for ACTH and a wide range of other hormones. Radioimmunoassay and bioassays showed that tumor extracts and further purified fractions were active in corticotropin-releasing factor, and the tumor material coeluted with corticotropin-releasing factor on high-pressure liquid chromatography. These studies demonstrate that ectopic secretion of corticotropin-releasing factor is a cause of Cushing's syndrome in human beings. The features of this syndrome include hypercortisolism, pituitary corticotroph hyperplasia, elevation of circulating ACTH levels, and failure to suppress the pituitary-adrenal axis with exogenous glucocorticoids.
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PMID:Ectopic secretion of corticotropin-releasing factor as a cause of Cushing's syndrome. A clinical, morphologic, and biochemical study. 632 3

Three Basenji dogs with renal tubular dysfunction were studied. Hyposthenuria and diminished urine concentrating ability, indicative of nephrogenic diabetes insipidus, were documented. Metabolic acidosis, hyperchloremia, and reduction in glomerular filtration rate also were detected in all dogs. In addition, an exaggerated response to the adrenocorticotropin test and hyperaldosteronism, believed to be secondary to decreased effective circulating blood volume, were detected in all 3 dogs. Thyroxine values were decreased in all dogs and could be correlated with histopathologic changes of the thyroid gland in 2 dogs. Gastropathy and hypergastrinemia were identified in 2 dogs. Diffuse lymphocytic-plasmacytic enteritis was evident in 2 dogs. It was concluded that a urine concentrating defect that may be secondary to hypercortisolism exists in Basenji dogs with renal tubular dysfunction.
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PMID:Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction. 668 36

The susceptibility of adrenocorticotropin (ACTH) in canine blood and plasma to enzymatic degradation has limited the availability of endogenous ACTH assay for veterinary use. This study examined if a proteinase (enzyme) inhibitor, aprotinin, mixed with blood at the time of collection, would limit the loss of immunoreactive (IR) ACTH from canine plasma stored at various temperatures. Blood was collected from laboratory-maintained dogs or dogs with hyperadrenocorticism and placed into EDTA-containing tubes in the presence or absence of aprotinin. Plasma obtained was stored for 4 d at temperatures ranging from -86 degrees C to room temperature (22 degrees C). Results showed that addition of aprotinin preserved IR-ACTH concentrations in plasma stored for 4 d at temperatures < or = 4 degrees C, or in unfrozen plasma stored inside insulated shipping containers containing frozen refrigerant packs. Plasma collected with aprotinin and stored at 22 degrees C showed a slight (17-23%) but significant (P < 0.05) decline in IR-ACTH. Unfrozen plasma collected without aprotinin showed significant (P < 0.05) loss of IR-ACTH during storage under identical conditions. These data indicate that aprotinin has a profound preservative effect upon canine plasma IR-ACTH and that it may be possible to submit unfrozen samples collected with this inhibitor to appropriate reference laboratories for analysis of IR-ACTH.
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PMID:Preservative effect of aprotinin on canine plasma immunoreactive adrenocorticotropin concentrations. 753 Jan 81

In pituitary-dependent hyperadrenocorticism (Cushing's disease), the disturbed regulation of ACTH secretion is associated with neoplastic transformation of corticotropic cells. As these two phenomena are almost indissolubly connected, it is of prime importance to elucidate the factor(s) that induce corticotropic cell proliferation. Here we report on the effects of hypophysiotrophic hormones and intrapituitary growth factors on the proliferation and hormone secretion of the murine corticotropic tumour cell line AtT20/D16v, as measured by DNA content, and ACTH concentration in culture media. In addition, sensitivity to the inhibitory effect of cortisol was assessed under various conditions. Corticotropin releasing hormone (CRH) and vasopressin (AVP) induced proliferation of AtT20-cells. In contrast to that caused by AVP, the CRH-induced proliferation was associated with increased ACTH secretion, which could be inhibited by cortisol. Insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) also stimulated the proliferation of AtT20-cells. The proliferation of AtT20-cells was significantly inhibited by cortisol in all tests. The IGF-I-induced proliferation was the least sensitive to inhibition by cortisol. The growth factors did not stimulate ACTH secretion but IGF-I differed in that it prevented the inhibition of basal ACTH secretion by cortisol. Additional experiments (Western ligand blot analysis) concerning the relative insensitivity of IGF-I induced proliferation to inhibition by cortisol revealed that IGF-I increased the concentration of a 29 kDa IGF binding protein (IGFBP) in the culture medium. The concentration of the 29 kDa IGFBP was slightly decreased by cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proliferation of the murine corticotropic tumour cell line AtT20 is affected by hypophysiotrophic hormones, growth factors and glucocorticoids. 754 6


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