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)

In a 49-year-old woman with empty sella syndrome, corticotropin (ACTH) deficiency and various abnormalities, including increased thyrotropin (TSH) secretion, growth hormone (GH) deficiency, and inappropriately high insulin with early phase hypoglycemia, during an oral glucose tolerance test were found. Existence of serum antipituitary antibody suggested that the empty sella and ACTH deficiency may be caused by an autoimmune destruction of the pituitary gland. All of the accompanying abnormalities except for increased TSH secretion were corrected with glucocorticoid supplement. Thyroidal responses to an increase and decrease of endogenous TSH were qualitatively normal, indicating that the patient's TSH was biologically active and the set point of hypothalamic-pituitary feedback regulation for TSH secretion was shifted.
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PMID:ACTH deficiency and TSH hypersecretion in a patient with empty sella turcica. 253 55

A 43-year-old woman with isolated ACTH deficiency in association with transient thyrotoxicosis is reported. The initial evaluation revealed that plasma ACTH and cortisol did not respond to corticotropin-releasing hormone (CRH) in the presence of hyperthyroxinemia and hyperprolactinemia. During the replacement therapy with dexamethasone, she developed transient hypothyroxinemia with persistent hyperprolactinemia. Although thyroid open biopsy did not show any evidence of autoimmune thyroiditis or subacute thyroiditis, the data appear to provide other evidence of a possible relationship between acute adrenal insufficiency and transient thyroid dysfunction.
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PMID:Isolated ACTH deficiency associated with transient thyrotoxicosis and hyperprolactinemia. 255 45

We report here three patients with hypopituitarism accompanied by primary empty sella, whose first manifestations were various mental symptoms. Endocrine studies revealed that two patients showed panhypopituitarism and the other had isolated adrenocorticotropin (ACTH) deficiency. Although several different types of pituitary dysfunctions have been described in a mild form, empty sella is usually asymptomatic. Their first manifestations were mental symptoms; consciousness disturbance, psychomotor agitation, visual hallucination and delusion. Isolated ACTH deficiency is an uncommon disease which etiology is still undetermined. A case with isolated ACTH deficiency associated with an empty sella has been reported before. It is suggested that empty sella might have a role in pathogenesis of isolated ACTH deficiency. The empty sella was confirmed by metrizamide cisternography and magnetic resonance imaging (MRI). These imaging studies are good tools to disclose empty sella. Replacement with cortisone and levothyroxine resulted in an improvement in the mental symptoms in two patients with panhypopituitarism. No alteration was observed following cortisone administration in the patient with isolated ACTH deficiency. Delusion and visual hallucination in this patient poorly responded to treatment with neuroleptics.
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PMID:[Three patients with hypopituitarism accompanied by primary empty sella presenting mental symptoms]. 259 26

We report on a brother and sister with adrenal insufficiency due to isolated adrenocorticotropin hormone deficiency discovered in the neonatal period. The first-born, a male infant, died; pathological findings suggested bilateral adrenal hypoplasia transmitted as an autosomal recessive trait. Plasma estriol levels were assayed during the mother's next pregnancy. The prenatal diagnosis allowed immediate and effective management of the second affected child. The supplementary evidence from the endocrine findings, unavailable on her brother, enabled us to make a diagnosis of isolated central ACTH deficiency. As the defect was found in infants of both sexes in the same family, it is in all likelihood transmitted as an autosomal recessive trait. We consider it important for genetic counselling to perform autopsies on all newborn infants whose death has no apparent cause. Maternal plasma estriol assays during pregnancy can help diagnose fetal adrenal insufficiency, whether the defect is central or adrenal.
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PMID:Isolated familial adrenocorticotropin deficiency: prenatal diagnosis by maternal plasma estriol assay. 283 Jul 87

A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. He presented with a 3-month history of weight loss, weakness, anorexia and persistent tendency to hypoglycemia that he had never experienced before. Basal and dynamic endocrine testing disclosed absent cortisol secretion caused by an isolated ACTH deficiency due to a primary pituitary defect. Corticosteroid replacement therapy allowed again a good glycometabolic control. The possible causes of hypoglycemia in insulin-treated diabetes and the pathogenetic basis of the reported association are discussed.
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PMID:Development of isolated ACTH deficiency in a man with type I diabetes mellitus. 284 79

Human corticotropin-releasing hormone (hCRH) test was performed in 57 normal volunteers and 102 patients with hypothalamic, pituitary and adrenocortical diseases. Intravenous bolus injection of synthetic hCRH, 100 micrograms for adults or 1.5 micrograms/kg for children, increased plasma ACTH and cortisol levels in about 90% of normal subjects. In 47 patients with Cushing's disease, plasma ACTH tended to show an exaggerated response to hCRH and peak ACTH was the most frequent abnormal component among the several reaction parameters. Poor responders among normal subjects and patients with Cushing's disease had significantly higher plasma cortisol levels before CRH administration. Patients with hypothalamic hypopituitarism showed exaggerated response, whereas patients with primary pituitary lesion, isolated ACTH deficiency or adrenal Cushing's syndrome showed no ACTH response. These differences in the response of patients suggest the value of the hCRH test in their differential diagnosis.
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PMID:Human corticotropin-releasing hormone test in normal subjects and patients with hypothalamic, pituitary or adrenocortical disorders. 284 92

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15

To investigate the efficacy of endocrine evaluation in diagnosing and localizing the cause of anterior pituitary failure, 17 patients with suprasellar space-occupying lesions, 4 patients with intrasellar tumors, 8 patients with no detectable anatomical lesion, 1 patient with posttraumatic failure and 1 patient with septooptical dysplasia were investigated. Endocrine evaluation consisted of measuring adrenocorticotropic hormone (ACTH), cortisol, and growth hormone (GH) levels during insulin hypoglycemia test (IHT) and after administration of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GRH). In addition, basal prolactin levels, gonadal and thyroid function were evaluated. The results showed that 4 of 17 patients with suprasellar tumors had normal ACTH and GH responses during IHT and after releasing hormone (RH) administration. Five of these patients had a normal ACTH or cortisol rise but no GH response during IHT. All 5 had a normal ACTH and 3 had normal GH rise after RH. Seven patients with suprasellar tumors had no ACTH or GH response during IHT, but all had an ACTH response to CRH. Only 3 of this group had a GH response to GRH. There was one exception of a patient who showed a GH and ACTH rise during IHT but only a blunted ACTH and no GH rise after RH administration. Four patients with pituitary failure and no demonstrable lesion had an ACTH rise after CRH but no GH rise after GRH, whereas in 3 patients with isolated ACTH deficiency no ACTH rise after CRH was seen. In 4 patients with nonsecreting pituitary tumors normal ACTH responses to IHT and CRH were seen, whereas GH rose during IHT only in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin hypoglycemia test and releasing hormone (corticotropin-releasing hormone and growth hormone-releasing hormone) stimulation in patients with pituitary failure of different origin. 285 21

Isolated adrenocorticotropic hormone (ACTH) deficiency was documented after cesarean delivery in a patient with type I diabetes. A preceding severe headache, subsequent declining insulin requirements, and hypotension are consistent with pituitary infarction in a patient without computed tomography evidence of a pituitary tumor. Antepartum incomplete pituitary infarction with isolated ACTH deficiency is an unusual but potentially catastrophic complication of the pregnant diabetic.
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PMID:Isolated adrenocorticotropic hormone deficiency with antepartum pituitary infarction in a type I diabetic. 298 76

Since ACTH and the opioids display opposite effects on experimentally-induced seizures, cerebrospinal fluid (CSF) levels of ACTH and beta-endorphin (beta-EP) were measured in 6 children (4-8 months) affected by infantile spasms with hypsarhythmia, an idiopathic early onset encephalopathy, and in 8 age-matched controls. beta-EP levels in the patients (76.3 +/- 14.7 fmol/ml, M +/- SD) did not differ from those in controls (109.8 +/- 42.7) while babies with epileptic encephalopathy showed reduced ACTH levels in the CSF (3.8 +/- 1.5) as compared to controls (9.0 +/- 3.7, p less than 0.01). This resulted in an increased beta-EP/ACTH ratio. Another patient previously treated with ACTH showed a normal CSF level of ACTH (9.0) with a normal beta-EP/ACTH ratio while in clinical and EEG remission. These results are consistent with the hypothesis that some infantile seizures unrelated to brain injuries could originate from an ACTH deficiency at central level and/or an imbalance of neuropeptidergic pathways.
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PMID:Reduced ACTH, while normal beta-endorphin CSF levels in early epileptic encephalopathies. 298 81


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