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 both human and animal studies a stimulatory effect of corticotropin-releasing hormone (CRH) on respiration and on cognitive parameters has been demonstrated. Our own studies employing human CRH (hCRH) iv in healthy volunteers and different groups of patients have shown hCRH to be a safe drug. We prospectively studied the clinical effects of a standardized dose of 100 micrograms hCRH iv in 12 elderly patients following major abdominal surgery who remained comatose and were under prolonged respirator therapy over a mean period of 37 days. Cardio-respiratory parameters, blood gas values, plasma cortisol and catecholamines were evaluated before and 30 min following hCRH injection. Furthermore, vigilance was tested using a score system. Ventilation was markedly enhanced following hCRH injection while the cardiovascular parameters were only moderately affected. Vigilance was augmented in all subjects and improved impressively in five patients. The changes were of great benefit for the patients treated and supported their respirator weaning procedures and mobilization training.
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PMID:Effects of corticotropin-releasing hormone on the postoperative course of elderly patients under long-term artificial respiration. 141 43

The opiate antagonist naloxone was suggested for the amelioration of cerebral ischemia after subarachnoid hemorrhage (SAH) following the 1981 report of clinical improvement of ischemic deficits in 2 patients. The deficit in 1 patient was exacerbated by morphine, suggesting that analgesics acting on opiate receptors should be avoided after SAH, and this would include codeine phosphate and dihydrocodeine, both widely used for post-SAH headache. We studied 21 consecutive patients with aneurysmal SAH whose condition was worse than Grade 1 on the Hunt and Hess scale. A single observer graded them to avoid interobserver error, and they were also given a score on the Glasgow coma scale. Each patient was then given an intravenous injection of 0.9% saline as placebo or 0.4 mg (7 patients) or 2.0 mg (14 patients) of naloxone. Five minutes later, the same observer regraded the patient. After 30 minutes, a second injection of placebo or naloxone was given, and the patient was regraded a third time. Each patient received placebo in one injection and naloxone in the other, but the order was randomized and unknown to the observer. There was no beneficial effect of 0.4 mg of naloxone after aneurysmal SAH, and we did not find an elevated level of the endogenous opiate beta-endorphin in the cerebrospinal fluid in the majority (6 of 8 of the patients in whom it was assayed). Five of the patients given 2.0 mg of naloxone did improve transiently, and none deteriorated after the drug, suggesting that naloxone in a high dose may have a place in the management of some post-SAH deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of naloxone on deficits after aneurysmal subarachnoid hemorrhage. 315 81

The effect of acute ethanol administration on plasma levels of beta-endorphin-immunoreactivity and opioid activity was measured in 4 normal volunteers. 60 min following ethanol consumption opioid activity levels, measured by radioreceptorassay, increased significantly with peak rises of more than 400%; levels of beta-endorphin-immunoreactivity did not change significantly. These results are compatible with the effect of the opiate-antagonist naloxone, reversing ethanol-induced coma.
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PMID:Ethanol increases opioid activity in plasma of normal volunteers. 627 Jul 9

A 32-year-old woman had seizures and coma due to severe hypoglycemia (26 mg/dL) in the 32nd week of an otherwise uncomplicated pregnancy. She responded dramatically to the administration of cortisol. Initial endocrine evaluation disclosed prolactin (PRL), corticotropin, and thyrotropin (TSH) deficiencies. The patient recovered completely with cortisol and thyroid hormone therapy and was delivered of a healthy male child at term. Endocrine reevaluations one week and six months postpartum disclosed luteinizing hormone, follicle-stimulating hormone, growth hormone, PRL, corticotropin, and probable TSH deficiencies. The cause of this panhypopituitarism has not been determined. This case suggests that the appropriate initial treatment for spontaneous symptomatic hypoglycemia in pregnancy, while awaiting further endocrine evaluation, is the administration of cortisol.
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PMID:Spontaneous hypoglycemic seizures in pregnancy. A manifestation of panhypopituitarism. 669 58

The changes in the cerebrospinal fluid (CSF) beta-endorphin (beta-end) levels within 24 h following the trauma were examined in 45 patients with head injuries. CSF samples obtained from 25 healthy subjects who had minor surgical operations under spinal anaesthesia were included as the controls. Patients with head injuries were evaluated according to their Glasgow Coma Scale (GCS) scores on admission to the neurosurgery clinic and four subgroups were formed as follows: Group I: minor head trauma (GCS: 13-15) without skull fracture; Group II: mild head injury (GCS: 13-15) with skull fracture; Group III: moderate head injury (GCS: 8-12) and Group IV: severe head injury (GCS: < 8). All patients with head injury had significantly higher CSF beta-end levels than the controls (P < 0.001). The levels in patients with mild head injury (Group II) were significantly higher than those with severe head trauma (Group IV) (P < 0.001). There was not any correlation between the CSF beta-end changes and the GCS scores of the patients. Endogenous opioid peptides are suggested to have a role in central nervous system (CNS) injuries. However, the CSF levels of beta-end in patients with varying degrees of head trauma have not yet been clearly documented in the literature. In the present study, significant changes in CSF beta-end levels are detected in patients with a wide range of head trauma (from minor head trauma to severe injury); however, the increased CSF beta-end levels were not correlated to the early prognosis of the patients.
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PMID:Endogenous neuropeptides in patients with acute traumatic head injury, I: cerebrospinal fluid beta-endorphin levels are increased within 24 hours following the trauma. 886 99

To determine the role of the sympatho-adrenal (SAS) and hypothalamo-pituitary-adrenocortical system (HPAS) after head injury, the relationship between venous blood epinephrine (E), norepinephrine (NE), adrenocorticotropic hormone (ACTH), cortisol levels, and clinical condition was examined in 55 patients. These observations suggest that head injury causes mainly activation of the above-mentioned systems depending on the severity of trauma. An inverse correlation between the levels of E, NE and Glasgow Coma Scale score, indicating the severity of head injury was revealed. ACTH and cortisol were similarly related to the clinical condition, although the observed correlation was less expressed. The changes in hormonal levels were present during the whole research period (1 week), although a certain shift to normalization was observed. However, catecholamines and ACTH levels in plasma were relatively low in severely head-injured patients whose CT scans revealed serious alterations in the mesencephalic-diencephalic area. At the same time their cortisol levels obtained maximal values and their chance to survive was diminutive. The results of this study indicate that investigation of hormones of SAS and HPAS might be useful as an additional method in the complex of ordinary examinations in establishing early prognosis in patients with brain injury.
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PMID:Changes of sympatho-adrenal and hypothalamo-pituitary-adrenocortical system in patients with head injury. 926 33

We studied head-injured patients treated at the Department of Neurosurgery, Silesian University School of Medicine, Katowice. The patients underwent lumbar puncture on days 1, 4 and 7 for diagnostic reasons. The levels of leu-enkephalin (LENK) and met-enkephalin (MENK) were examined in 4.5 ml of cerebrospinal fluid (CSF). The control group included patients with lumbar discopathy from whom CSF fluid was collected during myelography. Enkephalins were extracted by column chromatography and their levels were assayed radioimmunologically. The results indicate that enkephalins may play a certain role in the pathophysiological response of nervous tissue to traumatic injury. Constantly elevated MENK levels together with decreasing LENK levels in patients with a Glasgow coma scale score < or = 8 may be useful as a poor prognostic factor. It is also suggested that LENK and MENK play different pathophysiological roles.
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PMID:Concentration of enkephalins in cerebrospinal fluid of patients after severe head injury. 957 42

Combined pituitary hormone deficiency (CPHD) can be caused by mutation of the pituitary transcription factors POU1F1 or PROP1. More recently mutations in the HESX1, the LHX3 and LHX4 transcription factor genes have also been described as a cause in patients with CPHD. In most patients the disorder is characterized by an impaired production of GH, TSH, PRL and gonadotropins. In some cases of CPHD adrenocorticotropin deficiency is also present. We report the progressive CPHD and its molecular etiology in a woman with CPHD presenting with first symptoms of ACTH/cortisol deficiency at the age of 48 years. The 49 year old patient's initial symptoms were growth retardation at the age of 2 years and symptoms of hypothyroidism at the age of 5 years. The patient never entered puberty spontaneously. No familial history of delayed puberty, growth retardation or other symptoms of CPHD were present. At the age of 48 years the patient presented with the first symptoms of hypocortisolism such as recurring hypoglycaemias and hyponatriaemia with coma. Cortisol, ACTH, TSH, fT3, fT4 and GH as well as LH, FSH and PRL were measured in basal conditions. GH, cortisol and ACTH were also measured in response to an Insulin Tolerance Test. Molecular analysis was performed by PCR amplification and sequencing of exon 1-3 of the PROP1 gene. The patient had insufficiencies of TSH, LH, FSH and GH. PRL was normal. Serum cortisol was low and basal ACTH was normal. However, there were no responses of cortisol, ACTH and GH to hypoglycaemia. Magnetic resonance imaging showed a hypoplastic anterior pituitary lobe. Direct sequencing revealed a homozygous 2 base-pair deletion 301-302delAG in exon 2 of the PROP1 gene. This case suggests that in patients with CPHD ACTH producing cells may be involved at a rather late age.
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PMID:Adrenocorticotrope deficiency with clinical evidence for late onset in combined pituitary hormone deficiency caused by a homozygous 301-302delAG mutation of the PROP1 gene. 1281 7

Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive disease resulting from resistance to the action of adrenocorticotropic hormone (ACTH) on the adrenal cortex, which leads to isolated glucocorticoid deficiency with normal mineralocorticoid secretion. It may present in infancy or early childhood with hyperpigmentation, failure to thrive, recurrent infections, hypoglycemic attacks and convulsions that may result in coma or death. Laboratory investigations reveal low cortisol and androgen levels with high ACTH associated with normal reninaldosterone axis. The disorder may be caused by mutations in the gene of ACTH receptor (MC2R), or mutations in the newly described melanocortin- 2 receptor accessory protein (MRAP) namely, FGD type 1 and FGD type 2, respectively. Twenty five percent of FGD cases are due to the mutations of the ACTH receptor, while FGD type 2 accounts for approximately 15-20% of FGD cases. Here, we report a six-month-old male infant, who presented with recurrent hypoglycemic convulsions. Serum hormone analysis showed low cortisol and androgen levels associated with a high ACTH concentration. No mutation was found in the NR0B1 and MC2R genes excluding congenital adrenal hypoplasia and FGD type 1. We found a homozygous deletion (c. 106+1delG) in intron 3 of MRAP gene. To our knowledge, this is the first Turkish patient reported with FGD type 2 due to a known MRAP mutation.
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PMID:Familial glucocorticoid deficiency type 2: a case report. 2127 26

Familial glucocorticoid deficiency (FGD) or hereditary unresponsiveness to adrenocorticotropin (ACTH) is an autosomal recessive disorder characterized by isolated glucocorticoid deficiency associated with normal mineralocorticoid secretion. Mutations in genes encoding either ACTH receptor or melanocortin 2 receptor accessory protein are responsible for the disease in about 50% of cases, named FGD type 1 and type 2, respectively. Patients may present with hyperpigmentation, recurrent infections, failure to thrive, hypoglycemic seizures, and coma in infancy or early childhood. Here we report the case of a 17-day-old newborn diagnosed with FGD type 1 who presented with hyperbilirubinemia and hyperpigmentation, a sign which was erroneously assumed to be due to prolonged phototherapy by the referring physician. Hormone analysis showed low cortisol and high ACTH levels with normal serum electrolytes and renin-aldosterone axis. Genetic analysis revealed a novel homozygous melanocortin 2 receptor mutation p.Leu225Arg in the patient. The healthy parents were heterozygous for the mutation.
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PMID:A novel mutation in the MC2R gene causing familial glucocorticoid deficiency type 1. 2170 Dec 19


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