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)

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

A "closed space" subarachnoid hemorrhage (SAH) was produced experimentally in cats by rupture of the right middle cerebral artery to test the working hypothesis that a stressful event which provokes powerful sympathoadrenal discharge: causes a massive release of co-stored endogenous enkephalins together with catecholamines, induces an increased rate of opioid peptide precursor processing and/or synthesis, and eventually results in markedly elevated tissue levels of enkephalins relative to controls and to co-stored catecholamines. Adrenal medulla and other tissues were analyzed for met- and leu-enkephalins by RIAs and norepinephrine and epinephrine by HPLC-EC at 4 hrs, 3, 10, 16 and 30 days post-SAH. Catecholamines of adrenal medulla were already decreased at 4 hrs and by 3 days post-SAH depletion of epinephrine reached 86% and norepinephrine 53% compared to controls. Concurrently, at 4 hrs and 3 days post-SAH, the adrenal medulla was depleted 47% of met- and 53% of leu-enkephalins. By 10 days post-SAH, when catecholamines had regained control levels, met-enkephalin was elevated to 240% of control and 435% compared to the 3 day depletion; it remained elevated through 30 days post-SAH. In comparison, after 10 days reserpine treatment when catecholamines were markedly depleted, met-enkephalin rose to 970% and leu-enkephalin to 360% relative to controls, confirming recent reports in the literature. The data suggest that release of enkephalins originates primarily from epinephrine-type cells of the adrenal medulla in cat.
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PMID:Adrenal enkephalin and catecholamine contents following subarachnoid hemorrhage in cats. 376 79

The chronic stage of vasospasm occurring several days after subarachnoid hemorrhage (SAH) is characterized by the development of histopathologic changes in cerebral arteries causing cerebral ischemia. Numerous experimental data indicate the involvement of immune mechanisms in the angiopathy caused by SAH. Endogenous opioids play also an important role in the ischemic lesions of the brain. Corticotropin releasing hormone (CRH) induces the release of beta-endorphin (beta-END) from hypothalamic neurons and also from mononuclear white blood cells. The function of CRH and beta-END in vasospasm following SAH and the interrelationship between neuroendocrine and immune changes requires further elucidation. In the present study we investigated the influence of CRH injected into cerebral cisterna magna (CM) of rats on beta-END-like level in cerebrospinal fluid (CSF) in acute and chronic phase of cerebral vasospasm following artificial SAH. Acutely CRH induced a significant rise of beta-END-like in CSF both in SAH and sham SAH rats. However, in rats subjected to SAH, a single injection of CRH caused a prolonged rise of 5-END in CSF, which was also seen 2 days after SAH, during the chronic phase of vasospasm. The obtained results indicate that CRH increases neuroendocrine changes induced by SAH, probably by an activation of immune cells involved in the patomechanism of chronic vasospasm.
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PMID:Corticotropin releasing hormone (CRH) increases beta-endorphin (beta-end like) concentration in cerebrospinal fluid of rats with vasospasm following subarachnoid hemorrhage. 1057 71

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is a proopiomelanocortin derivative that has potent anti-inflammatory influences within the brain. The aim of the present research was to determine if there are changes in blood concentrations of this peptide in patients with acute traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). Concomitantly, we recorded clinical parameters and measured blood concentrations of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Twenty-three patients were enrolled in this study--18 had TBI and five SAH. Blood samples for determination of alpha-MSH and TNF-alpha were collected daily from day 1 to day 4 after injury. Baseline concentration of plasma alpha-MSH in patients with acute brain injury of either traumatic or vascular origin was significantly lower than in controls. Patients with TBI or SAH had similar alpha-MSH concentrations and the peptide remained consistently low over four post-injury days. Circulating TNF-alpha on day one was measurable in all patients and there was a negative correlation between plasma TNF-alpha and alpha-MSH. Alpha-MSH was measured again after the acute phase in eight patients. The peptide was substantially increased in all subjects except for two who had an unfavorable outcome. From the well-known protective anti-inflammatory influences of alpha-MSH in the host, reduction in this circulating peptide may have detrimental consequences in brain injury. The data raise the possibility that restoration of normal circulating alpha-MSH through administration of the peptide could be beneficial in patients with brain injury.
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PMID:Alpha-melanocyte-stimulating hormone is decreased in plasma of patients with acute brain injury. 1282 Jun 79

Incidence and prevalence of hypopituitarism are estimated to be 4.2 per 100,000 per year and 45.5 per 100,000, respectively. Although the clinical symptoms of this disorder are usually unspecific, it can cause life-threatening events and lead to increased mortality. Current research has refined the diagnosis of hypopituitarism. Identification of growth hormone and corticotropin deficiency generally requires a stimulation test, whereas other deficiencies can be detected by basal hormones in combination with clinical judgment. Newly developed formulations of replacement hormones are convenient and physiological. Work has shown that many patients with brain damage--such as traumatic brain injury or aneurysmal subarachnoid haemorrhage--are at high risk of (sometimes unrecognised) hypopituitarism. Thus, a much increased true prevalence of this disorder needs to be assumed. As a result, hypopituitarism is not a rare disease and should be recognised by the general practitioner.
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PMID:Hypopituitarism. 1776 14

This commentary on a paper by Bendel and colleagues in the previous issue of Critical Care describes the difficulty in assessing the sufficiency of adrenal responses to endogenous, stress-induced adrenocorticotropic hormone (ACTH) release by the pituitary or to exogenous ACTH administration in the critically ill patient in general, and after subarachnoid hemorrhage in particular. It is argued that comparisons with responses under circumstances of equal stress as well as assessments of severity of disease are necessary to judge the sufficiency of cortisol responses to endogenous and exogenous ACTH before treatment is considered. There are no universally applicable cutoff values for cortisol levels--and increases in cortisol levels with increasing levels of ACTH--for the diagnosis of relative adrenal insufficiency (or as it is now commonly termed, critical illnes-related corticosteroid insufficiency) following, for example, subarachnoid hemorrhage or other intracranial catastrophes. The paper by Bendel and colleagues is critically discussed in view of these concepts.
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PMID:Hypothalamo-pituitary-adrenal axis activity after intracranial catastrophies: what is enough? 1885 50

When performed properly, bilateral inferior petrosal sinus sampling (BIPSS) for adrenocorticotropic hormone (ACTH) is rarely associated with complications. Major complications reported to date include thromboembolism, brain stem infarction, pontine haemorrhage, isolated sixth nerve palsy and venous subarachnoid haemorrhage. We describe a rare case where a predominant contrast extravasation into the subarachnoid space, admixed with a small quantity of venous blood, occurring during BIPSS in a 58-year-old woman with ACTH-dependent Cushing's syndrome, was misinterpreted as venous subarachnoid haemorrhage.
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PMID:Contrast extravasation after bilateral inferior petrosal sinus sampling masquerading as venous subarachnoid haemorrhage. 1996 Jan 50

A 47-year-old man presented to our hospital after suffering transient loss of consciousness and falling to the floor. On admission, his Glasgow Coma Scale score was 11 (E3V3M5), and he exhibited restlessness. Blood examination revealed hyperthyroidism. Computed tomography showed slight traumatic subarachnoid hemorrhage. He developed fever and tachycardia, and was diagnosed with thyroid crisis. Magnetic resonance imaging showed a brain contusion in the right frontal lobe, and encephalopathy signs in the right frontal and insular cortex. Immunocytochemical examinations suggested Hashimoto's disease, and hormone examinations revealed plasma levels were undetectably low of adrenocorticotropic hormone (ACTH) and low of cortisol. Pituitary stimulation tests showed inadequate plasma ACTH and cortisol response, consistent with isolated ACTH deficiency (IAD). The final diagnosis was IAD associated with Hashimoto's disease. Hydrocortisone replacement therapy was continued, and the patient was nearly free from neurological deficits after 18 months. The neuroimaging abnormalities gradually improved with time.
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PMID:Isolated adrenocorticotropic hormone deficiency associated with Hashimoto's disease and thyroid crisis triggered by head trauma. Case report. 2227 27

Subarachnoid haemorrhage (SAH) is known to be related to pituitary dysfuntion in retrospective and short-term prospective studies. We aimed to investigate pituitary functions in patients with SAH in longer follow-up periods to demonstrate if pituitary hormone deficiencies recover, persist or new hormone deficiencies occur. Twenty patients with SAH, who were followed up for 3 years, were included in the present study. Patients were evaluated with basal hormone levels and glucagon stimulation test (GST).Serum basal cortisol and adrenocorticotropic hormone (ACTH) levels were found to be significantly elevated at 3rd year of SAH compared to 1st year. Other basal hormone levels at 3rd year did not show a significant change from the levels found at 1st year. One of the patients had ACTH deficiency at 1st year of SAH and recovered at 3rd year. Growth hormone (GH) deficiency, according to GST,was diagnosed in 4 patients. One patient with GH deficiency at first year was still deficient, 3 of them recovered and 3 patients were found to have new-onset GH deficiency 3 years after SAH. SAH is associated with anterior pituitary dysfunction and GH is the most frequently found deficient hormone in the patients. Although one year after SAH seems to be an appropriate time for the evaluation of pituitary functions, further follow-up may be required at least in some cases due to recovered and new-onset hormone deficiencies at 3rd year of SAH.
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PMID:Three years prospective investigation of pituitary functions following subarachnoid haemorrhage. 2231 89