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)

Synthetic human and ovine corticotropin-releasing hormone (hCRH, oCRH) are commonly used as a diagnostic tool of the hypothalamo-pituitary-adrenal axis. In this paper reports about side effects after various modes of CRH-application are analyzed and compared to our corresponding data of human studies with hCRH and oCRH. Generally, CRH is well tolerated after single administration and interval-application of standard doses, although minor side effects appear sometimes after higher doses (greater than 200 micrograms hCRH, oCRH) of CRH-bolus-injections. Predominantly the cardiovascular system (e.g. tachycardia, hypotension, flushing) is affected; neuropsychological symptoms are only seen sporadically (e.g. dizziness). Long term continuous infusion (several hours) of low CRH-doses (hCRH, oCRH) are well tolerated but side effects appear (see above) when cumulated doses of 200 micrograms-300 micrograms/h are given. Standard doses of hCRH and oCRH are also well tolerated in severely ill patients; it has to be considered that higher doses may provoke marked side effects in persons with neurologic disorders, in subjects with coronary heart disease and in patients with endocrinological disorders of the pituitary-adrenal axis, especially in those subjects in whom the blood-brain-barrier may have been damaged (e.g. head injury, intracranial operation). Single hCRH- and oCRH-bolus-injections in standard doses have a very low rate of complications, "non-standard" doses should provisionally be used only in clinical studies with well designed safety-precautions.
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PMID:Safety and side effects of human and ovine corticotropin-releasing hormone administration in man. 203 13

A tilt-table test was performed on 12 untrained subjects to evaluate the humoral adaptation to postural change. The observed peripheral reaction with a reversible short-term rise of norepinephrine (NE) and plasma renin activity (PRA) allowed us to divide the syndrome of the orthostatic dysregulation into a hyponoradrenergic and hypernoradrenergic type. This classification can be helpful for the clinical evaluation and therapy of orthostatic lability. The central excessive stimulation of the antidiuretic (ADH) and adrenocorticotropic hormone (ACTH) follow-ing orthostatic symptoms such as weakness or dizziness was not completely reversible within the observation period of 30 min. The ADH and ACTH increase was not different between the hypo- and the hypernoradrenergic type of dysregulation but was the most sensitive indicator of orthostatic lability: 41% of all subjects showed a hypernoradrenergic orthostatic dysregulation with pronounced NE response and alpha 2-adrenoceptor down-regulation. By use of antiembolism stockings (AES) or dihydroergotamine (DHE) this rate decreased to 16%. This was associated with a significantly reduced NE and PRA response and a diminished alpha 2-adrenoceptor number.
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PMID:Humoral regulation of the orthostatic reaction. 284 55

The efficacy of naloxone in reducing the incidence of side effects after intrathecal injection of morphine and the effects of maternal naloxone administration on the condition of the newborn were evaluated in 40 patients. Patients in labor were given a 1-mg intrathecal injection of morphine and, 1 hr later, either a 0.4-mg bolus of naloxone, followed by a 0.4-0.6 mg/hr intravenous infusion of naloxone, or an intravenous bolus of saline, followed by an intravenous infusion of saline. Intrathecal morphine provided at least 50% pain relief in 78% of patients given naloxone, and in 82% given saline. Intravenous naloxone significantly decreased the incidence of pruritus during labor and delivery. There was no significant decrease in the incidence of nausea, vomiting, somnolence, dizziness, or urinary retention in patients given naloxone. Despite placental transfer of naloxone, neonatal outcome was not adversely affected. For both groups, maternal beta-endorphin levels decreased significantly with the onset of analgesia and returned to control levels at delivery. We conclude that intravenous infusion of naloxone reduced pruritus after intrathecal injection of 1 mg of morphine for labor pain without lessening analgesia or adversely affecting maternal or neonatal status.
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PMID:The effects of naloxone associated with the intrathecal use of morphine in labor. 316 Feb 59

Eight psychiatric patients with tardive dyskinesia (TD) were treated with single doses of the synthetic met-enkephalin analogue FK 33-824 (1, 2, and 3 mg IM) morphine (10 mg SC) and naloxone, an opiate receptor antagonist (0.8 mg IM). The drug effects were assessed by blind evaluation of randomly sequenced videotapes made before and during treatment. FK 33-824 (1, 2, and 3 mg IM) slightly reduced TD (P < 0.05) and increased preexisting bradykinesia. The effect on TD, however, was pronounced only in patients concurrently treated with neuroleptics in relatively high doses. Morphine had a similar although weaker antihyperkinetic effect, whereas naloxone had no effect. Side effects of FK 33-824 included dizziness, heaviness in the extremities, slurred speech, and dryness of mouth. Morphine caused drowsiness, dizziness, ataxia, and nausea, and naloxone had no side effects. The results do not point to a primary role of enkephalin in the pathophysiology of TD, but enkephalin may interact with dopamine functions and potentiate some of the effects of neuroleptic drugs.
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PMID:Enkephalin, morphine, and naloxone in tardive dyskinesia. 677 5

Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15 mmHg (delta = -0.06 +/- (SEM) 0.04 pmol min-1 100mL-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (delta = 0.31 +/- 0.13 pmol min-1 100mL-1). Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope.
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PMID:Neurohumoral antecedents of vasodepressor reactions. 855 62

Fifty-nine patients underwent consecutive colonoscopic examination with premedication of electroacupuncture analgesia (EA) were compared with conventional meperidine analgesia (MA) in pain relief and changes of neurotransmitters in serum. The results showed that analgesic efficacy of both groups were the same but with less side effects in the EA group (P < 0.01) especially in regard to dizziness. Serum concentration of beta-endorphin in both groups has a similar curve change at 4 different phases during colonoscopy. Serum concentration of epinephrine, norepinephrine, dopamine and cortisol showed no significant difference between these two groups. The analgesic effect of EA and MA during colonoscopic examination may be closely related to beta-endorphin production in serum.
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PMID:A clinical study on physiological response in electroacupuncture analgesia and meperidine analgesia for colonoscopy. 916 93

The authors have investigated the effect of naltrexone (NTX) on lowering the urge of alcohol drinking and the action mechanism of NTX. Fifteen healthy male social drinkers voluntarily participated. The experimental method was a double-blind, placebo-controlled cross-over design. To eliminate NTX effect, 1 week washout cross-over interval was taken. Subjects ingested NTX, 50 mg/day, or placebo for 1 week. Then, the alcohol (0.5 ml/kg) challenge test was done in the evening. Blood samples were taken immediately before drinking, at 20 min and at 60 min after alcohol drinking. Plasma beta-endorphin, plasma ACTH and serum cortisol levels were checked. Subjects completed self-report questionnaires such as the visual analog scales of drink urge and the alcohol sensation scales at regular intervals. In the case of NTX pretreatment, the subjects reported significantly (P=.013) less urge to drink alcohol on the self-reporting urge scales, especially at postdrinking 20 min and 60 min than placebo pretreatment. After alcohol challenge, the subjects reported significantly more dizziness (P=.015) in the case of NTX pretreatment, and reported less mood elevation trend, though not significant (P=.052). Basal plasma beta-endorphin levels were not different, but in the case of NTX pretreatment, the increasing degree of plasma beta-endorphin during 20 min after alcohol challenge was significantly (P=.039) higher than with placebo pretreatment. This results show that the NTX reduced the urge to drink alcohol with the mechanism of partially blocking the opioid positive reward system and partially mimicking the alcohol effect.
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PMID:Alcohol urge and plasma beta-endorphin change after alcohol challenge with naltrexone pretreatment in social drinkers. 1218 97

Addison's disease due to adrenal lymphoma usually manifests as bilateral adrenal enlargement. We report a patient with Addsion's disease in whom the initial overt primary adrenal insufficiency was accompanied by an only slightly enlarged right adrenal gland. The 80-year-old man presented with nausea, anorexia, weight loss, and hyperpigmentation of the skin and buccal mucosa. Addison's disease was diagnosed based on this clinical presentation and laboratory findings of low cortisol and high adrenocorticotropin levels. Computerized tomography (CT) of the adrenal glands revealed a small right adrenal tumor. His family refused to allow percutaneous or surgical biopsy to determine the nature of the tumor. His general condition improved after steroid supplementation. However, about 1 year later, dizziness, fever, night sweats, and edema of the lower legs developed, and adrenal CT scanning revealed that the left adrenal gland had enlarged and now exceeded the size of the right one. Left adrenalectomy was performed and pathology showed a diffuse large B-cell lymphoma. Staging work-up using whole-body CT scanning suggested a stage IIIb lymphoma. Chemotherapy was given, but the disease still progressed and the patient died 4 months after diagnosis. Primary adrenal lymphoma should be considered in the differential diagnosis of Addison's disease, even if only slight enlargement of the adrenal glands is found initially.
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PMID:Adrenal lymphoma and Addison's disease: report of a case. 1263 19

Adrenocorticotroph cell pituitary adenomas immunoreactive for adrenocorticotropic hormone (ACTH) but unassociated with preoperative signs of hypercortisolism constitute between 6% and 43% of all ACTH adenomas. Few large series have been published. At our referral center for pituitary diseases, we have encountered 12 patients with silent ACTH adenomas, none of whom exhibited definite clinical features of hypercortisolism preoperatively. Two patients presented with apoplexy, and in 2 patients preoperative neuroimaging studies mimicked craniopharyngioma. Pathological examination revealed 8 adenomas with variably basophilic cytoplasm (type I, including 1 each with coarse basophilic granules and Crooke's hyaline change) and 4 with predominantly chromophobic cytoplasm (type II). Diffuse versus patchy (30% to 50% of cells) immunostaining best distinguished these 2 types; calcitonin staining was focal or negative in both. Two patients had unexpected postoperative courses consistent with acute cortisol insufficiency; 1 patient suffered from a severe flu-like illness, and the other had dizziness and was found to have a serum cortisol level of < 1.0 microg/dL. Both patients improved after cortisol replacement followed by a slow taper. Another patient developed 2 separate pituitary adenomas, a silent ACTH adenoma followed by a pure prolactinoma resected months later. Clonality studies demonstrated that the 2 tumors had arisen from different clonal populations. These cases offer additional insights into clinical, neuroimaging, histological, and biological features of silent ACTH adenomas. Because 2 of these patients seemed to require postoperative cortisol supplementation that otherwise would not have been given, clinicians should be notified about ACTH immunostaining in adenomas from patients without preoperative diagnoses of Cushing's disease, to optimize postoperative care.
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PMID:Silent corticotroph adenomas: further clinical and pathological observations. 1534 17

Insomnia is a sleep trouble in which the patient has difficulties in falling or in staying asleep. There are patients who fall asleep easily, but wake up too early; others have troubles in falling asleep and a third category has troubles with both falling and staying asleep. Independent of the type of insomnia, the final result is a poor-quality sleep, responsible for depressive or irritable mood, loss in concentration, learning and memory capacities. Sleep is essential to emotional and physical health. Inadequate sleep over a period of time is increasing the risks for obesity, diabetes, heart disease and depression. People suffering of chronic insomnia show an increased predisposition for psychiatric problems. People who had sleep troubles reported impaired ability to fulfill tasks involving memory, learning, logical reasoning and mathematical operations. New studies show that insomnia might be a result of the decrease of gamma-aminobutyric acid (GABA), a neurochemical responsible for the decrease of activity in many brain areas. Lower brain GABA levels were also found in people with major depressive disorder and anxiety disorders. Hypnotics, such as benzodiazepines are acting increasing the activity of the GABA neurons. Exposure to stress is associated with a greater risk for insomnia, with individual differences. Stress activates the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis. Increased activity of HPA axis is stimulating the secretion of corticotropin-releasing hormone, further inducing sleep disruption. Insomnia is also associated with depression and anxiety disorders, in which the HPA axis is characteristically overactive. People who show predisposition to sleep troubles have a hyperactive sympathetic nervous system, they are usually suffering from hyperarousal and they have a more intense response to stressful events. Primary sleep troubles (insomnia) has no apparent causes, is lasting more than one month, and is affecting approximately a quarter of the adult population. Secondary insomnia is associated with chronic heart and/or lung diseases, medication which interfere with onset or duration of sleep, constant change of the sleep habits, restless leg syndrome, etc. Besides lifestyle changes and cogn itive-behavioral therapy, in the treatment of insomnia are used hypnotic medicines, advised to be prescribed on short-term cures of one or two weeks. Benzodiazepines are inducing and maintaining sleep. Longer use is responsible for severe side effects--dependency and withdrawal syndrome, daytime drowsiness and dizziness, low blood pressure, memory troubles and change in the melatonin secretion during night-time period. For these reasons were created non-benzodiazepines hypnotics--zolpidem, zaleplon, which are as effective as benzodiazepines, but have fewer side effects. Nevertheless the use of these hypnotics is also restricted to 7-10 days. Zopiclone (Imovane) another short-acting non-benzodiazepine hypnotic has a different chemical structure, but a pharmacologic profile similar to that of the benzod iazepines; the treatment should be of maximum four weeks. Besides generally known concerns related to the use of hypnotics (residual sedative effects, memory impairment, rebound insomnia, abuse, dose escalation, dependency and withdrawal problems) it was signaled a risk of death associated with the use of current hypnotic medications.
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PMID:Main neuroendocrine features and therapy in primary sleep troubles. 2327 43


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