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 absorption of a synthetic ACTH-peptide (alpha1-18 corticotropin, Ba 41.795) via the nasal mucosa was investigated in twelve probands. After application of 1 mg into each nostril a rapid increase of the plasma cortisol was observed which returned to the initial value only after 7 hours. In two patients with rheumatoid arthritis and two patients with bronchial asthma who had been treated with regular steroid injections an attempt was made to replace the injections by nasal application. The same therapeutic effects could be obtained, but larger doses were required than when using injection therapy.
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PMID:[Nasal application of a synthetic alpha1-18 corticotropin: an effective form of ACTH treatment (author's transl)]. 18 98

Hypothalamic-pituitary-adrenal function in a well-defined, carefully selected group of 25 patients with extrinsic asthma was assessed by measuring plasma levels of adrenocorticotropic hormone (ACTH) and of 11-deoxycorticol after administration of metyrapone and by measuring the level of cortisol following stimulation with cosyntropin. No difference was demonstrated between asthmatic subjects and 20 normal age-matched controls. In addition, neither the response of the level of ACTH nor of 11-deoxycortisol correlated with the duration of asthma or the severity as assessed in 23 patients by tests of pulmonary function. We conclude that there is no abnormality in hypothalamic-pituitary-adrenal function in patients with extrinsic asthma, and we suggest that previous data suggesting such an abnormality may reflect heterogeneous groups of patients, inaccurate methods, and the variability of normal responses to ACTH and stimulation with metyrapone.
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PMID:Hypothalamic-pituitary-adrenal function in extrinsic asthma. 21 70

The effects of beclomethasone, dipropionate aerosol (DBA) (400 microgram/day) on clinical course, pulmonary function, and pituitary-adrenal function was studied in 34 steroid-dependent asthmatic children. Asthma severity was assessed by daily symptom and medication scores, peak flow measured three times a day, and weekly spirometry. Pituitary-adrenal function was evaluated by diurnal cortisol levels, cortisol responses to intravenous (IV) corticotropin (ACTH), and steroid responses to IV metyrapone. After 12 weeks of BDA therapy, 30 of 34 patients no longer required prednisone. Mean weekly symptom and medication scores and the number of attacks decreased significantly (P less than .01)). A significant improvement was demonstrated in the patients' peak flow (P less than .01), forced expiratory volume in one second, and maximum midexpiratory flow rates (P less than .01). Thirty of the 34 patients initially had abnormal metyrapone responses, 28 had abnormal diurnal cortisol levels, whereas only 14 had abnormal IV ACTH response tests. Although significant improvement was noted in the mean metyrapone and diurnal cortisol tests, only partial recovery of pituitary-adrenal function was observed in 20 patients, complete recovery in 5, and no change in 9. BDA was found to be therapeutically superior to oral steroids in the group of steroid-dependent asthmatic children and produced no serious adverse effects.
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PMID:Treatment of chronic childhood asthma with beclomethasone dipropionate aerosols: II. Effect on pituitary-adrenal function after substitution for oral corticosteroids. 35 20

Cloprednol is a new oral corticosteroid with a short half-life that is presently under investigation for use in asthma. Seventeen steroid-dependent children and adolescents were switched from daily treatment with prednisone to cloprednol for a one-year study. Patients showed a statistically significant improvement in symptoms while receiving cloprednol therapy. Two patients had extraordinarily good responses. Growth trends, bone age, and chest roentgenograms were not remarkably changed by cloprednol. Pulmonary function was stable. There was a significant improvement in fasting morning cortisol levels and ability to respond to metyrapone and adrenocorticotropic hormone (ACTH) challenge. Cloprednol appears to be a promising drug for steroid-dependent patients who require oral corticosteroid therapy.
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PMID:Cloprednol therapy in steroid-dependent asthma. 44 Aug 95

The effect of inhaled beclomethasone dipropionate (dose, 400 mug daily) was investigated in 31 prednisone-dependent asthmatics. In a double-blind noncrossover study of 25 patients dependent on a daily prednisone dose of 17.5 mg or less, the dose of ingested prednisone was significantly diminished through the use of beclomethasone as compared with placebo (P < 0.001). In a subsequent single-blind study of the 12 patients who had received placebo, a similar decrease in prednisone dose was possible when these patients received beclomethasone. In all 25 patients the effect of beclomethasone was maintained for 2 years; 9 came to require less beclomethasone and 1 required more. In an additional single-blind study of six patients with severe asthma, dependent on prednisone in a dose of 20 to 25 mg/d, the response to beclomethasone was more variable and less significant (P < 0.01). However, at 2 years there was no significant benefit (P > 0.05) and there were two treatment failures.In patients in whom reduction of dose or discontinuation of prednisone was possible plasma cortisol values before and after corticotropin administration increased significantly (P < 0.001). Prednisone reduction was associated with the appearance of mild musculoskeletal steroid-withdrawal symptoms of short duration in 15 patients, and recurrence of symptoms of rhinitis in 15 patients. Side effects of beclomethasone included episodes of hoarseness in 6 and easily treated oropharyngeal Candida albicans infection in 14.
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PMID:Subsittution of inhaled beclomethasone dipropionate for ingested prednisone in steroid-dependent asthmatics. 85 28

A 25-year-old female developed IgE-mediated sensitization against human recombinant corticotropin-releasing hormone (CRH) with symptoms of allergic rhinoconjunctivitis and bronchial asthma. The occupational allergy was proved by positive skin prick test, bronchial provocation, dose-dependent histamine release, RAST measurements with CRH allergen (RAST class 3) and RAST inhibition. Using the immunoblot technique, a single allergen band with a molecular weight of less than 14.4 kD in the range between the isoelectric point 5.2 and 5.7 was detected for the CRH extract. Since no endocrinological and behavioral disorders were found, increased CRH-specific IgE was not able to influence the regulatory control of this neuropeptide. After 18 months of avoiding the occupational CRH exposure allergen-specific histamine release and RAST were negative.
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PMID:IgE-mediated inhalant allergy against human corticotropin-releasing hormone. 195 74

The hormonal responses to exercise of 10 asthmatic patients and 12 normal subjects were compared by studying the changes in the plasma levels of growth hormone, prolactin, adrenocorticotropic hormone (ACTH) and cortisol induced by treadmill running. The asthmatic patients demonstrated absence of the plasma cortisol response to exercise (peak increment -15 +/- 21 (SEM) vs 108 +/- 34 nmol.l-1 p less than 0.02). None of these patients were being treated with systemic corticosteroids and there was no difference between the responses of users and non-users of beclomethasone dipropionate. The results suggest the presence of an impaired adrenocortical response to the stress of physical exercise in asthma and indicate the need for detailed evaluation of hypothalamic-pituitary-adrenal function in patients with the disease.
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PMID:The hormonal response to exercise in asthma. 215 17

The paper deals with the investigation of endorphin content in the blood of patients with asthma. The increase in alpha- and beta-endorphin concentration was shown to depend on the severity of clinical manifestations of infectious-allergic and atopic forms of bronchial asthma. This regularity was not observed for gamma-endorphin. The infectious-allergic form of asthma was characterized by drastic reduction in the content of all three endorphin types upon treatment with dexamethasone. The possible role of endorphin reactions in the pathogenesis of asthma is discussed.
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PMID:[Bronchial asthma and endorphins]. 241 23

Synthetic corticosteroids are frequently used to manage asthma and other inflammatory diseases. The timing of such drugs (whether ingested, inhaled, or infused) in relation to body rhythms influences the magnitude of both desired and undesired effects. It is crucial that corticotherapy be correctly scheduled to the circadian system of the hypothalamic-pituitary-adrenocortical (HPA) system. The secretion of cortisol from the adrenal cortex is not constant during each 24-hour period. Instead, production of this hormone varies as a high-amplitude circadian rhythm, with most of the secretion taking place during the initial hours of the activity span and very little late in the evening and during the first half of the sleep span. Results of laboratory and human studies indicate that the timing of exogenous corticosteroids, in relation to the circadian rhythm in HPA activity, is a critical factor. For example, the optimization of corticosteroid therapy for asthmatics entails daily (or alternate-day) administrations in the morning and, if necessary, early afternoon. By timing exogenous corticosteroids early during the activity span, the risk of adrenal suppression is minimized or avoided while bronchial patency is optimally enhanced, i.e., increasing the 24-hour average forced expiratory volume in 1 second (FEV1) and reducing its nocturnal dip. Clinical findings indicate that these results are obtainable with both acute and chronic corticosteroid therapies. In contrast, splitting the daily dose of corticosteroids into several small administrations, such as at mealtimes and before bedtime, markedly increases the likelihood of adrenal suppression without achieving the desired therapeutic effect. The dosing of synthetic corticosteroids late in the afternoon or evening, whatever the route of delivery, suppresses pituitary adrenocorticotropic hormone (ACTH) production during subsequent 24-hour spans, resulting in adrenocortical inhibition. Also, morning dosing of corticosteroids over many years seems to induce less--if any--osteopenia compared to dosing at other times. The adrenal response to exogenous administration of ACTH also is circadian-rhythmic. ACTH dosing in the morning results in greatest adrenal response in terms of cortisol secretion, while dosing in the evening results in least response. Knowledge of the circadian organization of the HPA axis is necessary to optimize the effect of synthetic corticosteroids, whether they be used to treat asthma, rheumatoid arthritis or other cortico-dependent diseases, or as a substitution therapy for Addison's disease.
J Asthma 1988
PMID:Chronobiology and asthma. III. Timing corticotherapy to biological rhythms to optimize treatment goals. 284 6

Concentrations of endogenous opioid peptides in the plasma are increased during exercise and these substances have been implicated in the pathogenesis of asthma induced by chloropropramide and alcohol in diabetic patients. This work was undertaken to determine whether exercise induced asthma might be mediated by endogenous opioids. Plasma beta endorphin, met-enkephalin, and adrenocorticotrophic hormone (ACTH) concentrations were measured in five asthmatic patients and five normal volunteers breathing cold air during exercise. In four of the patients the effect of an infusion of naloxone on FEV1 was also measured during exercise induced asthma. Exercise produced acute bronchoconstriction in all asthmatics, characterised by a fall in FEV1; whereas no change occurred in normal subjects. There was no difference in plasma met-enkephalin, beta endorphin, and ACTH concentration between the two groups. Infusion of naloxone neither prevented nor worsened exercise induced asthma. These data suggest that endogenous opioids probably do not play a part in the development of exercise induced asthma.
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PMID:Exercise induced asthma and endogenous opioids. 294 40


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