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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study aimed at evaluating the effects of a dynamic training program on circulating levels of corticotropin-releasing factor (CRF), beta-lipotropin (beta-LPH), and beta-endorphin (beta-EP) in 8 patients (5 females and 3 males, aged 39-65 years) with classical/definite rheumatoid arthritis (RA). Blood samples were collected immediately before, in the middle of, and after a 6-week high-intensity training period as well as after a subsequent 1-year period of low-intensity training. In addition, baseline data were obtained 3 weeks before the start of the training program. Use of multivariate analyses of variance, and of analyses of variance of contrast variables, indicated a short-term effect of the high-intensity training program for beta-EP with increased levels (P less than 0.05) between the 3rd and the 6th weeks, no significant differences being obtained for CRF or beta-LPH here. Corresponding analyses with regard to the combined high and low-intensity training program revealed CRF (P less than 0.01), and beta-LPH (P less than 0.01) levels to increase over time, no long-term effect being found for beta-EP. Despite the intensity of the dynamic training program, no change was found in pain experience as measured on a visual analogue scale.
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PMID:Dynamic training and circulating levels of corticotropin-releasing factor, beta-lipotropin and beta-endorphin in rheumatoid arthritis. 233 14

Inbred Lewis (LEW/N) female rats develop an arthritis in response to group A streptococcal cell wall peptidoglycan polysaccharide (SCW), which mimics human rheumatoid arthritis. Histocompatible Fischer (F344/N) rats do not develop arthritis in response to the same SCW stimulus. To evaluate this difference in inflammatory reactivity, we examined the function of the hypothalamic-pituitary-adrenal (HPA) axis and its ability to modulate the development of the inflammatory response in LEW/N and F344/N rats. We have found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin 1 alpha, the serotonin agonist quipazine, and synthetic rat/human corticotropin-releasing hormone. LEW/N rats also had smaller adrenal glands and larger thymuses. Replacement doses of dexamethasone decreased the severity of LEW/N rats' SCW-induced arthritis. Conversely, treatment of F344/N rats with the glucocorticoid receptor antagonist RU 486 or the serotonin antagonist LY53857 was associated with development of severe inflammatory disease, including arthritis, in response to SCW. These findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to defective HPA axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N rats to SCW arthritis is regulated by an intact HPA axis-immune system feedback loop.
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PMID:Inflammatory mediator-induced hypothalamic-pituitary-adrenal axis activation is defective in streptococcal cell wall arthritis-susceptible Lewis rats. 253 40

Thymopoietin and thymopentin are well characterized polypeptides influencing immunoregulation by several mechanisms. Proposed as a therapy in diseases with major immune abnormalities such as rheumatoid arthritis, thymopentin improved within 2 weeks some clinical parameters as pain and joint swelling. The hypothesis that this spectacular effect could be mediated through interactions with anti-inflammatory (ACTH) and pain relieving (beta-endorphin) hormones producing cells was tested on the rat isolated pituitary cell model. Thymopentin and thymopoietin can enhance in vitro the levels of ACTH, beta-endorphin and beta-lipotropin in a time- and dose-dependent fashion for physiological concentrations ranging from 10(-12) to 10(-8) mol/l. The action on pituitary cells was restricted to those molecules as no changes occurred in LH, FSH, GH, TSH and PRL levels, after otherwise identical experimental conditions.
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PMID:Thymopoietin and thymopentin enhance the levels of ACTH, beta-endorphin and beta-lipotropin from rat pituitary cells in vitro. 282 Jan 73

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.
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PMID:Chronobiology and asthma. III. Timing corticotherapy to biological rhythms to optimize treatment goals. 284 6

Serum beta-endorphin was assayed without knowledge of study subject category in 44 consecutive patients with primary fibromyalgia syndrome, 3 patients with rheumatoid arthritis (RA), and 30 normal controls, all females. Mean serum beta-endorphin levels were 81 +/- 28 pg/ml in patients with fibromyalgia, whereas those in normal controls and patients with RA were 73 +/- 17 pg/mg and 73 +/- 18 pg/ml, respectively. These differences were not statistically significant. Serum beta-endorphin levels did not correlate with relevant clinical variables in either fibromyalgia or RA groups.
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PMID:Serum beta-endorphin in primary fibromyalgia syndrome: a controlled study. 293 38

The relationship among therapeutically induced affective arousal, depressive symptoms, pain and beta-endorphin levels were explored on 6 patients with chronic, active rheumatoid arthritis. An ABA, n of 1 study methodology was utilized, replicated 5 times. This procedure allowed the analysis of individualized changes across time in response to the therapeutic regimen. The results indicated that the treatment regimen activated the beta-endorphin system, particularly during the early and late phases of treatment. However, beta-endorphin response had little effect on reports of subjective pain. Depressive symptoms were affected positively by the treatment but were not strongly correlated to the beta-endorphin response. The results suggest that pain and depression represent independent systems and that beta-endorphin levels serve more as stress markers than analgesics in chronic, organic pain.
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PMID:Effects of therapeutically induced affect arousal on depressive symptoms, pain and beta-endorphins among rheumatoid arthritis patients. 295 58

This study was designed to examine the effects of aspirin, naloxone and placebo treatment on serum beta-endorphin concentration and joint pain in patients with rheumatoid arthritis (RA). Ten patients with definite or classical RA were studied. All treatments were administered in a randomized sequence. On each study day, the following measurements were carried out at specified time intervals: serum beta-endorphin concentration, serum salicylate concentration and joint pain score on a visual analogue horizontal scale. We conclude that in patients with rheumatoid arthritis suffering from chronic joint pain, serum beta-endorphin does not appear to play a role in pain relief.
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PMID:Effects of aspirin, naloxone and placebo. 296 94

In patients with rheumatoid arthritis, corticosteroids are usually given as a single morning dose to minimize adrenal suppression, because of the well-known circadian rhythm of the secretion of cortisol and corticotropin. However, it has not been so far examined whether there really is a normal secretion pattern of those hormones in all patients with rheumatoid arthritis, as there is in healthy subjects. We therefore studied twelve patients with rheumatoid arthritis who had never been treated before with corticosteroids and disease-modifying drugs such as gold, D-penicillamine or immunosuppressive drugs. The study was designed to examine adrenal secretory activity by measuring the cortisol and corticotropin levels at 2 h intervals throughout a 24 h cycle. The circadian secretion patterns of cortisol and corticotropin were disturbed in most patients. High inflammatory activity of the disease was accompanied by a severe disturbance of the circadian rhythm, whereas patients with low inflammatory activity showed a nearly normal secretion pattern. Besides other causes, the influence of mediators of inflammation on hypothalamic centers, analogous to endogenous pyrogen in fever, must be discussed.
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PMID:[Circadian rhythm of cortisol and corticotropin (ACTH) in patients with rheumatoid arthritis in relation to inflammatory activity]. 303 23

Serum concentrations of luteinizing hormone, follicle-stimulating hormone, prolactin, 17 beta-estradiol, testosterone, androstenedione, dehydrotestosterone, dehydroepiandrosterone sulfate, and cortisol were examined in 14 men with rheumatoid arthritis (RA) and in age-matched osteoarthritis controls. Hypophyseal, adrenal, and testicular responses to stimulation with luteinizing hormone-releasing hormone, adrenocorticotropin, and human chorionic gonadotropin, respectively, were evaluated in 8 RA patients and in 8 age-matched healthy volunteers. Basal serum testosterone concentrations were significantly lower in male RA patients than in the osteoarthritis control subjects (P less than 0.01). After human chorionic gonadotropin stimulation, serum concentrations of testosterone were also lower in the RA patients than in normal healthy controls (P less than 0.05). These findings suggest that diminished testicular steroid biosynthesis might contribute to the serum testosterone deficiency observed in male RA patients.
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PMID:Sex hormone status of male patients with rheumatoid arthritis: evidence of low serum concentrations of testosterone at baseline and after human chorionic gonadotropin stimulation. 314 Aug 23

Serum beta-endorphin levels have been determined in patients with a wide variety of rheumatic disorders as well as a group of healthy men and women controls. Normal levels of endorphin have been found in patients with juvenile rheumatoid arthritis. Patients with rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, gout, ankylosing spondylitis, pseudogout and psoriatic arthritis have diminished levels of endorphins. Speculation is offered to explain these changes. Perturbations in endorphins are postulated to be part of the organism's protective mechanism in inflammatory arthritis.
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PMID:Serum beta-endorphin in rheumatic disorders. 716 73


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