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 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

To evaluate the neurochemical, neuroendocrine, and behavioral effects of exogenous corticosteroids in humans, we administered prednisone (80 mg/d orally for 5 days) in a double-blind manner to 12 medically healthy volunteers. Behavioral measures were assessed before, during, and after prednisone administration in all 12 subjects, and cerebrospinal fluid biochemistry was assessed before and during prednisone administration in 9 of the subjects. Prednisone administration was associated with decreases in cerebrospinal fluid levels of corticotropin, norepinephrine, beta-endorphin, beta-lipotropin, and somatostatinlike immunoreactivity. No significant changes were noted in cerebrospinal fluid levels of alpha-melanocyte-stimulating hormone, corticotropin-releasing hormone, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, or 5-hydroxyindoleacetic acid. No consistent or significant group mean changes were observed in structured behavioral ratings, although 9 (75%) of the volunteers studied reported mild behavioral changes while receiving prednisone. Correlations between the neurochemical and behavioral changes are discussed.
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PMID:Prednisone effects on neurochemistry and behavior. Preliminary findings. 197 71

A case report is presented of the need for both bromocriptine and human menopausal gonadotropin (hMG) for induction of ovulation in a patient who developed partial hypopituitarism and persistent hyperprolactinemia even after a transsphenoidal pituitary microadenectomy. The patient, a 27-year old white female, initially presented in 1979 with a history of amenorrhea and galactorrhea after discontinuing oral contraceptives (OCs). Her menstrual cycles had been regular since her menarch at age 13 until she began taking OCs at age 20. Preoperative endocrine evaluation in 1979 revealed serum luteinizing hormone (LH), 9.1 mIU/ml; serum follicle stimulating hormore (FSH), 6.4 mIU/ml; serum thyroid stimulating hormone (TSH), 3.8 mIU/ml; serum prolactine (PRL), 300 ng/ml; serum thyroxine (T4), 6.4 mcg/dl; and an attenuated PRL response to thyrotropin releasing hormone (TRH). Radiographic studies revealed a pituitary tumor of approximately 1 cm in diameter. In July 1979 a transsphenoidal hypophysectomy was performed. Pathologic examination revealed a pituitary adenoma with a monomorphic basophilic cell population with fibrosis and chronic inflammation. The patient required prednisone therapy postoperatively for 3 months secondary to compromised adrenal status. Prednisone therapy was discontinued in October 1979 after a normal cortisol (F) response to induced hypoglycemia was documented. The patient's serum PRL levels remained elevated at 111 ng/ml in August 1979 and 269 ng/ml in October 1979. Her amenorrhea and galactorrhea persisted. Bromocriptine therapy, 2.5 mg 3 times daily, was instituted in October 1979. She became normoprolactinemic, with a serum PRL of 6 ng/ml, and the galactorrhea disappeared but the amenorrhea persisted. In February 1981 she was referred for further consultation on her fertility status. Bromocriptine therapy was discontinued. In April 1981 she underwent a thorough endocrine evaluation. The results indicate that GnRH stimulation was unable to elicit a pituitary gonadotropin response anywhere near normal levels of FSH and LH, thus suggesting pituitary hypogonadotropism. Growth hormone release was subnormal in response to the insulin induced hypoglycemia and L-dopa ingestion. Hyperprolactinemia was obvious but the patient's serum TSH, T4, and adrenocorticotropin (ACTH) levels were normal. A diagnosis of hyperprolactinemia with partial hypopituitarism and gonadotropin deficiency was made. Bromocriptine therapy was reinstituted at 2.5 mg twice daily in June 1981, with good results. In November 1981 her serum PRL was normal, and as she was desirous of pregnancy, ovulation induction with bromocriptine and Pergonal was carried out. The patient is now 6 months pregnant and doing well. This case illustrates the poor functional results for surgery for pituitary microplactinomas.
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PMID:Partial hypopituitarism and hyperprolactinemia: successful induction of ovulation with bromocriptine and human menopausal gonadotropins. 681 37

The brain is an important target organ for both endogenous and synthetic corticosteroid hormones, but the nature of steroid action there is complex. We review a series of studies that was designed to elucidate possible relationships between the behavioral and biological effects of exogenous corticosteroids. In these studies, corticosteroids were administered to intact animals or to currently healthy volunteers, and behavioral and biological indices of corticosteroid effects were jointly assessed. In the first study, chronic corticosterone administration to intact rats resulted in increased locomotor activity (consistent with increased caudate or nucleus accumbens dopamine activity) and increased caudate homovanillic acid (HVA) levels. In the second study, acute dexamethasone administration to healthy human volunteers resulted in increased plasma HVA levels. These findings in animals and humans may help explain vulnerability factors for experiencing psychotic reactions during chronic corticosteroid treatment. To more closely mimic clinical conditions in which "steroid psychoses" develop, we administered a higher dose and more chronic corticosteroid medication (prednisone, 80 mg/day for 5 days) in a double-blind manner to healthy volunteers. Consistent with prior clinical observations, behavioral changes were variable across subjects. Seventy-five percent of the individual volunteers developed mild behavioral side effects during prednisone administration; in addition, significant, specific deterioration in cognitive performance was observed. Prednisone administration was also associated with significant decreases in plasma levels of adrenocorticotropic hormone (ACTH), cortisol, and 3-methoxy,4-hydroxyphenyl glycol (MHPG) and in cerebrospinal fluid (CSF) levels of ACTH, beta-endorphin (BE), beta-lipotropin (BLPH), somatostatin-like immunoreactivity (SLI), and norepinephrine (NE). It was also associated with significant slowing of brain wave electrical activity (viz., an increase in theta wave activity) on quantitative electroencephalography. Several behavioral changes, particularly those relating to mood or cognition, were related to changes in CSF levels of NE, MHPG, ACTH, BE, BLPH, and SLI and to the slowing of brain wave activity. Our preliminary data raise the possibility that the behavioral effects of exogenous corticosteroids have specific neural concomitants and that the pattern of biological changes produced contributes to the behavioral variability observed. Steroid effects on levels of biogenic amines, pro-opiomelanocortin (POMC)-related peptides and somatostatin, among others, as well as on brain electrophysiology, may be behaviorally relevant and are highlighted as being worthy of further investigation.
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PMID:Prospective controlled studies of the behavioral and biological effects of exogenous corticosteroids. 751 7

Elevated levels of circulating corticosteroids are frequently associated with behavioral alterations in man, although the mechanisms by which corticosteroids may affect behavior are poorly understood. To evaluate possible effects of exogenous corticosteroids on brain electrophysiological functioning and the relationship of such effects to behavioral and biochemical changes, we administered prednisone (80 mg p.o. daily for 5 days) in a double-blind manner to 11 medically healthy volunteers. Quantitative electroencephalogram analysis was performed following 4 days of prednisone administration and during the preceding and ensuing placebo administration periods. Central theta wave brain electrical activity significantly increased following prednisone administration and returned to baseline following prednisone withdrawal. This effect was directly correlated with prednisone-induced increases in subjective sadness ratings and with decreases in self-rated energy and well-being. Prednisone-induced reductions in peak alpha wave activity were also directly correlated with increases in subjective sadness and Symptom Checklist-90 ratings and with decreases in self-rated 'hypomanic' symptoms. Further, prednisone-induced increases in theta activity were significantly correlated with prednisone-induced decreases in CSF levels of somatostatin-like immunoreactivity, and prednisone-induced decreases in peak alpha activity were significantly correlated with decreases in CSF levels of norepinephrine and with relative increases (or lesser decreases) in CSF levels of beta-endorphin and beta-lipotropic hormone. This preliminary report of the concomitant development of prednisone-induced changes in brain electrical activity, neurochemistry and behavior highlights areas for future exploration in the study of corticosteroid effects on behavior in man.
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PMID:Quantitative electroencephalographic correlates of steroid administration in man. 823 43

The influence of adrenocorticotropic hormone (ACTH) and prednisone on the effects of amitriptyline (AMI), imipramine (IMI), mianserin (MIA) or nomifensine (NOM) was investigated in forced swimming and in open field tests. ACTH (50 I.U./kg) or prednisone (1 mg/kg) were given in a single dose or for 7 consecutive days alone or together with AMI (10 mg/kg), IMI (10 mg/kg), MIA (10 mg/kg) or NOM (2 mg/kg). It was found that neither ACTH nor prednisone administered alone in a single dose or for 7 days influenced the behavior of rats. ACTH co-administered with AMI or NOM in a single dose or with AMI, IMI or NOM for 7 days potentiated the antiimmobility effect of antidepressant drugs. Prednisone potentiated only antiimmobility effect of NOM in forced swimming test. ACTH as well as prednisone co-administered with NOM (but not with the other drugs), in a single dose as well as for 7 days, increased also locomotor activity in open field. Neither ACTH nor prednisone influenced the effect of MIA in both tests used. It was concluded that the specific synergism exists only between ACTH and tricyclic antidepressants (AMI, IMI). The observed behavioral interaction between ACTH and AMI or IMI does not seem to be mediated by adrenocorticoids (prednisone was without effect). The potentiation of NOM effects by ACTH as well as by prednisone and lack of any interaction with MIA seems to be related with different mechanism of action of those antidepressant drugs.
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PMID:Studies on the interaction of antidepressant drugs with adrenocorticotropic hormone or prednisone in rats. 911 44

The impact of the synthetic glucocorticoid prednisone on adrenal steroid hormone production was examined using 24-hour urinary steroid hormone profiling. Five women, who were chronically taking low-dose prednisone, were tested, and the relevant literature was reviewed. As expected, adrenal glucocorticoid production, measured by urinary terminal cortisol and cortisone metabolites, was markedly suppressed compared to reference range values (p=0.03). Urinary cortisol and cortisone, reflecting circulating glucocorticoids, were decreased to a lesser extent than their terminal metabolites. Urinary dehydroepiandrosterone (DHEA) excretion was dramatically suppressed (p=0.03), while the downstream androgen metabolites androsterone and etiocholanolone were suppressed to a lesser extent. Aldosterone and tetrahydrocorticosterone production demonstrated modest suppression after prednisone administration, but allo-tetrahydrocorticosterone, which is highly sensitive to adrenocorticotropic hormone (ACTH) secretion, was suppressed to a greater extent. Prednisone administration results in a decrease in ACTH secretion by the anterior pituitary, suppressing synthesis of glucocorticoids, DHEA, and DHEA metabolites. Decreased glucocorticoid synthesis is adaptive, because prednisone is active at the glucocorticoid receptor, but suppression of DHEA synthesis is not mitigated by prednisone. DHEA is an important sex hormone precursor, neurosteroid, and endocrine and immune modulator; therefore, DHEA depletion may have significant adverse consequences in terms of sex hormone production, bone health, endocrine and immune system function, and neuropsychiatric status. Studies of DHEA replacement in patients taking prednisone for lupus demonstrate amelioration of some of these adverse effects.
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PMID:Suppression of adrenal function by low-dose prednisone: assessment with 24-hour urinary steroid hormone profiles--a review of five cases. 1659 93

Objective Patients with adrenal insufficiency (AI) need to adapt their glucocorticoid replacement under stressful conditions to prevent adrenal crisis (AC). Prednisone (PN) suppositories are used for emergency treatment. Pharmacokinetics of 100 mg PN suppositories after vaginal or rectal administration was evaluated. Design Single-center, open-label, sequence-randomized, cross-over, bioequivalence study. Methods Twelve females with primary AI were included. Comparison of pharmacokinetics after vaginal and rectal administration of 100 mg PN suppositories. Main outcome measures: bioequivalence (Cmax: maximum plasma concentration of prednisolone; AUC0 -360: area under the plasma concentration curve of prednisolone from administration to 360 min), adrenocorticotropin (ACTH) levels, safety and tolerability. Comparison of ACTH-suppressive effect with subcutaneous and intramuscular administration of 100 mg hydrocortisone. Results Vaginal administration of PN suppositories was not bioequivalent to rectal administration: Cmax and AUC0-360 were significantly lower after vaginal compared to rectal administration: 22 ng/mL (109%) vs 161 ng/mL (28%), P < 0.001; 4390 ng/mL * min (116%) vs 40,302 ng/mL * min (26%), P < 0.001; (mean (coefficient of variation), respectively). A suppression of ACTH by >50% of baseline values was observed 149 min (32%) after rectal PN administration; after vaginal PN administration, the maximum decrease within 360 min was only 44%. Adverse events were more frequent after vaginal administration and mainly attributable to the glucocorticoid deficit due to inadequate vaginal absorption. The ACTH-suppressive effect was more pronounced after parenteral hydrocortisone compared to rectal or vaginal PN. Conclusion Vaginal administration of PN suppositories in the available form is not useful for prevention of AC. Pharmacokinetics after rectal use of PN show inferiority compared to available data on parenteral glucocorticoids. In adrenal emergencies, hydrocortisone injection should be the first choice.
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PMID:Emergency treatment of adrenal crisis with prednisone suppositories: a bioequivalence study in female patients with Addison's disease. 3095 11