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)

To elucidate further the pathogenesis of steroid-induced ulceration, plasma gastrin levels, both basal and after a test meal, were studied in normal volunteers and patients treated with glucocorticoids or corticotropin. In normal subjects the acute intravenous administration of 100 mg prednisolone had no effect on plasma gastrin levels. After oral administration of prednisolone (40 mg daily, for four days) a significant increase of the basal, the reactive, and the over 90-min integrated gastrin release was observed. In this group, the glucocorticoid treatment had a slight, but significant influence on gastric acid and pepsin secretion, while acidity and pepsin output stimulated by pentagastrin was not affected. In patients treated with prednisolone for more than 24 weeks, the oral administration of this hormone failed to alter basal gastrin values but affected significantly secretion after the test meal. In patients with multiple sclerosis, after intramuscular administration of corticotropin (60 IU daily, for 12 days), an increase of the basal, the reactive, and the integrated gastrin release also was found. Glucocorticoid-induced hypergastrinemia provides information on the pathogenesis of steroid-induced ulceration.
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PMID:Hypergastrinemia induced by glucocorticoid and corticotropin treatment in man. 18 Jul 97

Corticotropin is one of the few accepted treatments for acute exacerbations of multiple sclerosis and retrobulbar neuritis. Psychosis is a serious side effect usually necessitating discontinuation of the drug therapy. Because mood disorders preponderated in most patients previously described with this psychosis, 27 patients were empirically treated with lithium carbonate concurrently with corticotropin. In none of the patients treated with lithium did a psychotic reaction occur, although in a comparable group of 44 patients previously treated identically with corticotropin but without lithium, six (14%) became psychotic.
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PMID:Lithium prophylaxis of corticotropin-induced psychosis. 21 18

The pineal gland has been implicated recently in the pathogenesis of multiple sclerosis (MS). To investigate this hypothesis further, we studied nocturnal plasma melatonin levels and the presence or absence of pineal calcification (PC) on CT scan in a cohort of 25 patients (5 men, 20 women; mean age: 41.1 years; SD = 11.1; range: 27-72) who were admitted to a hospital Neurology service for exacerbation of symptoms. Plasma alpha-melanocyte stimulating hormone (alpha-MSH) estimations were included in the study since there is evidence for a feedback inhibition between alpha-MSH and melatonin secretion. Abnormal melatonin levels were found in 13 patients (52.0%), 11 of whom had nocturnal levels which were below the daytime values (i.e., < 25 pg/ml). Although melatonin levels were unrelated to the patient's age and sex, there was a positive correlation with age of onset of symptoms (p < .0001) and an inverse correlation with the duration of illness (p < .05). PC was noted in 24 of 25 patients (96%) underscoring the pathogenetic relationship between MS and the pineal gland. Alpha-MSH levels were undetectable in 15 patients (60.0%), low in two patients (8.0%), normal in seven patients (28.0%), and elevated in one patient (4.0%). Collectively, abnormal alpha-MSH levels were found in over 70% of patients. These findings support the hypothesis that MS may be associated with pineal failure and suggest, furthermore, that alterations in the secretion of alpha-MSH also occur during exacerbation of symptoms. The relevance of these findings to the pathogenesis of MS are discussed.
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PMID:Nocturnal plasma melatonin and alpha-melanocyte stimulating hormone levels during exacerbation of multiple sclerosis. 130 32

Comparative study of neurologic, immunologic, and endocrinologic signs of disseminated sclerosis and lateral amyotrophic sclerosis was carried out by radioimmunoassay, monoclonal antibodies, and microcytotoxic Terasaki's test. The data have shown a tendency to hyperthyroid and hypocorticoid states in 60 percent of lateral amyotrophic sclerosis patients. Fluctuations in hormonal levels of disseminated sclerosis patients were quite the opposite in 37.5 percent of cases. Thyrotropic hormone content was rarely changed (in 20 and 18.75 percent of cases, respectively), this permitting a conclusion on the possibility of an extrahypophyseal (thymic) effect on the thyroid in these conditions and on the advisability of using thyrotropin- and corticotropin-releasing hormones (8-arginine-vasopressin) in combined therapy thereof.
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PMID:[Neuroendocrine aspects of the pathogenesis and treatment of disseminated sclerosis and lateral amyotrophic sclerosis]. 211 78

Twenty-five patients with chronic progressing multiple sclerosis were examined for the content of beta-endorphin in blood serum, supernatants of activated lymphocytes and CSF by RIA. At the same time the parameters of cellular immunity were appraised. Different relations were discovered between cellular immunity and the content of beta-endorphin in biological fluids which may play a material part in the pathogenesis of multiple sclerosis.
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PMID:[Study of cellular immunity and the opioid peptide system in patients with multiple sclerosis]. 216 Jan 62

T-cell subpopulations were tested in multiple sclerosis (MS) patients before and after cyclophosphamide (n = 38) and corticotropin (n = 37) treatment and physiotherapy (n = 30). There were no specific changes of subset ratios immediately after immunosuppressive treatment. However, T-cell subpopulations showed great day-to-day variations in MS patients.
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PMID:T-lymphocyte subpopulations in multiple sclerosis--do they help to judge immunosuppressive therapy? 285 Jan 89

In a double-blind placebo-controlled crossover study of ten patients with multiple sclerosis, we found amantadine hydrochloride therapy to be effective in improving fatigability in six. Administration of the drug was associated with significantly higher levels of beta-endorphin-beta-lipotropin and responders had significantly higher levels than nonresponders. Lactate levels were significantly higher and pyruvate levels lower in nonresponders. Amantadine given for fatigue to patients with multiple sclerosis is associated with measurable changes in levels of metabolites and peptides in the circulation.
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PMID:Amantadine, fatigue, and multiple sclerosis. 297 70

The mode of action of adrenocorticotropic hormone (ACTH) treatment in exacerbating multiple sclerosis was studied by short-term infusions of agents that mimic specific and limited pharmacological actions of ACTH and observing for temporally phase-locked clinical changes. The study was double blinded, and agents were administered while the patients were being treated with a standard course of 10-day intramuscular ACTH therapy (40 U twice daily). Antiedema, alkalotic-hypocalcemic, extraadrenal, and sodium-retaining actions were studied using infusions of mannitol, sodium bicarbonate, ACTH, and sodium chloride, respectively. Seven of 8 patients receiving placebo infusions (2.5% glucose) showed no significant clinical change and 1 exhibited an equivocal improvement. Five of 9 patients receiving mannitol showed definite signs of clinical improvement phase-locked to drug administration, with subsequent gradual reversal to baseline. Similar improvements occurred with infusions of NaHCO3 in 5 of 8 patients and of ACTH in 4 of 8 patients. Three of 7 patients given NaCl infusion showed possible mild improvements. The results indicate that mannitol and NaHCO3 induced transient acute improvement in signs at the 95% confidence level in patients with exacerbating multiple sclerosis, with ACTH having a similar effect at the 90% confidence level. These agents mimic some of the known effects of ACTH, which may be important in the therapeutic action of ACTH in multiple sclerosis. A possible role for mannitol and high-dose ACTH in the treatment of demyelinating disease warrants further study.
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PMID:Acute improvement in exacerbating multiple sclerosis produced by intravenous administration of mannitol. 300 Feb 78

Subsequent use of an adrenocorticotropic hormone (ACTH) preparation may be considered in some instances in a patient who has demonstrated a suspected or proven allergic reaction to corticotropin on prior administration. We describe a patient with multiple sclerosis with a history of anaphylaxis to porcine ACTH in whom another course of treatment with ACTH was being considered. The patient had immediate cutaneous reactivity to porcine ACTH but not to the synthetic ACTH peptide, cosyntropin. With a test-dose schedule, we were able to uneventfully administer cosyntropin to the patient. The presence of serum IgE antibody directed against porcine ACTH and absence of IgE antibody against cosyntropin were demonstrated by ELISA technique, corroborating the skin test results. These studies are consistent with previous evidence that immediate hypersensitivity reactions to corticotropin are IgE mediated and support the value of skin testing in the clinical evaluation and management of known or suspected corticotropin hypersensitivity.
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PMID:Evaluation and management of corticotropin allergy. 303 95

In 1984 and at the beginning of 1985 the authors carried out radioimmunoassays (SORIN-CIS kit) the plasma levels of ACTH in 116 multiple sclerosis patients (m-52, f-64) and in 10 cases this radioimmunoassay was done in the cerebrospinal fluid (m-5, f-5). The control group comprised 90 patients with ischialgia and neuroses. The normal value in the plasma was from 0 to 80.86 pg/ml, and in the fluid it was from 0 to 77.08 pg/ml. In multiple sclerosis patients the plasma ACTH level was from 0 to 286.9 pg/ml, in the cerebrospinal fluid from 0 to 89 pg/ml. The values of ACTH were significantly higher in multiple sclerosis patients, mainly in males. In the fluid the level of ACTH was significantly higher in the studied patients. No significant differences in ACTH levels were found between males and females with multiple sclerosis, and in the control group this level was higher in females. Raised ACTH level was found mainly in multiple sclerosis with lung duration of the disease (10 years) at the time of exacerbations. The authors continue studies on the axis hypothalamus-hypophysis-adrenals, on various hormones, prostaglandins, beta-endorphin, biochemical markers, cAMP, cCMP, arylosulphatase A and B MBC etc.
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PMID:[ACTH in the plasma and cerebrospinal fluid in patients with multiple sclerosis]. 303 9


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