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)

With the aim of evaluating the glucocorticoid function and the role of the adrenal gland in hypogonadism and feminization of cirrhotic patients, we examined 11 patients with virus-induced liver cirrhosis and 8 normal subjects as controls. In each subject serum levels of cortisol (C), progesterone (P), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), delta 4-androstenedione (A), estrone (E1), testosterone (T), luteinizing hormone (LH) were assayed in basal conditions and after adrenocorticotropic hormone (ACTH) stimulation. Serum levels of ACTH, C, E1, estradiol (E2), T were assayed in basal condition and after dexamethasone suppression test. Moreover, a circadian study of ACTH, C and corticosteroid-binding globulin (CBG) was performed, with blood samples drawn at 8:00 and 20:00 on two consecutive days. Our results demonstrate that in cirrhosis: 1) normal levels of C, when metabolism is altered and CBG levels are reduced, are maintained by inhibition of ACTH secretion; 2) circadian rhythmicity of the pituitary-adrenal axis is well preserved; 3) in non-alcoholic cirrhosis, too, there is a reduction of androgens (T, DHEA, DHEAS, A) and a rise of estrogens (E2 and, more markedly, E1) and P; 4) in cirrhotic men E1 is mainly of adrenal origin and contributes, through negative feedback on LH secretion, to low levels of T.
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PMID:[Hypothalamo-pituitary-adrenal function in liver cirrhosis of viral etiology]. 174 24

A histological and ultrastructural study has demonstrated that cutaneous pigmentation in primary biliary cirrhosis (PBC) is due to the presence of increased amounts of melanin, widely dispersed throughout both epidermis and dermis. No deposits of stainable iron were observed. Compared with skin from matched sites from control patients with alcoholic cirrhosis and no pigmentation, the melanocyte: keratinocyte ratio was not significantly higher in PBC. However, in PBC, melanosomes persisted to unusually high levels in the epidermis and were packaged in larger membrane-bound clusters than was the case in the controls. Whether excess melanin results from increased melanogenesis or defective melanin degradation remains unclear, although there is some evidence favouring the latter mechanism. No hormonal (beta-MSH and ACTH) or chemical (bile salt irritation) stimuli to increase melanogenesis were demonstrated.
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PMID:Melanin pigmentation of the skin in primary biliary cirrhosis. 627 1

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
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PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

A novel poly(vinyl chloride) matrix membrane sensor responsive to 4-nitrophenylphosphate (4-NPP) substrate is described, characterized and used for the potentiometric assay of acid (ACP) and alkaline (ALP) phosphatase enzymes. The sensor is based on the use of the ion-association complex of 4-NPP anion with nickel(II)-bathophenanthroline cation as an electroactive material and nitrophenyloctyl ether (NPOE) as a solvent mediator. The sensor displays good selectivity and stability and demonstrates a near-Nernstian response for 4-NPP over the concentration range 9.6x10(-6) to 1.0x10(-2) M with an anionic slope of 28.6+/-0.3 mV decade(-1) and a detection limit of 6.3x10(-6) M over the pH range 4.5-10. The sensor is used to measure the decrease of a fixed concentration of 4-NPP substrate as a function of acid and alkaline phosphatase enzyme activities at optimized conditions of pH and temperature. A linear relationship between the initial rate of 4-NPP substrate hydrolysis and enzyme activity holds over 0.05-3.0 and 0.03-3.4 IU L(-1) of ACP and ALP enzymes, respectively. Validation of the method by measuring the lower detection limit, range, accuracy, precision, within-day repeatability and between-day-variability reveals good performance characteristics of the proposed sensor. The sensor is used for the determination of acid and alkaline phosphatase enzyme activities in biological fluids of some patients suffering from alcoholic cirrhosis, acute myelocytic leukemia, pre-eclampsia and prostatic cancer. The sensor is also utilized for assessment of alkaline phosphatase enzyme in milk and dairy products. The results obtained agree fairly well with data obtained by the standard spectrophotometric methods.
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PMID:A simple-potentiometric method for determination of acid and alkaline phosphatase enzymes in biological fluids and dairy products using a nitrophenylphosphate plastic membrane sensor. 1936 23

A 62-year-old man, receiving chronic haemodialysis and suffering from alcoholic liver cirrhosis and chronic pancreatitis, presented with hypoglycaemic coma. Plasma cortisol was undetectable (< 5.5 nmol/L) with suppressed adrenocorticotropic hormone (ACTH), which established a diagnosis of adrenal failure due to ACTH deficiency. Twenty-five milligrams of oral hydrocortisone eradicated hypoglycaemia. Presentation of adrenal failure in this patient was atypical because he was hypertensive, serum electrolytes including sodium were normal and anaemia was unremarkable, which were all due to end-stage renal disease and its treatment with haemodialysis. As far as we are aware, this is the first case report of hypoglycaemic coma due to adrenal failure in a chronic haemodialysis patient.
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PMID:Hypoglycaemic coma due to adrenal failure in a chronic haemodialysis patient. 2598 98