Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of the vitamin D-binding protein was measured in human serum by single radial immunodiffusion. Normal serum concentrations were slightly higher in normal women than in normal men. No race-related difference was found between white people from Belgium and black people from Zaire. Lower concentrations were found in cord serum and in patients with cirrhosis of the liver. Increased serum levels were observed during pregnancy or during the intake of estro-progestogens. The serum level of the vitamin D-binding protein was not altered in various diseases of calcium metabolism (primary osteoporosis, primary and secondary hyperparathyroidism, rickets, osteomalacia or vitamin D intoxication). No correlation was found between serum levels of 25-hydroxy vitamin D and those of its binding protein. From these data the following conclusions can be drawn: 1) The serum concentration of the vitamin D-binding protein (about 6.10(-6)M) largely exceeds the normal serum concentration of 25-hydroxy vitamin D (about 4.10(-8)M), so that this protein is normally for less than 1% saturated, 2) Normal serum levels of the vitamin D-binding protein were observed in several diseases of calcium metabolism, and 3) The free concentration of 25-hydroxyvitamin D is not regulated at a constant level.
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PMID:The measurement of the vitamin D-binding protein in human serum. 88 87

The levels of circulating 25 OH-D were determined by a direct radio-competition methods both in normal subjects and in subjects with various pathological conditions. In normal subjects, the average level of 25 OH-D was higher in summer (42.3 ng/ml) than in winter (29.1 ng/ml), P less than 0.005. Monthly variations in the 25 HO-D levels were found in relation to insolation The level of 25 OH-D was practically normal in osteoporosis (28.9 ng/ml), clearly lower in the mixed forms called "osteoporomalacia" (13.5 ng/ml, P less than 0.005) and very low in osteomalacia (5.8 ng/ml, P less than 0.001). In cases of cortisone osteopathy the average level was 22.8 ng/ml (NS). The level of 25 OH-D was also found to be lower in hepatic cirrhosis (11.7 ng/ml, P less than 0.01), in subjects treated with anticonvulsants (P less than 0.01), and in the course of hyperparathyroidism (P less than 0.002). There was no corelation between the level of 25 OH-D and calcaemia, phosphoraemia, circulating immunoreactive parathyroid hormone, or the relative osteoid volume. In contrast, there seemed to be a good correlation with the level of alkaline phosphatasaemia. The level of 25 OH-D was also determined in 4 subjects with vitamin-resistant osteomalacia: in 3 cases hepatic hydroxylation seemed normal, indicating the possibility of a subsequent disorder of vitamin D metabolism; in one case the absence of hepatic hydroxylation was noted.
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PMID:[Study of circulating 25 hydroxyvitamin D]. 98 30

Fifty patients with liver cirrhosis (36 alcoholic, 1 drug-induced, 7 posthepatitic, and 6 cryptogenic) and normal renal function were investigated to determine whether PTH levels in serum, measured using the common midregion human PTH-(44-68) RIA, are elevated in such patients and whether this is related to impaired liver function rather than to the effect of secondary hyperparathyroidism. Their data were compared with those from 25 control subjects. The median PTH level of 462 +/- 18 ng/L (+/- SEM) was significantly increased (P less than 0.01) in cirrhotics compared with that of 236 +/- 13 ng/L in the control group. Significant correlations were found between PTH levels and parameters of liver function such as prothrombin time (r = -0.40; P less than 0.01), albumin as a percentage of total protein (r = -0.48; P less than 0.01), bilirubin (r = 0.35; P less than 0.05), albumin (r = -0.34; p less than 0.05), and cholesterol (r = -0.32; P less than 0.05), but not for antipyrine clearance, suggesting increasing PTH with decreasing liver function. The median calcium level (2.26 +/- 0.03 mmol/L), corrected for changes in albumin, was near the lower limit of the normal range (2.25-2.60), but corrected calcium and PTH were positively correlated (r = 0.33; P less than 0.05), indicating that the elevation is not reactive to calcium depletion. A negative correlation existed between PTH and 25-hydroxy-cholecalciferol (r = -0.49; P less than 0.05), the main circulating metabolite of vitamin D. Normal values in an immunoradiometric assay that detects the whole sequence of human PTH-(1-84) suggest that fragments rather than the intact hormone are responsible for PTH elevations in cirrhosis. The positive correlation between midregion PTH and corrected calcium is probably an artifact of the correction formula. In conclusion, midregion PTH fragments are increased in patients with liver cirrhosis. The reason for this elevation may well be the impaired liver function rather than secondary hyperparathyroidism.
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PMID:Parathyroid hormone and cirrhosis of the liver. 222 13

Elevated serum levels of intact parathyroid hormone (PTH) have been reported in severe versus mild biliary cirrhosis. The aim of this study was to determine whether hyperparathyroidism was present in severe liver disease on the basis of the inability of the liver to catabolize the hormone. Because biologic activity resides in the amino terminal, and amino terminal PTH determinations have not been routinely made in liver disease, it is possible that hyperparathyroidism was previously missed in these patients. Accordingly, we obtained fasting blood from 11 patients with severe liver disease and 8 age-matched controls. We measured intact, amino terminal, and mid-region PTH, vitamin D metabolites, bone gamma carboxyglutamic acid protein (BGP), ionized calcium, phosphorus, magnesium, and liver function tests. Serum levels of PTH were normal with all assays and 1,25(OH)2D levels were not elevated. These findings argue against the possibility that hyperparathyroidism plays a role in the pathogenesis of hepatic osteodystrophy.
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PMID:Absence of hyperparathyroidism in severe liver disease. 249 4

Hypertension can be ameliorated by certain concomitant disease states, especially those in which serum globulin is elevated. Blood pressure has been reduced in cases of cirrhosis of the liver, chronic alcoholism, congestive heart failure, arthritis, hypothyroidism, and myeloma. These clinical findings were confirmed experimentally when animals with various models of hypertension became normotensive after the development of a modest degree of liver damage with hyperglobulinemia. Other diseases, not associated with hyperglobulinemia, that can lower blood pressure are stroke, uremia, hyperparathyroidism, and malnutrition. When any of these diseases occur in hypertensive patients, their influence on blood pressure must be considered when determining treatment and prognosis.
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PMID:Disease states in which blood pressure is lowered. 261 Jul 59

If conservative treatment of hypercalcemic crises is ineffective, low calcium bath or zero calcium bath hemodialysis represent good alternatives. We report 5 patients (from 54 to 82 years old) treated with calcium free acetate hemodialysis because of hypercalcemic crises due to breast cancer with bone metastases, thiazids' medication and immobilisation, liver cirrhosis, hepatocellular carcinoma and hyperparathyroidism. By 3 hours' therapy calcium concentration could be reduced from a mean value of 3.74 mmol/l (3.13-4.46) to 2.47 mmol/l (1.38-3.12). In 3 cases rapid clinical improvement was achieved and in 4 cases the subsequent conservative therapy was sufficient to maintain serum calcium levels within reference range. In accordance to other investigators we consider hemodialysis as an effective method of low risk in hypercalcemic crises. Calcium rebound may occur in patients with hyperparathyrodism.
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PMID:[Calcium-free hemodialysis--value in therapy of hypercalcemic crisis]. 292 46

In addition to direct toxic effects on endocrine organs chronic alcohol intake affects regulation of endocrine systems by disturbed liver function. As a result in patients with alcohol-induced liver cirrhosis gonadal axis is characterized by low total and free testosterone, elevated estradiol. LH, FSH, and sexual hormone binding globulin and an enhanced conversion of testosterone to estradiol. Prolactin also is found to be elevated. The thyrotropic axis is characterised by low T3- und T4- as well as elevated rT3-values and normal TSH. STH is elevated, while somatomedin C is decreased. The corticotropic axis may show an abolished circadian rhythm, a negative Dexamethasone-test, low transcortin and elevated free cortisol levels. The disturbance of the calcitropic axis leads to osteoporosis and osteomalacia, due to intestinal hyperparathyroidism and vitamin D malnutrition. In 50% of chronic alcoholics there are elevated insulin and glucagon values and a pathological glucose tolerance test.
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PMID:[Alcohol and endocrinologic homeostasis]. 306 42

A 25-yr-old black man with cystic fibrosis and cirrhosis developed symptoms of osteomalacia and hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and low circulating 25-hydroxyvitamin D (25-OHD). Serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) was within the normal range. Iliac crest bone biopsy confirmed the diagnosis of osteomalacia. Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal. Intramuscular vitamin D2, 10,000 IU every 8-12 week, improved symptoms, raised serum 25-OHD to normal, and increased circulating 1,25-[OH]2D to values five times normal. Over the next 10 mo circulating 1,25-[OH]2D remained elevated despite normalization of serum calcium, phosphorus, and parathyroid hormone. Repeat bone biopsy 1 yr after parenteral vitamin D showed healing of the osteomalacia. Malabsorption of vitamin D appears secondary to profound steatorrhea due to pancreatic insufficiency and secondary biliary cirrhosis. Although extensive hepatocellular disease was present, hepatic conversion of vitamin D to 25-OHD was intact. Both high and low circulating 1,25-[OH]2D levels during active osteomalacia have been reported; initially, the level was in the normal range and higher values in this patient occurred with repletion of 25-OHD substrate. This study shows that symptomatic osteomalacia may be a major manifestation of cystic fibrosis in those patients surviving into adulthood. Measurements of serum 25-OHD in cystic fibrosis patients may identify those who should receive supplemental vitamin D.
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PMID:Vitamin D metabolism and osteomalacia in cystic fibrosis. 387 14

A laboratory study including estimation of 25 OH vitamin D, terminal parathormone (PTH) C and N fractions, urinary cyclic AMP (AMP cU) and ionised calcium, was carried out in 25 patients, 10 cases of alcoholic cirrhosis without decompensation (group 1) and 15 cases of decompensated cirrhosis (group 2) in order to seek evidence in favour of hyperparathyroidism secondary to cirrhosis. The results show: 1) The existence of hypovitaminosis D which seems to be independent of the liver failure. 2) A very definite increase in terminal PTH N in group 2 compared with group 1 (p < 0.01), without any increase in terminal C fraction. 3) An insignificant increase in urinary cyclic AMP in group 2 compared with group 1. 4) A low serum ionised calcium in group 2 compared with 14 controls (p < 0.05). The terminal N PTH was correlated significantly with urinary cyclic AMP and ionised calcium. The evidence is in favour of secondary hyperparathyroidism where the ionised calcium plays a role, but one wonders whether other factors do not intervene, e.g. serum iron, owing to the discovery of a significant link between serum iron and terminal N PTH levels.
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PMID:[Hyperparathyroidism secondary to cirrhosis. Arguments supplied by ionized calcium, urinary cyclic AMP and blood N-terminal parathyroid hormone]. 625 46

Serum parameters of calcium metabolism were measured in 32 consecutive patients with biopsy-proven cirrhosis due to either hepatitis (n = 13), alcohol abuse (n = 11), Wilson's disease (n = 3), or primary or secondary biliary cirrhosis (n = 5). All measurements were normal in the small group of patients with Wilson's disease. The serum concentrations of albumin, vitamin D-binding protein, total calcium, phosphorus, and 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) were decreased in the other patients with cirrhosis, but their mean serum concentrations of ionized calcium, 25-hydroxyvitamin D3 (25-OHD3) and free 1,25-(OH2)D3 index were normal. A slight but significant increase in the serum PTH measured using a carboxyl-terminal antiserum was found. A significant correlation was found between the serum concentration of either albumin or vitamin D-binding protein and the serum concentrations of total calcium, 25-OHD3, 1,25-(OH2)D3, and PTH but not with ionized calcium or free 1,25-(OH2)D3 index. The observed abnormalities of calcium metabolism in unselected patients with cirrhosis were mainly due to decreased protein synthesis. Only the patients with severe cirrhosis had decreased concentrations of 25-OHD3 but they were nevertheless able to maintain a normal ionized serum calcium and free 1,25-(OH2)D3 level, possibly by means of compensatory hyperparathyroidism.
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PMID:Serum vitamin D metabolites and their binding protein in patients with liver cirrhosis. 654 47


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