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)

Serum Group-specific component (a probable vitamin D transport protein) concentrations have been measured in 72 patients with chronic liver disease. Low mean values were found in groups of patients with cirrhosis and metastatic liver disease. In a group of patients with biliary tract disease the mean value was not significantly different from normal except for seven patients with severe bone disease who were found to have the lowest levels. The mechanism for the reduction remains to be clarified, but low Group-specific component values may play a contributory role in the osteodystrophy of chronic obstructive liver disease.
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PMID:Group-specific component [Gc] levels in chronic liver disease. 7 53

To investigate osteodystrophy in liver cirrhosis, 99Tcm MDP (methylene diphosphonate) bone scintigraphy was performed on 36 patients with liver cirrhosis. Abnormal lesions were detected in 17 out of 36 scans (47.2%). On the other hand, areas of increased uptake were uncommon in patients with chronic active hepatitis (1/11 cases). Plasma vitamin D3 fractions [25(OH)D3, 24.25(OH)2D3 and 1.25(OH)2D3] were decreased. Statistically significant depletion of 1.25(OH)2D3 was observed in cases with positive bone scintigraphy. 1 alpha(OH)D3 (1-2 micrograms/day) was administered for 6 months to nine patients having abnormal bone scans. Six of them showed improvement without any apparent side-effects. We conclude that hepatic cirrhotic osteodystrophy can be diagnosed positively by 99Tcm MDP bone scintigraphy and can be treated accordingly.
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PMID:Osteodystrophy in liver cirrhosis: detection and treatment evaluation using 99Tcm methylene diphosphonate bone scintigraphy. 184 51

In order to determine the prevalence and severity of hepatic osteodystrophy by non-invasive means we compared 115 consecutive ambulant patients with histologically proven chronic liver disease to 113 age and sex matched control subjects. Methods used included the assessment of fracture prevalence rates, spinal radiography, and measurements of bone mineral density in the spine and the forearm. Spinal and peripheral fractures were more prevalent in the patients than in the control subjects (p less than 0.03 and p less than 0.01 respectively). The type of the underlying liver disease did not significantly affect the fracture prevalence rates, but alcoholic patients sustained more peripheral fractures than patients with other hepatic disorders (p less than 0.05). The bone mineral densities of the spines and the forearms were significantly reduced in male patients of all age groups and in female patients aged 60 years or more (p less than 0.001 for men and p less than 0.01 for women for both measurements). The prevalence rates of spinal and forearm osteoporosis were twice as high among patients with liver disease than in control subjects regardless of the definitions used. The presence of cirrhosis and hypogonadism were major risk factors for development of both spinal (Beta coef = 0.190 and 0.176; SE = 0.079 and 0.086 respectively) and forearm osteoporosis (Beta coef = 0.20 and 0.29; SE = 0.073 and 0.80 respectively). Spinal bone density was the predominant determinant of spinal fractures (Beta coef = -0.007; SE = 0.001), while hypogonadism (Beta coef = 0.363; SE = 0.075) and cirrhosis (Beta coef = 0.185; SE = 0.068) were the major predictors of peripheral fractures. The concentrations of serum calcium and serum vitamin D metabolites and the use of corticosteroids were apparently without effect on the prevalence of skeletal fractures or bone density.
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PMID:Osteoporosis and skeletal fractures in chronic liver disease. 231 34

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

Elevated serum calcitonin (SC) levels have been observed in cirrhotic patients although the biological activity of this hormone in such patients is not known. Twenty one patients diagnosed histologically of alcoholic hepatic cirrhosis (AC) and 12 healthy controls were studied evaluating the degree of hepatocellular failure by means of clinical and biological criteria. Serum calcitonin was determined by means of a radioimmuno assay (RIA) and a radioimmunometric assay (IRMA) in which by combining two monoclonal antibodies, mature calcitonin is determined. These levels almost correspond to levels of biologically active calcitonin. The results obtained show a significant increase in SC in patients with AC when compared to controls, both by RIA (280 +/- 197 pg/ml, p less than 0.001) and IRMA (18 +/- 6 pg/ml, p less than 0.01). Control values were 57 +/- 23 pg/ml and 12 +/- 7 pg/ml respectively. Mean SC values in cirrhotic patients obtained by RIA were 4.9 times greater than their controls while the increase in SC in cirrhotics determined by IRMA was 1.5 times the control, thus obtaining a significant direct correlation between SC and severity of hepatic failure. According to our results, the elevated SC found in cirrhotics is mainly due to immature or non active forms directly related with the degree of severity of the hepatic failure and probably to high Molecular Weight molecules. The slight increase in mature SC in this type of patients is probably due to hormonal mechanism of bone regulation, defendants of hepatic osteodystrophy.
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PMID:[Heterogeneity of calcitonin in liver cirrhosis]. 260 81

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.
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PMID:Hyperparathyroidism, cirrhosis, and portacaval shunt. A new clinical syndrome. 325 57

Metabolic bone disease has long been recognized in chronic liver disease, especially cholestatic or alcoholic liver diseases. The aim of the present study was to investigate the prevalence and severity of osteodystrophy in cirrhotic men and the correlation of its incidence with the clinical severity of cirrhosis in an endemic area of post-necrotic hepatitis. We measured serum levels of osteocalcin, 25-hydroxyvitamin D, parathyroid hormone mid-molecule, calcium and testosterone in 74 cirrhotic men (Child-Pugh's classification grade A n = 30, B n = 21 and C n = 23) and 16 healthy controls. Standard X-rays and bone mineral densities of lumbar spine were performed in 30 patients with post-necrotic cirrhosis and 10 healthy controls. Serum levels of osteocalcin, parathyroid hormone and testosterone were significantly lower in patients with cirrhosis than in controls. Changes paralleling an increased severity of cirrhosis were found in serum levels of 25-hydroxyvitamin D and testosterone, but not in the serum levels of osteocalcin and parathyroid hormone. The lumbar bone mineral density was significantly lower in patients with post-necrotic cirrhosis than in controls (0.97 +/- 0.13) vs 1.07 +/- 0.12 g/cm2, P < 0.05) and was correlated with serum 25-hydroxyvitamin D levels (r = 0.467; P < 0.005). There was no correlation between the bone mineral density and serum osteocalcin or the clinical severity of cirrhosis. The prevalence of spinal osteoporosis, as defined by a lumbar bone mineral density greater than two standard deviations below the mean value of the controls, was 20% in cirrhotic patients compared with 10% in controls. Two (6.7%) patients (both grade C) had spinal compression fractures compared with none in the control group. In conclusion, serum osteocalcin and lumbar bone mineral density were significantly lower in cirrhotic men than in controls. However, they were not correlated with each other or the clinical severity of cirrhosis.
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PMID:Metabolic bone disease of liver cirrhosis: is it parallel to the clinical severity of cirrhosis? 874 12

Bone mineral density (BMD) of the lumber vertebrae and factors related to bone metabolism were determined in patients with chronic viral hepatitis and patients with liver cirrhosis to clarify correlations between hepatic dysfunction, considered to be one of the causes of hepatic osteodystrophy, and decrease in bone mass. BMD of the second to fourth lumbar vertebrae was determined with a Lunar (Madison, WI, USA) DPX, a dual-energy X-ray absorptiometry diagnostic system. BMD was significantly lowest in patients with liver cirrhosis, followed by patients with chronic hepatitis, and healthy subjects, in this order. There was a significantly positive but weak correlation between albumin and BMD. Levels of 25(OH)D and 1,25(OH)2D were significantly lower in patients with liver cirrhosis than in those with chronic hepatitis. BMD and vitamin D were decreased in all patients whose cholinesterase (ChE) was below 0.3 delta pH. Urinary pyridinoline (Upyr) was significantly higher in the patients with liver cirrhosis, in whom bone mass was decreased, than in the patients with chronic hepatitis, whereas serum osteocalcin levels were distributed in the upper normal range in patients with chronic hepatitis and those with liver cirrhosis. There was a positive correlation between 25(OH)D and serum osteocalcin levels in patients with liver cirrhosis. These results indicate that osteogenesis is decreased and suggest that the decrease in BMD which occurs in viral liver cirrhosis, probably related to decreased, bone formation and slight promotion of bone resorption, reflects deranged hepatic function. This is the first report of Upyr and urinary deoxypyridinoline (UDpyr) determination in patients with liver cirrhosis and patients with chronic hepatitis. The negative correlation of Upyr and UDpyr with ChE is a novel finding.
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PMID:Osteodystrophy in patients with chronic hepatitis and liver cirrhosis. 888 33

To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl4) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non-cirrhotic liver injury and CCl4-induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl4-treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine ratio increased. In all CCl4-treated rats, bone volume was significantly correlated with both the serum albumin concentration and the number of goblet cells reflecting intestinal villous atrophy. The serum concentration of vitamin D metabolites was not correlated with bone volume. Whole body retention of 47Ca was significantly lower in CCl4-treated cirrhotic rats than in controls. Furthermore, the bone volume in thioacetamide-treated cirrhotic rats was significantly lower than in controls. These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis (i.e. HOD) due to a combination of low bone formation rates and high resorption rates, that HOD begins at the stage of chronic non-cirrhotic liver injury, that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy, while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD.
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PMID:Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis. 903 34

Bone thinning causing both fractures and severe pain not associated with fractures has been recognized in patients with chronic liver diseases. The patients most commonly affected are those with primary or secondary biliary cirrhosis, but those with alcoholic liver disease and cirrhosis after active chronic hepatitis may also be involved. Chronic liver disease has also been recognized as an important cause of osteoporosis in both sexes, with the mechanism thought to be a combination of calcium and/or vitamin D. The 9.1% patients with chronic active hepatitis accompanied with osteodystrophy. But 50% cirrhotic patients accompanied with osteodystrophy. Bone densitometry was determined by Digital Image Processing Method (Osteodystrophy < mean-2SD: age- and sex-matched normal value). Serum levels of osteocalcin (BGP) and parathyroid hormone (PTH) in patients of hepatic cirrhosis without osteodystrophy were lower than those with osteodystrophy. These results were suggested that hepatic osteodystrophy was rapidly turnover osteodystrophy. To function physiologically, vitamin D must be hydroxylation in liver to 25-(OH)-D and subsequently by the kidney to 1 alfa, 25-(OH)2-D. Osteodystrophy associated with hepatic cirrhosis is due to a defect in the 1 alfa-hydroxylation by the kidney rather than a hepatic hydroxylation defect. 1 alfa OH-D3 is very useful for treatment for hepatic osteodystrophy.
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PMID:[Hepatic osteodystrophy]. 964 89


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