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)

Protein-dispersive enteropathy was noted in three children with chronic constrictive pericarditis. Increased intestinal permeability to proteins was detected by using lavelled albumin in one patient. Biopsy showed absence of mucosa lesions and normal villi in another case. Partial pericardiotomy led to rapid resolution of pseudo-cirrhosis and normalisation of serum proteins in all three cases.
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PMID:[Protein-losing enteropathy in chronic constrictive pericarditis in children]. 65 92

Serum zinc conentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy and impaired wound healing) are common in these patients. It remains unresolved whether these low serum zinc concentrations in these disease states are indicative of true symptomatic or asymptomatic zinc deficiency, or merely reflect a decrease in available zinc-binding proteins, as well over 90% of serum zinc is bound to protein in normal subjects. The correlation between serum zinc and albumin concentrations, reportedly the major zinc-binding protein, is unimpressive. Studies of serum and urine binding of added radiozinc65 using Sephadex G-200 gel column chromatography and polyacrylamide gel electrophoresis suggest most of the radiozinc is bound to a protein with a molecular weight near albumin (68,000). Polyacrylamide gel electrophoresis suggests this might be a prealbumin. The low serum zinc concentration in the patient with nephrotic syndrome does not appear to be due to loss of zinc bound to urinary protein.
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PMID:Serum concentrations and urinary excretions of zinc in cirrhosis, nephrotic syndrome and renal insufficiency. 66 9

In a retrospective analysis of 78 patients with liver cirrhosis, we found low serum levels of calcium and phosphorus. The low calcium levels showed a better correlation with high activity of aspartate aminotransferase than with low levels of albumin. In addition, there was a relationship between low calcium and low phosphorus levels. Therefore, factors other than, and in addition to, hypoalbuminemia seem to be responsible for the low calcium and phosphorus levels in cirrhosis patients. Although low levels of serum 25-hydroxyvitamin D were found in 23 of our patients, there was no indication that hypovitaminosis D was causative factor in the hypocalcemia and hypophosphatemia.
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PMID:Low levels of serum calcium, phosphorus and plasma 25-hydroxy vitamin D in cirrhosis of the liver. 68 Nov 62

The behaviour of albumin during the development of chronic progressing liver damages was investigated on the model of the thioacetamide cirrhosis in Wistar-rats. Simultaneous estimations of the albumin concentrations in extractable liver protein and in the serum as well as accompanying measurements of the total protein and of the transaminases SGOT and SGPT in the serum allow a complex judgment. The albumin concentration in the liver significantly decreased after 4 and 8 weeks and reached highly normal values in fully developed cirrhosis. In each case the serum level changed in the same sense, but less expressed. The total protein in liver and serum showed an analogous course of the curve, whereas the albumin-total protein-quotient in the liver remained unchangedly low. The relative proportion of albumin in the serum did not show a diminution in every phase. The simultaneous decrease of albumin and total protein are explained as an expression of an inhibition of the synthesis due to destruction of protein-synthesizing subcellular structures. The normalisation of the serum levels and of the highly normal albumin contents despite the developed cirrhosis become understandable by the loss of efficiency of the foreign substance thioacetamide in consequence of structural and biochemical adaptation. The thioacetamide cirrhosis of the rat in the investigated phase despite the microscopically provable so-called degenerative parenchymal damages is accompained by parameters of the increased protein metabolism. The relative serum albumin content apparantly in the first place undergoes the oncotic pressure regulation and is not suited as the measure of a hepatocellular lesion. From the diagnostic point of view the reduction of the albumin concentrations seems to be of importance in the developmental phase to cirrhosis.
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PMID:[The behavior of albumin in acute and chronic liver diseases. I. The behavior of albumin during the development of rat thioacetamide cirrhosis]. 68 33

In 305 patients examined by liver biopsy albumin and the entire soluble protein in the liver puncture as well as albumin in the serum were estimated quantitatively. A significant decrease of the serum albumin level in active cirrhoses and biliary liver damages confirmed the importance of the hypalbuminaemia as facultative symptom of a liver damage. The lacking specifity was emphasized by the low albumin serum concentrations in malignomas and after the intake of contraceptive hormones. The hypalbuminaemia and the increased content of soluble liver protein in the bioptic material might enrich the diagnostics of the activity in cirrhoses. The diagnostic value of the decrease of the relative proportion of albumin is low, since of all liver diseases examined the active cirrhosis alone was accompanied by a significant decrease. The estimation of the albumin content in the bioptically got liver tissue had in contrast to the animal experiment no diagnostic value for liver diseases.
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PMID:[The behavior of albumin in acute and chronic liver damage. III. Intrahepatic and serum albumin concentrations in human liver diseases]. 69 90

The urinary excretion of D-glucaric acid, a catabolite of glucuronic acid, is considered to be a reliable index of the state of hepatic microsomal enzyme activity. Because enzyme activity may be altered in liver disease, we examined the effect of liver disease on the excretion of this metabolite and its correlation with liver function tests. We studied 89 patients with nonhemolytic jaundice, 39 with viral hepatitis, 33 with obstructive jaundice, six with cirrhosis, and 11 patients with jaundice of mixed etiology. Glucaric acid excretion was significantly increased in all these patients as compared to controls, most pronounced in the obstructive jaundice group. No correlation was found between glucaric acid excretion and concentrations of bilirubin, albumin, globulin, aspartate aminotransferase, alkaline phosphatase, cholesterol, or gamma-glutamyltransferase in serum, even though the concentrations of these analytes did vary with the type of liver disease. We suggest that this increase in glucaric acid excretion is an indication of normal or even increased glucuronidation (UDP-glucuronosyltransferase activity), which occurs in liver disease.
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PMID:Increased D-glucaric acid excretion by jaundiced patients. 69 85

The plasma proteins are constantly shuttling between intravascular and extravascular mass of a specific plasma protein is determined by its individual rate of synthesis and the mean total time it spends in plasma. The ratio of intravascular to total mass (distribution ratio) is determined by the relative rate, at which it passes from plasma to interstitial spaces (transcapillary escape rate: TER) and the relative return rate via lymph. TER in a specific organ depends on the local leakiness of the microvasculature. The overall value in normal man varies with the molecular weight of the protein being about 5%/h of the intravascular albumin mass, 3%/h for IgG and less than 1%/h for IgM. The higher the TER, the lower is the intravascular fraction. Hypertension, diabetes mellitus, burns, myxedema and certain types of liver cirrhosis will increase TER. In hypertension and diabetes this may be compensated for by an increased lymphatic return rate. Hypoproteinemia due to malnutrition or urinary or gastrointestinal loss is accompanied by a shift from the extravascular to the intravascular space.
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PMID:Intra- and extravascular distribution of albumin and immunoglobulin in man. 73 85

Between 1968 and 1974, azathioprine has been used in a controlled prospective trial to treat patients with symptomatic but precirrhotic primary cirrhosis. Forty-five patients were admitted, of whom 22 were given azathioprine in a dose of 2 mg per kg of body weight. During the 1st year, serum aspartate transaminase levels showed a significant change in favor of the treated group, but improvement did not continue. Throughout the trial, serum alkaline phosphatase, bilirubin, cholesterol, albumin and immunoglobulin M values showed no significant change. Titers of serum mitochondrial antibodies tended to become negative more often in the treated than the untreated. Pruritus cannot be assessed objectively, but seemed less in the treated than in controls. Serial hepatic biopsy specimens showed the development of cirrhosis equally in the two groups. Survival, as judged by the life table method, was similar for the first 5 years of the trial. There was, however, a significant difference in favor of the treated group in the 6th year, although the number of patients available for assessment at that time was extremely small.
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PMID:A prospective controlled trial of azathioprine in primary biliary cirrhosis. 77 Feb 24

Amino acid imbalance ratio was determined in apparently healthy Pakistanis and patients with hepatitis and cirrhosis of the liver. The ratio was normal in 75% of the patients with actue viral hepatitis but in only 5% with cirrhosis of the liver. The ratio was abnormal in 25% cases of acute viral hepatitis possibly due to aminoaciduria. The abnormal ratio in cirrhosis of the liver indicated the functional capacity for albumin synthesis and correlated well with serum albumin concentration.
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PMID:Aminoacid imbalance ratio in liver disease. 82 73

Amino acid imbalance ratio was determined in apparently healthy Pakistanis and patients with hepatitis and cirrhosis of the liver. The ratio was normal in 75% of the patients with acute viral hepatitis but in only 5% with cirrhosis of the liver. The ratio was abnormal in 25% cases of acute viral hepatitis possibly due to aminoaciduria. The abnormal ratio in cirrhosis of the liver indicated the functional capacity for albumin synthesis and correlated well with serum albumin concentration.
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PMID:Aminoacid imbalance ratio in liver disease. 82 59


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