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)

Ascitic fluid samples from 19 patients with ovarian carcinoma, 3 with a benign ovarian tumor, and 5 with cirrhosis of the liver were examined for their content of coagulation factors and components of the fibrinolytic system. The concentration of trypsin inhibitors in the ascitic fluid was significantly higher in the presence of carcinoma. Large amounts of FDP were found in the ascitic fluid in all patients with malignant tumors, but not in the other two groups. Determination of FDP may therefore make it possible to differentiate between malignant and nonmalignant ascitic fluid.
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PMID:Coagulative and fibrinolytic properties of ascitic fluid associated with ovarian tumors. 4 63

Kininogen level, that of active kinins and kininase activity in the plasma of patients suffering from cirrhosis of the liver and of healthy people were studied. The kininogen content was determined by different available methods i.e. the trypsin and acetone techniques and by means of the plasma and glandular kallikrein preparation. An increase in kininase activity and a lowered kininogen level as determined by all the methods were found in the sick persons. The maximal decrease in the kininogen level determined by means of the plasma kallikreins is substantiated in connection with the increased fibrinolytic activity of the plasma of the patients with hepatic cirrhosis.
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PMID:Studies of the plasma kinin-forming system in cirrhosis of the liver. 16 51

Antitrypsin activity was measured in 50 healthy controls and 100 cases of Indian Childhood Cirrhosis (ICC). The incidence of alpha-I anti-trypsin (Alpha I-AT) enzyme deficiency was strinkingly higher in cases of cirrhosis (39.0%) than in healthy controls (4%). The enzyme deficiency was more prevalent in severe grades of cirrhosis (51.5%) as compared to mild (17.6%) and moderate cirrhosis (38%). Liver function tests were severely deranged in enzyme deficient cirrhotics and the damage to the liver was directly proportional to the extent of the enzyme deficiency. The incidence of the family history of ICC was noted significantly higher in enzyme deficient cases (20%) as compared to non-deficient cases (3.3%). The enzyme deficiency was also measured in 160 first blood relatives of the deficient cirrhotics and was found to be deficient in 19.4% subjects. It is probable that the deficiency runs in families with an autosomal recessive mode of inheritance.
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PMID:alpha-I antitrypsin enzyme deficiency in Indian childhood cirrhosis. 31 92

Human arylesterase is localized in liver microsomes where the presence of different electrophoretic bands corresponding to the serum bands can be recognized. Serum arylesterase is mainly a result of liver activity and its high level might be explained by a low rate of elimination in urine. The behaviour of arylesterase towards inhibitors shows certain similarities to that of some of the proteases, such as trypsin. The clinical value of serum arylesterase determination in assessing liver function is confirmed by its isoenzyme behaviour in cirrhosis and porto-caval shunt.
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PMID:Characteristics and behaviour of arylesterase in human serum and liver. 40 72

The combination of pulmonary emphysema and liver cirrhosis in early childhood is documented for the first time in a 31/2 year old girl with homozygous (ZZ) deficiency of a1-antitrypsin. Examination of relatives in the generation of parents and grand parents revealed 7 heterozygous (MS) and five normal members (MM). Lung function tests showed altered respiratory function in 4 out of these 7 heterozygous subjects. Measurement of trypsin inhibitory capacity in plasma gave a good correlation to the genotype, however determinations of a1-antitrypsin coincided with it to a lesser degree. A high trypsin inhibitory capacity was detected in the tears of the propositi, which was shown to be immunologically distinguishable from serum a1-antitrypsin. Similarly, antiprotease activity was demonstrated in nasal secretions. This too did not reflect the serum profile.
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PMID:[Alpha 1-anti trypsin-deficiency: combination of pulmonary emphysema and liver cirrhosis in infancy (author's transl)]. 80 42

Exocrine pancreatic function was assessed by the standard test meal method of Lundh in a control group, and 13 patients with nonalcoholic, postnecrotic cirrhosis of the liver. In six of these patients, splenorenal shunts were performed and exocrine pancreatic function was assessed before and three months after operation. In three of the six, the secretin-pancreozymin stimulation test was also performed. An increased volume but normal trypsin output was observed in the unoperated cirrhotic patients. An increase both in volume and in trypsin was found in the cirrhotic patients after shunting using the test meal stimulation. There was no appreciable difference, however, when tested with secretin and pancreozymin. Hypersecretion in cirrhotics, with or without shunts, is probably due to a by-pass of the hepatic degradation of normal pancreatic secretogogues produced by the intestine.
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PMID:Exocrine pancreatic function in hepatic cirrhosis. 93 24

Hypercholesterolemia was induced in rats by feeding them a high cholesterol olive oil diet. The livers were homogenized in modified Krebs-Ringer medium and centrifuged at 35,000 x g. The supernatants from livers of both hypercholesterolemic and normal rats were found to stimulate collagen synthesis in freshly isolated embryonic chick-tendon fibroblasts. However, this was significantly greater in the supernatants from fatty livers. The stimulating principle proceed to be dialyzable, non-lipid and heat-stable. There were at least two factors involved, the more effective of which was trypsin-sensitive, with a molecular weight below 2,000. The results suggest that a mediator is formed in the livers of hypercholesterolemic rats which might be responsible for the enhanced collagen synthesis of fibrotic processes vivo, e.g., in atherosclerosis and liver cirrhosis.
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PMID:Factors stimulating collagen synthesis from the livers of hypercholesterolemic rats. 94 25

Intestinal perfusion methods with a nonabsorbable marker allow an exact quantitative determination of intestinal absorption and secretion provided that methodological pitfalls are avoided. A modified technique is applied to the simultaneous measurement of biliary and pancreatic secretion during and depending on emptying of a mixed test meal. A duodenal segment was perfused with an isotonic polyethyleneglycol solution (PEG). Reinjection of duodenal aspirates maintained a normal enterohepatic circulation of bile acids (interruption less than 10%). The perfusion was performed in healthy volonteers over a period of 12 to 24 hours, with three mixed formula meals containing 51CrCl3 as a marker ingested at conventional feeding hours. Influence of meal size was studied by means of a high caloric (40 Kcal/b. wt. per day) test meal. Patients with cholesterol gallstones and cirrhosis of the liver only received one formula test meal of 300 Kcal. Instead of concentrations output of trypsin, lipase, bile acids and cholesterol (the latter corrected for duodenal absorption) was calculated from the dilution of PEG in the duodenal juice and gastric emptying was determined by following quantitatively the flow of 51CrCl3. Gastric emptying can be expressed by a single exponential function over most of the time. Only the last 60-100 Kcals were expelled by the stomach at a faster rate. The daily biliary and pancreatic secretion depend indirectly on the amount of food ingested. But during the day light hours (with continuous meal flow), secretion was similar in high and low caloric subjects, while a significant difference became obvious during night hours corresponding to differences in gastric emptying time. Mean hourly output of bile acid, biliary cholesterol, trypsin and lipase is independent from meal size and secretion of pancreatic enzymes reaches the values close to those after maximal stimulation by i.v. CCK-PZ. Output of pancreatic enzymes does not differ in health and gallstone disease or cirrhosis of the liver respectively. Since during digestion in normals approximately one forth of the bile acid pool is secreted hourly into the gut, the number of daily enterohepatic cycles of bile acids can be calculated by 4-6. Patients with cholesterol gallstones maintain normal bile acid output by enhanced cycling of the small pool: An average of 50% of the pool passed the duodenum per hour. A decreased bile acid pool is also present in cases of advanced cirrhosis of the liver. However, hourly output of bile acids in these patients is significantly less than in mild cirrhosis (with normal bile acid pool) or normal controls. Therefore the hourly fraction of the pool secreted is similar to healthy subjects. These findings provide an important information to explain abnormalities in bile acid metabolism in cirrhosis.
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PMID:[Simultaneous determination of gastric emptying and bile and pancreatic enzyme secretion]. 106 80

A study of 27 relatives of a child with fatal hepatic cirrhosis due to homozygous Z variant alpha-1-antitrypsin deficiency revealed 15 members with heterozygous MZ phenotypes. Levels of circulating alpha-1-antitrypsin and trypsin-inhibiting capacity were shown to be unreliable in identifying the heterozygous state, Pi typing being necessary for definitive diagnosis. The morphologic evolution of the hepatic changes in this condition have been studied, and the importance of the PAS stain in identification of the characteristic cytoplasmic bodies is stressed.
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PMID:Childhood cirrhosis associated with alpha-1-antitrypsin deficiency. A genetic, biochemical, and morphologic study. 107 52

A 4-year-old girl with hepatic cirrhosis was found to have alpha1-antitrypsin deficiency. The method of FAGERHOL detected that she is a heterozygous carrier of the Pi SZ type. Investigations with the light and the electron microscope and immunofluorescence tests confirmed the diagnosis. The values of alpha1-antitrypsin and trypsin inhibitory capacity gave intermediate values. The fact that in the patient, the Z allele was combined with an S allele may have contributed to the severity of the illness.
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PMID:Cirrhosis and heterozygous alpha1-antitrypsin deficiency in a 4-year-old girl. 108 53


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