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 authors describe a method for combined measurements of the plasma trypsin-like proteinases, alpha 1-antitrypsin and alpha 2-macroglobulin. The values of these parameters' activities in the plasma of normal subjects and patients with peritonitis and liver cirrhosis are presented. The suggested method may be used for identification of the type of disorders in the system of trypsin-like proteinases and endogenous inhibitors in other diseases.
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PMID:[Use of a method of combined determination of the activity of the trypsin-like proteinases, alpha 1-antitrypsin and alpha 2-macroglobulin, in a gastroenterology clinic]. 169 55

Conditioned media of Kupffer cells from normal rat liver produce in culture two factors that inhibit fibroblast proliferation. The inhibitory factors have molecular masses of approximately 25 and 5 kDa. In contrasts to these results, the conditioned media of Kupffer and mononuclear macrophagic cells, obtained 48 hours after CC1(4) administration to rats, contains a 17 kDa factor that stimulates fibroblast proliferation (FSF). FSF also stimulates [3H]-thymidine incorporation into DNA of cultured rat liver fat-storing cells. Two peaks with FSF activity were demonstrated after isoelectrofocusing; one with a pI of 6.1 and a second with a pI of 7.5. The fraction containing FSF is devoid of interleukin-1 (IL-1) activity and no inhibitory activity is detected in this conditioned media. Production of FSF is inhibitable by colchicine but not by indomethacin, it is thermolabile and trypsin-sensitive. In animals treated chronically with CC1(4) to produce cirrhosis, FSF activity is demonstrable from the first to the 8th week of treatment. However, the activity is lower at 8 weeks post-CC1(4) as compared with 2 weeks. The results suggest that homeostasis of cells in the liver is controlled by factors produced locally, that act by autocrine and paracrine mechanisms. When homeostasis is altered, fibroblast proliferation occurs, and excess collagen deposition leads to fibrosis. We propose that the antifibrogenic activity of colchicine is associated, in part, with its capacity to inhibit the release of FSF by Kupffer cells and liver mononuclear macrophage cells.
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PMID:Kupffer cells from CC1(4)-treated rat livers induce skin fibroblast and liver fat-storing cell proliferation in culture. 272 21

Immunolocalization of type III collagen and procollagen in cirrhotic human liver was studied using monoclonal antibody specific for the helical determinant of type III collagen extracted from human placenta. Deparaffinized, trypsin-treated cirrhotic liver sections from 8 autopsy cases were examined by the unlabeled peroxidase-antiperoxidase and immunofluorescence techniques. These techniques revealed the localization of this epitope shared by type III collagen and procollagen not only in the extracellular matrix of hepatocytes and sinusoidal cells but also in the cytoplasm. In hepatocellular carcinoma concurrent with cirrhosis, neoplastic cells were shown to react with this antibody as well. These results are consistent with data obtained using antiserum specific for bovine type III procollagen aminopeptide which appeared in our previous report.
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PMID:Immunolocalization of type III collagen and procollagen in cirrhotic human liver using monoclonal antibodies. 308 39

Alpha-1-antitrypsin level and serum trypsin inhibitory activity were measured in patients with viral hepatitis, chronic hepatitis and liver cirrhosis. The most pronounced discrepancy between these two parameters were observed in patients with liver cirrhosis: the increase of alpha-1-At level was not accompanied by adequate increase of trypsin inhibitory activity. Some mechanisms potentially responsible for this discrepancy are discussed.
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PMID:Serum trypsin inhibitory activity and alpha-1-antitrypsin level in liver diseases. 349 Apr 9

To estimate the diagnostic value of elastase output in the duodenal aspirates during a pancreozymin secretin test, elastase as well as amylase, chymotrypsin, trypsin, and lipase was determined in 46 controls and 61 patients with various disease. The elastase output decreased significantly in chronic pancreatitis (mild exocrine insufficiency 13 and advanced eight), pancreatic cancer (n = 10), and liver cirrhosis (n = 14) when compared with the controls. The outputs of the four other enzymes also decreased in chronic pancreatitis and pancreatic cancer, not in liver cirrhosis. Low elastase output was found in four of 13 chronic pancreatitis patients with mild exocrine insufficiency, whereas low outputs of the other enzymes were observed in only one or less of the 13. The ratio of elastase to amylase alone was significantly lower in the pancreatic diseases. The results suggest that elastase is the most susceptible enzyme to pancreatic dysfunction and that its output and its ratio to amylase output provide a valuable index to assess the enzyme secretory capacity in the pancreatic diseases.
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PMID:Elastase secretion in pancreatic disease. 384 84

Immunolocalization of type III procollagen (pro III) in normal and cirrhotic human liver was studied using rabbit antiserum specific for bovine type III procollagen aminopeptide. The material examined was deparaffinized, trypsin-treated hepatic tissue sections from 28 autopsy cases, including 19 cirrhotic and 9 normal liver donors. Immunostaining, performed by the unlabeled peroxidase-antiperoxidase antibody technique demonstrated that extracellular matrices corresponding to perisinusoidal reticulin, collagen in periportal areas, and blood vessel walls were the common sites of pro III antigenicity in both normal and cirrhotic liver. Moreover, in the cirrhotic liver, the fibrous septa of pseudolobules, and cytoplasm of hepatocytes and sinusoidal cells were positive when stained for pro III peptide. The differential counts of pro III positive cells in cirrhotic liver, however, revealed that the average ratio of these hepatocytes to sinusoidal cells was 25 to 1, indicating complete dominance of hepatocytes with respect to stainability for pro III peptide compared to sinusoidal cells. In hepatocellular carcinomas coexisting with cirrhosis, neoplastic cells also displayed pro III antigenicity. These data suggest that hepatocytes of cirrhotic liver and hepatocellular carcinoma cells play a significant role in type III collagen synthesis in vivo.
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PMID:Localization of type III procollagen aminopeptide antigenicity in hepatocytes from cirrhotic human liver. 393 61

The susceptibility of hepatic collagen to homologous collagenase in human and experimental CCl4 cirrhosis of the liver has been explored in vitro by exposure of cryostat liver sections to the corresponding enzymes for different time periods. The morphology and extent of collagen degradation was studied by the Picrosirius red/polarizing microscopy technique. The results of various experiments indicate that collagen present in cryostat sections of both human and rat normal and cirrhotic livers is resistant to trypsin digestion for periods of exposure of up to 48 hours but that heating the sections to 60 C for 1 hour renders the collagen susceptible to degradation by trypsin. Incubation of cryostat liver sections with bacterial collagenase revealed progressive degradation of collagen with a uniform pattern of changes in the original color and diameter of the fibers. Exposure of liver sections to homologous collagenases gave rise to the same pattern of changes observed with bacterial collagenase, although less extensive when equal incubation periods were compared. Nevertheless, sufficiently prolonged incubation of liver sections with their homologous collagenases eventually showed degradation of all collagen present in all normal and cirrhotic liver sections. These observations suggest that in the presence of non rate-limiting concentrations of homologous collagenase, the susceptibility of hepatic collagen to the corresponding degrading enzyme is probably not responsible for the irreversibility of the disease.
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PMID:The susceptibility of hepatic collagen to homologous collagenase in human and experimental cirrhosis of the liver. 615 26

alpha 1-Antitrypsin is the most abundant of several serum protease inhibitors. Its deficiency is associated with an increased incidence of emphysema in adults, jaundice in newborns, and childhood cirrhosis. We describe an automated functional assay for the Instrumentation Laboratory's Multistat III Microcentrifugal Analyzer with N-alpha-benzoyl-DL-arginine-p-nitroanilide as trypsin substrate. The assay is standardized in terms of moles of trypsin active sites inhibited per liter of serum, by use of a chromogenic titrant for trypsin active sites, p-nitrophenyl-p'-guanidinobenzoate. The method is rapid, precise, and independent of trypsin supplier, and results correlate well with those by a manual chromogenic and a nephelometric assay.
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PMID:Automated assay for alpha 1-antitrypsin with N-alpha-benzoyl-DL-arginine-p-nitroanilide as trypsin substrate and standardized with p-nitrophenyl-p'-guanidinobenzoate as titrant for trypsin active sites. 628 Aug 95

We have studied the volume, protein concentration, total protein, and chymotrypsin and trypsin outputs in pure pancreatic juice (PPJ) following endoscopic cannulation of the pancreatic duct in 11 male and 2 female patients with advanced alcoholic cirrhosis (AC). Results were compared to those obtained from 21 nonalcoholic volunteers (NAV) and 26 chronic alcoholic (CA) patients without cirrhosis. Intravenous stimulation with secretin followed 10 min later by intravenous cholecystokinin-pancreozymin (CCK-PZ) resulted in highly significant increases in volumes during both phases of pancreatic stimulation in AC compared to NAV and CA. Protein concentration and total output during secretin stimulation was not different among the three groups. During CCK-PZ stimulation, CA exhibited a significant elevation in protein concentration and total output compared to NAV and AC. Although total chymotrypsin output was lower in secretin-stimulated CA than other groups, no other differences between the groups were observed in either of the hormone-stimulation phases. Marked elevations in trypsin output were observed in secretin-stimulated AC and in CCK-PZ-stimulated AC and CA. The high PPJ volume and the relatively low protein concentration observed in AC may effect a washout phenomenon resulting in a decreased tendency for ductal protein precipitation in these patients.
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PMID:Pancreatic secretion after secretin and cholecystokinin stimulation in chronic alcoholics with and without cirrhosis. 665 99

Intestinal bile salt deficiency marginally impairs fat absorption in cholestatic patients. The finding of massive steatorrhea in some patients with primary biliary cirrhosis led us to systematically study and compare fat digestion in control subjects (n = 4) and patients with biliary cirrhosis with (n = 11) and without (n = 3) steatorrhea. The jejunum was anatomically and functionally intact in all subjects, as demonstrated by normal gastrointestinal radiology and xylose absorption, respectively. The intestinal contents were recovered during digestion of a fat meal. Lipolysis, pH, and trypsin activity were measured in whole intestinal contents, whereas bile salts, total lipid, and fatty acid were determined in both total and aqueous phases. The results obtained in controls and patients without steatorrhea were similar. Percentage of lipolysis and intraluminal pH were normal in controls and in both patient groups. The intestinal contents of the patients with steatorrhea had a significantly lesser capacity to solubilize both total lipid and fatty acid in relation to abnormally low aqueous bile salt concentrations. No bile salt deconjugation and only minimal bile salt precipitation were found, thus low aqueous bile salts were strictly related to bile secretory failure. Steatorrhea was always present when aqueous bile salt levels were below 3.0 mM. Intestinal trypsin activity was subnormal in patients with steatorrhea; decreased trypsin activity was related (r = 0.82, p less than 0.001) to reduced intestinal bile salt levels. One patient was found to have severe exocrine pancreatic failure. Administration of medium chain triglycerides was uniformly effective in improving nutrition in patients with steatorrhea, but the course of the disease was unaffected. These results indicate that overt pancreatic failure is uncommon in primary biliary cirrhosis, and that fat maldigestion and steatorrhea, regardless of what degree, are due mainly to low intestinal bile salt levels secondary to bile secretory failure. Finally, subnormal pancreatic function in this disease appears to be related to the bile secretory failure, suggesting either that the lack of bile or bile salts in the intestine depresses pancreatic exocrine function or that both biliary and pancreatic secretions decrease in parallel as part of a widespread secretory failure syndrome.
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PMID:Fat digestion and exocrine pancreatic function in primary biliary cirrhosis. 672 61


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