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)

Monocyte function in patients with cirrhosis of the liver was measured by phagocytosis and killing of Candida pseudotropicalis and C albicans. Both variables were significantly decreased in the patients compared with controls. Control monocytes exposed for two hours to patients' serum showed a significant decrease in intracellular killing compared with control monocytes incubated in autologous serum. This suggests the presence of an inhibiting factor in the patients' serum. This inhibitory factor passed through a dialysis membrane that permitted the passage of molecules of less than 12 000 daltons. Treating monocytes from patients with trypsin significantly increased phagocytosis, indicating that the possible inhibitory factor was attached to the monocyte surface. Metabolism of monocytes during phagocytosis as determined by chemoluminescence was significantly lower in monocytes from patients compared with controls, indicating metabolic impairment. Monocytes are a component of the monocyte-macrophage system, which includes Kupffer's cells. Impairment of the function of these cells, which have a pivotal role in clearing portal blood, might well be extremely important in the development of chronic liver disease.
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PMID:Impaired monocyte function in liver cirrhosis. 678 6

Recent evidence suggests that the cirrhosis of alpha-1-antitrypsin deficiency is not invariably fatal as it was previously thought. Portal hypertension is often the major determinant of survival. The few reports of porta-systemic venous anastomosis in this disorder have shown poor results or uncertain outcome. Thus, doubts exist as to whether porta-systemic shunts should be performed in alpha-1-antitrypsin deficiency. Two patients with alpha-1-antitrypsin deficiency (PiZZ) and associated portal hypertension, cirrhosis, and hypersplenism underwent splenorenal shunt and splenectomy 8 yr ago, and both have done well. One of the patients has chronic severe headaches, diarrhea, exudative enteropathy, sinusitis, and hematuria, all uncommon in alpha-1-antitrypsin deficiency but possibly related to the antienzyme deficiency. She also has a higher trypsin inhibitory capacity than is generally reported in ZZ individuals. Based on the experience with these 2 patients, it appears that alpha-1-antitrypsin deficiency with cirrhosis is not a valid contraindication to the performance of a portasystemic shunt.
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PMID:Successful spleno-renal shunt and splenectomy in two patients with alpha-1-antitrypsin deficiency. 697 26

In 121 patients with either liver cirrhosis or chronic renal failure, abnormal values for the concentrations of two pancreatic enzymes in serum were a frequent finding. In renal insufficiency a decreased rate of enzyme elimination is the most likely cause of the above-normal values we observed for serum immunoreactive trypsin and pancreatic isoamylase activity. As for patients with liver cirrhosis, we believe that changes in entrance rates into the blood--i.e., an affected pancreas--is a likely explanation of the abnormally high values we often found for these serum enzymes.
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PMID:Immunoreactive trypsin and pancreatic isoamylase activity in serum of patients with chronic renal failure or hepatic cirrhosis. 697 16

The presence of liver IgG Fc receptor sites was demonstrated in the liver tissue from 23 patients with liver diseases and 2 patients without liver lesions by the localization of soluble immune complexes of peroxidase-antiperoxidase (PAP). Cryostat sections of liver tissues were incubated with the complexes and the peroxidase activity was revealed histochemically. In the normal liver tissue, PAP were localized on the liver cell membrane, the Kupffer cells, and some of the sinusoidal walls. In acute hepatitis, a strongly positive reaction on swollen Kupffer cells was remarkable but positive reaction on the liver cell membrane was very weak. In chronic aggressive hepatitis, PAP were strongly positive on multiplied Kupffer cells and many PAP-positive infiltrated cells were observed at the area of piecemeal necrosis. However, the positive reaction on the liver cell membrane in patients with chronic aggressive hepatitis was generally fainter than in the normal cases without liver diseases. These results correlated well with the severity of liver cell necrosis. In chronic persistent hepatitis, the number of PAP-positive infiltrated cells in the portal area and positive Kupffer cells were fewer than in chronic aggressive hepatitis. Similar results were obtained with liver cirrhosis, and in particular, the liver cell membrane with regenerative nodules gave a positive reaction. A negative result was obtained by incubation with PAP-F(ab')2 alone. PAP reaction was significantly inhibited by pretreatment with aggregated human IgG, trypsin, and pronase but not with neuraminidase.
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PMID:Detection of liver IgG Fc receptors using soluble immune complexes of peroxidase-antiperoxidase. I. Detection in liver tissue from patients with liver diseases. 701 47

Sinusoidal "inclusion-containing endothelial cells" were studied histopathologically and immunohistochemically in various liver diseases, and their clinical importance was investigated. A total of 498 needle liver biopsies were examined. Endothelial inclusions inside the cells were recognized as eosinophilic granules in hematoxylin-eosin-stained sections. Electron microscopy showed that these inclusions corresponded to round cytoplasmic dense bodies with a single limiting membrane. The contents of these bodies were generally homogeneous, but sometimes heterogeneous. The inclusions appeared to contain protein, but were resistant to trypsin digestion, and immunohistochemistry failed to identify any immunoglobulins or hepatocyte-derived proteins. These endothelial cells also contained an increased number of micropinocytotic vesicles when compared with ordinary cells. The inclusion-containing endothelial cells appeared frequently in chronic hepatitis, but were relatively rare in other liver diseases. The incidence was higher in chronic aggressive hepatitis than in chronic persistent hepatitis or inactive cirrhosis. Although the density of these cells varied considerably even among patients with the same histological diagnosis and the phenotypical changes of these endothelial cells, assessed by monoclonal antibodies, were not apparent, the serum gamma globulin level tended to increase in relation to the density of inclusion-containing endothelial cells and the correlation was significant in hepatitis C.
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PMID:Appearance of sinusoidal inclusion-containing endothelial cells in liver disease. 752 15

We analyzed the serial changes in serum pancreatic enzyme activities by transcatheter arterial embolization (TAE) in 20 hepatoma patients with liver cirrhosis in an attempt to evaluate the incidence of the pancreatic tissue damage by TAE. Serum amylase activities increased in two (10%) cases, elastase 1 levels in six (30%) cases, and trypsin and pancreatic secretory trypsin inhibitor (PSTI) levels in each of five (25%) cases. Consequently, TAE resulted in the elevation of at least more than one serum pancreatic enzyme in eight (40%) of 20 cases, although none had clinical symptoms related to pancreatitis. When the adverse effect on the pancreatic tissue was compared among 6 cases of the superselective TAE and 14 cases of the nonsuperselective TAE, which were performed from the segmental and the nonsegmental hepatic arteries, respectively, the elevation of serum pancreatic enzymes was caused only by nonsuperselective TAE, not by superselective TAE. The volumes of Spongel and Lipiodol used or the injected doses of the anticancer agent mitomycin C were not different between the two groups. These results indicate that TAE for the treatment of hepatoma frequently causes pancreatic tissue damage, and the position of the inserted catheter tip is very important to avoid the pancreatic tissue damage by TAE.
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PMID:Pancreatic tissue damage by transcatheter arterial embolization for hepatoma. 767 84

High levels of tissue plasminogen activator (t-PA) have been reported to be the main component of the high fibrinolytic activity measured in patients during orthotopic liver transplantation. However, a previous study of our group suggested that specific t-PA may not completely account for the massive fibrinolytic activities recorded. In the present study we investigated the fibrinolytic patterns in 10 consecutive liver cirrhosis patients undergoing OLT. Euglobulin fibrinolytic activity, measured either on physiologic (fibrin plates) or amidolytic substrates, increased as expected during anhepatic and reperfusion phases, but largely exceeded the specific activity of t-PA, as proved by quenching procedures using anti-t-PA antibodies. The presence of plasmin- and trypsin-like amidolytic activities was detected in native plasmas at the end of anhepatic and reperfusion phases, together with decreased levels of protease inhibitors, especially alpha 1 Antitrypsin. In conclusion, the hyperfibrinolytic pattern recorded in the central OLT phases is not only attributable to an increased t-PA concentration, and is better described as a complex "lytic" state also including the presence of free proteases (plasmin- and trypsin-like), with limited participation of u-PA. Although t-PA increase is probably the main mechanism of stimulation of the fibrinolytic system during OLT, actual and not just potential proteolytic activities can be found in this condition independent of the occurrence of major hemorrhagic complications.
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PMID:Protease activities, as well as plasminogen activators, contribute to the "lytic" state during orthotopic liver transplantation. 769 27

Exocrinous performance of the pancreatic gland under secretin-pancreozymin stimulation was studied in 76 patients with chronic diffuse diseases of the liver who were distinguished into 6 groups: those who suffered from chronic persistent hepatitis of viral and alcohol origin, chronic active hepatitis of viral origin, cirrhosis of the liver of viral and alcohol origin, primary biliary hepatocirrhosis. The results obtained were correlated with those from 11 normal persons (controls). Out of 76 examinees the disorders of exocrinous performance of the pancreatic gland were revealed in 75 persons. The most characteristic features were: a decrease in the basal and an increase in the stimulated volume of the pancreatic juice; a reduction of both basal and stimulated production of bicarbonates; a decrease in the trypsin and amylase fasting levels and their increment in the stimulated juice of the pancreatic gland. Disorder in the production of bicarbonates was stated as a most characteristic feature in the patients both with viral and alcohol origin of the disease but it was mostly manifest in the patients with hepatocirrhosis. Pronounced elevation of the activity of amylase and trypsin in the pancreatic juice was observed in patients with very high activity of disease development and in the patients who continuously used large amounts of alcohol. The authors suspected that alcohol abuse and the effect of hepatitis virus had an equal pathogenic impact on the liver and pancreatic gland.
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PMID:[Exocrine function of the pancreas in patients with chronic hepatitis and liver cirrhosis of various etiologies]. 814 1

Platelet glycocalicin (GC) is the extramembranous portion of GPIb alpha that can be rapidly cleaved by enzymes such as calpain, plasmin, trypsin, elastase, etc. Quantitative cleavage will ultimately result in an acquired Bernard-Soulier-like bleeding disorder, and circulating GC may act as a potential inhibitor of platelet adhesion. We have developed and standardized a new enzyme-linked immunosorbent assay (ELISA), which uses two monoclonal antibodies (mAbs), both of which bind to the amino-terminal 45-kD fragment of GC and inhibit platelet-von Willebrand interactions and the streptavidin-biotin system. First, the methodology was evaluated and standardized with special emphasis on the anticoagulant and the inhibitors (EDTA, prostaglandin E1 [PGE1], aprotinin, N-ethyl-maleimide), the mode of high-speed centrifugation (to avoid platelet microparticles), and the standards used (purified GPIb and GC). This assay was then used to analyze the GC levels of healthy subjects (2.04 +/- 0.46 micrograms/mL) and of patients with selected diseases. The results of patients with aplastic anemia and thrombocytosis confirmed that GC levels are clearly dependent on the platelet count, which was the basis for the introduction of the GC index, the standardization of GC for a platelet count of 250 x 10(9)/L. The GC index discriminates reliably patients with active immune thrombocytopenic purpura from those in remission. GC levels are elevated in patients on hemodialysis (3.62 +/- 0.75 micrograms/mL, P < .001). The high GC index (6.93 +/- 4.21, P < .001) in cirrhosis patients suggests an increased platelet turnover and/or abnormal proteolysis. In contrast to other groups, we have not found that recombinant tissue plasminogen activator (rtPA) treatment of patients with myocardial infarction increases GC levels. However, concentrations are elevated in leukemia and the highest levels found are approximately 40 micrograms/mL. These studies suggest that GC is a useful platelet marker in certain diseases, which directly reflects platelet damage and possibly platelet dysfunction.
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PMID:Glycocalicin: a new assay--the normal plasma levels and its potential usefulness in selected diseases. 829 32

Pancreatic phospholipase A2 (PLA2) is secreted into the pancreatic juice by pancreatic acinar cells as a proenzyme (proPLA2), which is activated by trypsin. Radioimmunoassays with monoclonal antibodies to PLA2 and proPLA2 were used to examine the serum PLA2 and proPLA2 levels simultaneously in patients with various pancreatic diseases. In healthy subjects, proPLA2 proved to be the major form of the enzyme. The serum PLA2 level were found to be significantly increased in patients with acute pancreatitis, the active phase of chronic relapsing pancreatitis, and the early stage of pancreatic cancer. In the terminal stage of pancreatic cancer the serum PLA2 level became low. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and the serum total PLA2 and proPLA2 level, but not the PLA2 level. The serum PLA2 and proPLA2 concentrations, and the proportion of proPLA2 in the total, were within normal ranges in patients with liver cirrhosis, hepatocellular carcinoma, and chronic renal failure. These results suggest that simultaneous measurements of serum PLA2 and proPLA2 are clinically useful for diagnosis and monitoring of the active phase of pancreatitis.
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PMID:Simultaneous determinations of pancreatic phospholipase A2 and prophospholipase A2 in various pancreatic diseases. 844 83


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