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)

Bacterial peritonitis in patients with cirrhosis has a wide variety of clinical presentations. We report a group of 21 cirrhotic patients with secondary peritonitis from intra-abdominal sources. Seven had infected ascites. All of them had unrecognized secondary peritonitis which was diagnosed and treated as spontaneous (primary) bacterial peritonitis (SBP). Ascitic fluid analysis yielded a mean white blood cell count of 23,750 +/- 10,935/cu mm with 91.5% polymorphonuclear leukocytes, significantly higher than patients surveyed with SBP, 1,757 +/- 2,154/cu mm (P less than .001). Ascitic fluid protein levels were also higher than those typically seen in SBP: 4.4 +/- 1.5 gm/dl vs 0.8 +/- 0.4 gm/dl (P less than .001). The ascites: serum protein ratio was consistent with an exudate in those patients with secondary peritonitis (0.7 +/- 0.2) in contrast to typically infected transudate in patients with SBP (0.15 +/- 0.05) (P less than .001). Bacteriologic determination was similar: single organisms with Escherichia coli the most common. Often the clinical features and ascitic fluid analysis will not differentiate spontaneous from secondary peritonitis. It is, therefore, clinically prudent to consider secondary bacterial peritonitis in cirrhotic patients, especially with ascitic fluid WBC counts in excess of 5,000/cu mm and protein levels of greater than or equal to 2.5 gm/dl. Noninvasive diagnostic procedures should be included to search for sources of intra-abdominal infection.
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PMID:Secondary bacterial peritonitis in cirrhotic patients with ascites. 637 7

Human serum contains amyloid A degrading activity. This activity is decreased in patients with reactive systemic amyloidosis. To study the specificity of this finding, we evaluated the effect of liver disease per se on the amyloid degrading activity in serum as well as its relation to serum amyloid A (SAA), the putative precursor of amyloid A fibrils, and other serum protein levels in alcoholic and non-alcoholic non-malignant liver diseases without signs of amyloidosis. The amyloid A-degrading activity was significantly decreased in liver cirrhosis. The lowest activity was seen in patients with advanced cirrhosis. There was a positive correlation between the degradative activity and indices of hepato-cellular synthetic function (serum albumin, r = 0.77; serum prealbumin, r = 0.65). Most of the patients with liver disease had a detectable SAA level; 77% had a level higher than 5 mg/l (compared to 12% among blood donors). However, the SAA increase was generally only slight, e.g. in alcoholic liver cirrhosis the median SAA level was 15 mg/l. The results show that liver dysfunction per se decreases amyloid A-degrading activity in serum. A reduced activity cannot therefore be regarded as specific for reactive amyloidosis. Since reactive amyloidosis is extremely rare in liver cirrhosis, it seems obvious that a reduced amyloid degrading activity alone, in the absence of a markedly elevated SAA level, does not predispose, at least in patients with liver disease, to amyloidosis.
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PMID:Amyloid A fibril degrading activity in serum in liver disease--relation to serum acute phase and other protein levels. 688 7

The P-component of amyloid is a normal serum protein designated SAP. In view of recent in vivo experiments that suggested a possible role for the liver in the synthesis of SAP, we decided to evaluate the usefulness of its serum level as a marker of liver involvement. The study included 198 healthy adults, 154 patients with liver diseases, and 27 HBsAg carriers. Normal serum level of SAP was 66.12 micrograms/ml for males and 57.17 micrograms/ml for females. Patients with liver disease had a significantly decreased level of SAP. The mean serum level of SAP in cirrhosis was 30.15 in chronic active hepatitis--37.16 and in acute hepatitis--44.86 micrograms/ml. Asymptomatic HBsAg carriers had a normal SAP level (mean 65.48 micrograms/ml). Thirty-two patients with acute hepatitis were tested during the acute stage of the disease and after complete recovery. In all but three patients, a significant increase in SAP level, from a mean of 35.8 to 58.48 micrograms/ml, was observed. These results suggest a close correlation between serum levels of SAP and the degree of disease activity and hepatic impairment in patients with liver diseases, especially in those with acute hepatitis. Repeat determinations of SAP in patients with liver diseases could possibly help in their routine management.
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PMID:Serum amyloid P-component as a marker of liver disease. 709 Nov 28

The binding capacities of SHBG and CBG were measured by agar gel electrophoresis in 63 men with cirrhosis of the liver and in 42 healthy male subjects. The normal range (X- +/- 2s) for SHBG was 8.3-17.1 microgram/l, for CBG 46.4-82.8 micrograms/l. SHBG binding capacity was significantly higher in men with liver cirrhosis (mean 18;1 microgram/l; p less than 0.001) but CBG binding capacity was significantly lower (mean 49.7 microgram/l; p less than 0.001). Although SHBG was lower in patients with decreased CBG binding capacity, a correlation between both steroid binding proteins did not exist. Moreover, there was no correlation between SHBG or CBG on one hand and other parameters of hepatic protein synthesis such as serum protein concentration, cholinesterase activity and the coagulation factors V and VII on the other hand. In contrast to liver cirrhosis, 12 patients with fatty liver and 11 patients with toxic fibrosis of the liver did not reveal changes in SHBG or CBG. Treatment with spironolactone (200 mg daily for one week in 9 subjects) did not change the steroid binding capacity of human serum.
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PMID:[Binding capacity of sex hormone binding globulin and corticosteroid binding globulin in serum of male patients with liver cirrhosis (author's transl)]. 718 44

Endogenous digitalis-like factor (EDLF), an inhibitor of membrane Na+/K(+)-ATPase, is discussed to be involved in the pathogenesis of cirrhogenic portal hypertension, ascites formation and development of functional hepatorenal failure. Therefore, we investigated the serum content of this mediator in patients with liver cirrhosis Child-Pugh stage A, B, and C (n = 27) by means of enzyme immunoassay with a specific digoxin antibody. Furthermore, a correlation analysis was performed in order to find out correlations between signs of cell injury, cholestasis, synthetic cell function, ascites formation, and hepatorenal failure. Our results demonstrate that EDLF is significantly elevated in Child C cirrhosis (0.61 +/- 0.15 ng/ml) in comparison to Child A cirrhosis (0.013 +/- 0.2 ng/ml) and is also higher than in Child B cirrhosis (0.23 +/- 0.25 ng/ml). In patients without ascites EDLF (0.056 +/- 0.19 ng/ml) differs significantly from that of patients with non-complicated ascites (0.156 +/- 0.176 ng/ml) and from that of patients with therapy refractory ascites (0.66 +/- 0.17 ng/ml) or hepatorenal failure (1.56 ng/ml). There are no correlations between EDLF and renal function. Significant correlations were demonstrated for cholestasis (serum bilirubin), synthesis function (serum protein, Quick's value, cholinesterase, fibrinogen, albumin), and the degree of portasystemic encephalopathy (number connection test). We conclude that EDLF may act as a mediator in the process of progressive portal hypertension and its complications due to cirrhosis. This process of progression is caused by the inhibition of Na+/K(+)-ATPase, vasoconstriction, and endothelin secretion.
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PMID:[Endogenous digitalis-like factor in liver cirrhosis and cholestasis]. 748 6

An increase in total (72.67-8.24 mumol/l) and free (14.14-1.97 mumol/l) hydroxyproline and total (7.16-0.72 mumol/l) and free (1.06-0.24 mumol/l) hydroxylysine was found in the serum of 30 patients with decompensated hepatic cirrhosis as compared to the values in 40 healthy subjects (48.70-5.89; 8.41-4.73; 4.34-2.71; 0.77-0.25 mumol/l, respectively). The results were not related to total serum protein concentration. The level of peptide-bound hydroxyproline and peptide-bound hydroxylysine was significantly higher in cirrhotic patients despite the decrease in serum protein content.
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PMID:Serum hydroxyproline and hydroxylysine levels in patients with decompensated cirrhosis. 761 99

Injection of hepatocytes or cell-free supernatant into the lung was able to prevent death from surgically induced fulminant hepatic failure in the rat in over 90% and 53% of subjects, respectively. The aim of this study was to investigate whether this technique can be applied in chronic liver failure. Chronic liver failure was induced in Lewis rats by ligation and transection of the common bile duct, which led to cirrhosis after 3-5 wk in all animals. Four groups of animals were formed: group 1 (n = 5), normal rats, serving as control; group 2 (n = 15), cirrhotic rats, no further treatment; group 3 (n = 14), hepatocyte transplantation by injection of cell suspension transcutaneously into the right lung of cirrhotic animals four wk after bile duct ligation; group 4 (n = 17), injection of 1 mL cell-free supernatant intravenously at two-day intervals, starting 4 wk after ligation. Liver function tests, prothrombin time and serum protein levels were measured weekly before and every two days after transplantation. In group 2 all animals had died 56 (49-69) days after ligation. Survival in groups 3 and 4 was similar: all rats had died from liver failure 61 (51-72) and 60 (49-76) days following bile duct ligation. Survival rates and laboratory investigations showed no significant differences between treated and untreated cirrhotic animals. These data suggest that hepatocyte transplantation into the lung as well as supernatant injection do not have any significant effect on chronic hepatic failure, at least in the rat model.
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PMID:Hepatocellular transplantation into the lung in chronic liver failure following bile duct obstruction in the rat. 782 78

We report on a case of early portal vein thrombosis occurring after liver transplantation in a patient with alcoholic cirrhosis. Although this complication is usually accompanied by acute graft failure and/or gastroesophageal bleeding, in this patient the portal thrombosis occurred with the appearance of general dropsy and encephalopathy, serum protein deficiency and a slight rise in liver function test values. Echo-Doppler and arteriography showed portal thrombosis, arterial hyperflow and the persistence of a large spontaneous spleno-renal shunt, identified before the transplant had taken place. Endoscopy did not reveal gastroesophageal varices. Since there was no sign of serious ischemic damage or of a serious deterioration of liver function, the patient was treated non-operatively. Some particular hemodynamic aspects implicated in the appearance of portal thrombosis in our case are discussed. However, the authors consider that spontaneous portal-systemic shunt, in the presence of advanced cirrhosis, inverted portal flow, without gastroesophageal varices, can be considered as a surgical total diverting shunt and should be taken as a risk for portal thrombosis after transplantation.
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PMID:[Early thrombosis of the portal vein after orthoptic liver transplantation. A case report]. 832 40

The aim of this study was to investigate the regulation of various proteins of the GHIGF axis during progression of liver failure and to search for potential prognostic markers of functional hepatic reserve. Serum levels of growth hormone (GH) and high affinity growth hormone binding protein (GHBP), insulin-like growth factor I (IGF-I) and IGF binding proteins (IGFBP) -1, -2 and -3 were determined in patients with liver cirrhosis. A continuous decline in the concentrations of IGF-I, IGFBP-3 and serum GH-binding activity (GHBP) was observed during progression of cirrhosis and the data correlated significantly with choline esterase, total serum protein and the Child score. In addition, GHBP showed a significant correlation with the enzymatic activity of glutamate dehydrogenase or transaminases and seems so to be influenced by the degree of liver cell damage. In contrast, IGFBP-1 and IGFBP-2 levels were significantly elevated in preterminal disease suggesting an upregulatory mechanism is still effective in this situation. Only when liver function had markedly deteriorated, the serum levels of these two parameters decreased again, possibly due to an impaired synthesis. The excellent correlation between the serum levels of IGF-I (r = -0.64, p < 0.001) or IGFBP-3 (r = -0.67, p < 0.001) and the Child score index suggests that they reflect the hepatic functions just as conventional indicators. For an appropriate interpretation of the liver function the measurement of the growth related peptides can be a valuable tool to estimate pathological alteration in the functional hepatic reserve or in the glucose homeostasis.
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PMID:Regulation of growth hormone (GH), insulin-like growth factor (IGF)I, IGF binding proteins -1, -2, -3 and GH binding protein during progression of liver cirrhosis. 853 56

Thermolabile beta-2 macroglycoprotein is a novel serum protein that was detected by an autoantibody in sera of a Japanese woman with systemic lupus erythematosus. We developed an enzyme-linked immunosorbent assay for this glycoprotein and measured its serum levels in patients with chronic liver disease. There were significant correlations between serum levels of this glycoprotein and those of albumin and cholinesterase. The serum levels of TL beta 2MG decreased with increasing severity of cirrhosis. Immunohistochemical staining using monoclonal anti-thermolabile beta-2 macroglycoprotein antibody revealed positive staining in the cytoplasm of the hepatocytes. These data strongly suggested that hepatocyte may be one of the production sites of this glycoprotein. Measurement of serum levels of this glycoprotein was useful for evaluation of hepatic function in chronic liver disease.
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PMID:Thermolabile beta-2 macroglycoprotein (Hakata antigen) in liver disease: biochemical and immunohistochemical study. 893 53


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