Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha 1-Acid glycoprotein, an acute phase reactant synthesised by the liver, has been reported to be increased in neoplastic conditions and reduced in chronic liver disease. We measured serum alpha 1-acid glycoprotein by a nephelometric method in 186 subjects (112 males, 74 females): 55 had mild chronic liver disease (chronic hepatitis and steatofibrosis), 45 cirrhosis, 38 hepatocellular carcinoma, 15 extra-hepatic malignant disease; 33 healthy subjects were used as controls. Analysis of variance demonstrated a significant variability among groups (F = 17.08, P = 0.0000). Higher concentrations of alpha 1-acid glycoprotein were detected in malignant extra-hepatic disease than in all other groups (P < 0.01); concentrations of alpha 1-acid glycoprotein were higher in hepatocellular carcinoma than in cirrhosis (P < 0.01). Multiple regression analysis by groups (dependent variable = alpha 1-acid glycoprotein; group 1 = mild chronic liver disease + cirrhosis; group 2 = hepatocellular carcinoma) showed a significant correlation for both group 1 (r = 0.6264, F = 8.005, P = 0.0000) and group 2 (r = 0.8947, F = 13.643, P = 0.0000). The significant standardised regression coefficients were: cholinesterase, C-reactive protein, gamma-glutamyltransferase and iron (negative) for regression upon group 1; C-reactive protein, alpha 1-antiproteinase, gamma-glutamyltransferase, iron (negative) for regression upon group 2. A difference between the 2 regression equation coefficients was detected (F = 5.209, P = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase of serum alpha 1-acid glycoprotein despite the decline of liver synthetic function in cirrhotics with hepatocellular carcinoma. 810 7

The concentrations of platelet-derived growth factor in serum in 7 healthy controls (61 +/- 9 years; mean +/- SD) and 10 patients (62 +/- 8 years) with chronic liver disease (chronic hepatitis and/or liver cirrhosis) were compared. The plasma concentration of platelet-derived growth factor was below the detection limit (< 0.45 microgram/l) in all the subjects studied. The peripheral blood platelet count in patients with chronic liver disease was significantly lower than that in control subjects. However, the concentration of platelet-derived growth factor in serum, which was assumed to be released from platelet, was similar in patients with chronic liver disease and control subjects. These results indicate that the mean amount of platelet-derived growth factor released from the same number (10(9)) of platelets, calculated from the serum platelet-derived growth factor concentration and the peripheral blood platelet count, in patients with chronic liver disease (33 +/- 11 ng/10(9) platelets) was significantly (p < 0.01) higher than that in control subjects (14 +/- 5 ng/10(9) platelets). Moreover, the amount of platelet-derived growth factor released from 10(9) platelets inversely correlated with the serum concentration of pseudocholinesterase activity (r = -0.65, p < 0.01), and correlated positively (r = 0.91, p < 0.01) with the percent retention of indocyanine green in serum, in all subjects studied. These findings suggest that the amount of platelet-derived growth factor releasable from platelets of patients with chronic liver disease is higher than that in normal subjects and that it correlates with the severity of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased release of platelet-derived growth factor from platelets in chronic liver disease. 816 96

We measured serum erythropoietin (EPO) immunoenzymatically in 245 subjects (151 male, 94 female) to investigate the pathophysiology of its liberation in patients with liver disease. Twelve patients had acute hepatitis, 60 mild chronic liver disease (CLD), 50 cirrhosis (CIR), 43 hepatocellular carcinoma (HCC), 16 malignant extrahepatic disease, 32 benign extrahepatic disease (BEN); 32 subjects served as healthy controls. Higher EPO levels were found in all groups of patients as compared with controls (Bonferroni's test, P < 0.01); CIR and HCC had higher values than CLD and BEN (P < 0.01). By multiple regression analysis, EPO correlated with haematocrit, cholinesterase and C-reactive protein (F = 18.63, P < 0.0001). Thus, circulating EPO increases in patients with liver disease, particularly in its more advanced forms. Besides anaemia, both impairment of liver function (possibly via decreased EPO metabolism) and inflammation seem to play contributory roles in elevating serum EPO.
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PMID:Evidence for a multifactorial control of serum erythropoietin concentration in liver disease. 755 88

We studied 608 consecutive cases of anti-HCV-positive chronic liver disease. In 358 patients the diagnosis was established by needle liver biopsy. In 250 patients with liver cirrhosis the diagnosis was made on the basis of the unequivocal clinical signs and the results of imaging procedures. Chronic HCV infection is usually observed in adults or elderly patients; the age of the patients steadily increases with the progression of the illness to the more severe stages. Jaundice was infrequent in patients with chronic hepatitis or early cirrhosis; clinical symptoms and laboratory tests are of little value in differentiating CPH from CAH or in detecting early cirrhosis. Serum aminotransferases were usually only slightly elevated in all stages of the disease. Despite the mildness of the hepatic cytolysis, the progressive reduction in serum cholinesterase and albumin concentrations and the progressive increase in the serum alkaline phosphatase activity indicate progressive failure in the hepatic function in the course of the illness. The histological study showed that steatosis, follicular portal inflammation and eosinophilic changes in the hepatocytes were prominent features of chronic HCV infection. In contrast, severe piecemeal necrosis without bridging was rarely observed.
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PMID:Clinical and histological aspects of chronic HCV infection and cirrhosis. 840 7

Molecules governing cellular interactions have been suggested to be involved in the spurious elevation of alpha 1-fetoprotein (AFP) in non-neoplastic liver disease. To explore this controversial issue, we measured AFP, circulating intercellular adhesion molecule 1 (cICAM-1), and common liver function tests in 111 patients (71 male, 40 female). Eighty-four patients had non-neoplastic chronic liver disease and 27 had hepatocellular carcinoma. The concentration of cICAM-1 was determined immunoenzymatically. In patients with non-neoplastic chronic liver disease, univariate analysis demonstrated a significant correlation between AFP and cholinesterase (R = -0.397, P < 0.001), aspartate aminotransferase (R = 0.421, P < 0.001), bilirubin (R = 0.231, P < 0.05) and cICAM-1 (R = 0.430, P < 0.001). Multivariate analysis among these variables and AFP indicated cICAM-1 to be the strongest independent predictor of AFP. We conclude that cICAM-1 compares favourably with liver function tests in predicting non-specific AFP variations in non-neoplastic chronic liver disease, suggesting a link between targeting of the inflammatory damage to the hepatocyte and development of neoplasia.
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PMID:Circulating intercellular adhesion molecule 1 predicts non-specific elevation of alpha 1-fetoprotein. 864 48

We designed a clinical study to determine the effect of prostaglandin E1 (PGE1) on functional recovery of the liver after hepatectomy. Thirty-five patients with primary hepatic neoplasms accompanied by chronic liver disease were randomly divided into two groups: 13 patients received intravenous PGE1 at 0.06 micro g/kg per minute for 3 postoperative days (PGE1[+] group) and 22 patients did not (PGE1[-] group). All postoperative values of hepatic function tests were calculated as a ratio to each preoperative value. Significantly higher cholinesterase ratios were observed in the PGE1[+] group than in the PGE1[-] group 2 weeks postsurgery (P < 0.05). The alanine aminotransferase (ALT) ratios at 1 and 2 weeks postsurgery were 118% and 123% in the PGE1[+] group and 207% and 175% in the PGE1[-] group, respectively. The ratio of the maximum postoperative ALT level was 503% in the PGE1[+] group and 792% in the PGE1[-] group (P < 0.05). We concluded that PGE1 would have the effect of conditioning the postoperative ALT elevation and cholinesterase deterioration and that the patient's postoperative course might be more favorable with the use of PGE1.
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PMID:Effect of prostaglandin E1 on hepatic function after hepatectomy in patients with chronic liver disease. 875 Apr 3

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

We studied the hepatic functional reserve in the lobes of the liver in 28 patients with chronic liver disease and 13 controls using single photon emission computed tomography (SPECT) imaging with a radiolabeled asialoglycoprotein analog, Technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin (Tc-99m GSA). Counts of Tc-99m GSA radioactivity in the liver on SPECT images significantly correlated (P < .0001) with the serum albumin level (r = .612), log (serum cholinesterase activity) (r = .618), serum bilirubin level (r = .628), prothrombin time (r = .715), hepaplastin test (r = .637), and indocyanine green retention rate at 15 minutes (r = .771), making it possible to estimate the distribution of functional reserve in the liver based on counts. Using the intact hepatocyte theory, we estimated the number of viable hepatocytes based on the counts. With progression of hepatic functional degeneration, counts per unit hepatic volume decreased (rho = .779, P < .0001), and left lobe to right lobe ratio of this parameter increased (rho = .491, P = .0019) significantly. These findings suggest that the reduction of hepatic functional reserve per unit hepatic volume and numerical density of the hepatocytes, and the proliferation of fibrosis in patients with chronic liver disease is slower in the left lobe than in the right. We discuss a possible biological basis for these apparent lobar differences and for hepatic morphological changes seen in cirrhosis.
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PMID:Hepatic lobar differences in progression of chronic liver disease: correlation of asialoglycoprotein scintigraphy and hepatic functional reserve. 909 83

The intercellular adhesion molecule 1 (ICAM-1, CD54) and the lymphocyte associated antigen 3 (LFA-3, CD58) have been found in soluble form (sCD54 and sCD58) in human sera. Data concerning their role in chronic liver disease and their usefulness in disease monitoring are contradictory. We addressed the question whether elevated sCD54/sCD58 correlated either with disease activity or with decreased elimination secondary to reduced liver function in chronic hepatitis B. We studied 31 patients with chronic hepatitis B undergoing interferon alpha therapy in a longitudinal fashion. Serum concentrations of sCD54 and sCD58 were measured at four weeks interval by specific Sandwich ELISA during a follow-up period of ten months. The maximal difference in concentration of each biochemical parameter, e.g., delta AST, delta gGt, delta bilirubin, was determined for each patient during the whole follow-up period. These differences were correlated with the variation in sCD54 (delta sCD54) and sCD58 (delta sCD58) at the respective time points. Using this method, we were able to eliminate interindividual differences in serum concentrations for sCD54 and sCD58 and to avoid bias due to preselection of patients. We found that delta sCD54 correlated with delta AST (p = 0.001) and delta ALT (p = 0.002), whereas there was no such correlation for delta sCD58. Interferon therapy did not affect sCD54 or sCD58 levels. Neither hepatitis B viremia nor the immune response to hepatitis B during the time of seroconversion to anti-HBe did significantly increase sCD54 or sCD58 levels. However, delta sCD54 was associated with delta gamma GT (p = 0.005) and delta sCD58 correlated with delta bilirubin (p = 0.037); a negative correlation was found for delta sCD54 with delta cholinesterase (p = 0.007). Our findings imply that sCD54 and sCD58 may be associated with a decrease in liver function that accompanies hepatic disease activity. sCD54 and sCD58 did not prove useful to monitor disease activity or response to interferon therapy in chronic hepatitis B. From our data we conclude, that decreased elimination of soluble adhesion molecules sCD54 and sCD58 in advanced liver disease may be responsible for increased serum concentrations detected.
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PMID:Circulating ICAM-1 (sCD54) and LFA-3 (sCD58) in chronic hepatitis B--a longitudinal study in patients treated with interferon-alpha. 923 90

Chronic liver disease is often accompanied by hypoxaemia. We investigated the clinical factors that were related to the arterial oxygen tension (PaO2) in 40 women, all non-smokers with chronic liver disease. They were positive for hepatitis C virus (HCV) antibody and had no evidence of cardiopulmonary disease. Arterial blood was collected from patients at rest (> 15 min) for analysis of blood gases. We determined the correlation between blood gas tension and the clinical variables, i.e. the presence or absence of skin manifestations such as cutaneous spider nevi and palmar erythema, the presence or absence of splenomegaly, vital capacity, forced expiratory volume in one second, V25/body height, serum alanine aminotransferase (AST), serum asparate aminotransferase (ALT), serum cholinesterase, serum gamma-globulin/total protein, excretion of indocyanine green at 15 min (15-min retention rate, ICG level), blood level of ammonia, blood level of endotoxin, plasma level of glucagon and the serum level of type IV collagen-7S. The mean level of PaO2 was 78 +/- 11 (range: 43-95) torr. The mean alveolar-arterial oxygen tension gradient (A-aDO2) was 19 +/- 13 (range: 2-60) torr. Multiple regression analysis used PaO2 and A-aDO2 as objective variables, and the clinical findings as explanatory variables. The explanatory variables that were significantly correlated with blood gas values were ICG level, blood level of endotoxin and presence of skin manifestations. The ICG level showed a high correlation with blood gas values; the ICG level increased, the PaO2 decreased (r = -0.69), while the A-aDO2 showed a high positive correlation (r = +0.78, P < 0.001). Findings suggest that a reduction in hepatic blood flow and hepatocellular function interfere with the inactivation of vasoactive substances such as endotoxin by the liver, leading to the development of skin manifestations, the dilatation of intrapulmonary capillaries and the induction of hypoxaemia.
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PMID:Clinical factors that affect blood gases in non-smoking women with chronic liver disease. 951 26


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