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)

A 10-yr-old boy with an injured lower extremity received sevoflurane anesthesia 5 times within 40 days. Laboratory tests for hepatic and renal function i.e., serum transaminase (glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma-glutamyl transpeptidase), serum cholinesterase, plasma protein, serum cholinesterase, serum bilirubine, serum lactic dehydrogenase, serum prothrombin time, blood urea nitrogen, serum creatinine, beta 2-microglobulin, N-acetyl-D-glucosamidase and 24 hr-creatinine clearance remained within normal ranges throughout his perioperative period. Repeated sevoflurane anesthesia did not exert any adverse effect on hepatic and renal function in this patient.
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PMID:[Effects of repeated sevoflurane anesthesia on hepatic and renal function in a pediatric patient]. 781 13

We measured urokinase-type plasminogen activator (u-PA) plasma levels in patients with various chronic liver diseases, including hepatocellular carcinoma (HCC), also measuring these levels in healthy volunteers. Plasma u-PA levels in the group of patients with decompensated liver cirrhosis (mean modified Pugh score of 14 points) were markedly elevated and significantly higher than those in the patients with decompensated liver cirrhosis with HCC (modified Pugh score of 10 points), those with compensated liver cirrhosis with HCC, and those with compensated liver cirrhosis. Patients in all these three latter groups had moderately and significantly elevated u-PA levels compared to levels in the chronic hepatitis group and the healthy volunteers, but the levels were not significantly different from each other. There was no relationship between u-PA plasma level and the type of HCC tumor invasion or number or size of tumors. Significant correlations were found between u-PA plasma levels and the results of seven different liver function tests in three groups without associated HCC; u-PA antigen and prothrombin time (%), hepaplastin test (%), serum cholinesterase, serum albumin, serum total cholesterol, and indocyanine green clearance correlated negatively, while u-PA antigen and serum total bilirubin correlated positively. These results suggest that plasma u-PA is associated with deterioration of liver function but not with HCC invasion.
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PMID:Elevated urokinase-type plasminogen activator plasma levels are associated with deterioration of liver function but not with hepatocellular carcinoma. 787 70

Thirty-two crossbred (Suffolk x Rambouillet) wether lambs were used to examine the effectiveness of protein source (soybean meal [SBM] or fish meal [FM]) in alleviating decreased performance associated with dietary aflatoxin (AF) in growing lambs. After a 21-d adaptation period to concentrate diets, lambs were assigned to the following dietary treatments: 1) SBM, 0 mg of AF; 2) FM, 0 mg of AF; 3) SBM + 2.5 mg of AF/kg diet; or 4) FM+2.5 mg of AF/kg diet (two lambs/pen; four pens/treatment). Diets were fed 35 d, at which time AF was removed from the diet (except one pen/protein source) and lambs continued on study for an additional 32 d. On d 67, all lambs were killed and necropsied. Average daily gain, feed intake, and gain/feed were similar (P > .10) among lambs fed SBM or FM; however, lambs fed AF had lower (P < .01) feed intakes, daily gain, and gain/feed. Feed intake remained lower (P < .01) after AF was removed from the diet. Aflatoxin elevated (P < .01) aspartate amino transferase and gamma-glutamyl transferase activities and total protein and cholesterol concentrations while decreasing (P < .05) alkaline phosphatase, glucose, cholinesterase, albumin, inorganic phosphorus, iron, and total-iron-binding capacity. Hematocrit, white blood cell count, and prothrombin time increased (P < .01) in lambs fed AF. No AF or protein effects were seen on ruminal VFA, pH, or lymphocyte blastogenesis (P > .10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of aflatoxin in growing lambs fed ruminally degradable or escape protein sources. 805 74

Alpha 1-Antitrypsin deficiency predisposes to pulmonary emphysema, liver cirrhosis and hepatocellular carcinoma. Anecdotal evidence and a large autopsy study suggest that severe lung and liver disease rarely coexist in the same subject, but this has not been studied in patients. Therefore we investigated 27 patients with severe alpha 1-deficiency (Pi ZZ) and pulmonary emphysema for signs of liver disease and impaired hepatic function. A subgroup of 7 patients underwent quantitative liver function tests. On physical examination or ultrasonography, cirrhosis or tumor was not suspected in any patient. Conventional liver function tests were completely normal in 17 patients. Elevated serum activities of gamma-glutamyltranspeptidase and/or aminotransferases were seen in 10 patients. In some, the elevation was only marginal and in none more than twice normal. The serum bilirubin concentration and activity of alkaline phosphatase were increased in 1 patient. Serum protein, albumin, fibrinogen, antithrombin III, alpha 1-fetoprotein concentrations, serum activities of cholinesterase and glutamate dehydrogenase, activated partial thromboplastin time and prothrombin time were normal in all patients. The indocyanine green half-life was abnormal only in 1 of 6 patients, suggesting that hepatic blood flow was not impaired in the study group. However, the lidocaine half-life and galactose elimination capacity, parameters of hepatic metabolization, were impaired in 4 and 6 of 7 patients, respectively. We conclude that liver disease or impaired liver function is not a clinically relevant problem in most patients with pulmonary emphysema due to alpha 1-antitrypsin deficiency. But results of quantitative liver function tests, although performed in only a small group of patients, suggest that hepatic metabolization might be impaired even in those patients who present with pulmonary disease.
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PMID:Liver function in patients with pulmonary emphysema due to severe alpha-1-antitrypsin deficiency (Pi ZZ). 873 89

A survival analysis was carried out based on the data of 190 male patients with alcoholic liver cirrhosis (Child A: 82.2%; Child B: 17.8%). Patients (mean age: 49.6 +/- 7.1 years) were examined during the period 1983-1990. Censoring in May 1993 was based on the recordings of the "Rentenversicherungsanstalten". There were no "drop-outs". During follow-up (mean: 4.2 years) 64 (33.7%) of the patients died. 13 potential prognostic variables were examined individually by drawing Kaplan-Meier curves and performing log-rank tests. Portal pressure, determined during hepatic vein catheterization as hepatic vein pressure gradient HVPG (P), size of esophageal varices, serum bilirubin, serum albumin, prothrombin time (Quick), thromboplastin time (PTT), cholinesterase (ChE) and Child scores were correlated to survival (p < 0.05), whereas age, gamma GT, IgA, drinking habits and additional diagnoses were not. A multivariate Cox regression analysis stepwise eliminated all but three variables: ChE, albumin and variceal size were included in the prognostic index PI of the final model. The usefulness of the model was tested by a cross validation method. No significant difference was found between estimated and observed survivorship functions. To compare the PI of the Cox model with Child's scores, ROC curves of sensitivity and specificity of predicting death within one, three and five years were constructed. Better prognostic efficiency was indicated for PI. Because ChE, albumin and the size of varices are determined as a routine in our clinic, we consider the construction of PI an advisable alternative to Child's classification.
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PMID:Survival in alcoholic liver cirrhosis: prognostic value of portal pressure, size of esophageal varices and biochemical data. Comparison with Child classification. 877 35

The objective of this prospective study was to assess the prognostic value of dynamic and static liver function tests and clinical symptoms in pediatric patients with chronic end-stage liver disease in a serial examination including three evaluations at 3-month intervals. Of the 24 patients entering the study, six were given transplants within the observation period of 10 months. Of the remaining 18 patients who were considered in the final evaluation, five died before transplantation was possible. The variables included in the analysis were monoethylglycinexylidide (MEGX) formation from lidocaine, bilirubin, albumin, and creatinine serum concentrations, catalytic serum concentration of cholinesterase (CHE), prothrombin time (PT), factors II and V, serum amino acids, body weight, and presence of ascites. In nonsurvivors (n = 5), MEGX serum concentrations 30 min after intravenous administration of lidocaine (1 mg/kg body weight) were < 10 micrograms/L at the first examination. Statistically significant differences between nonsurvivors and survivors were observed for initial MEGX test results (p = 0.0089) and serum bilirubin concentrations (p = 0.009), as well as for the last available MEGX and bilirubin data from each patient (p = 0.017 and 0.016, respectively). At a diagnostic sensitivity of 100%, the corresponding diagnostic specificities for MEGX and bilirubin from the first examination were 77 and 62%, respectively. These data show that consistently low MEGX test results < 10 micrograms/L, obtained 30 min after intravenous administration of lidocaine (1 mg/kg body weight), are a prognostically unfavorable sign in pediatric transplant candidates.
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PMID:Prognostic value of the monoethylglycinexylidide test in pediatric liver transplant candidates. 885 54

To identify pretransplant factors that are influencing survival after orthotopic liver transplantation a Cox proportional hazards regression model was applied to 118 children with chronic terminal liver failure transplanted at Medical School Hannover during the period of 1978 to 1994. The response variable was survival, as covariates a total of 19 pretransplant variables were entered--i.e. age, diagnosis (biliary cirrhosis, metabolic cirrhosis, postnecrotic cirrhosis, cryptogenetic cirrhosis) sex, laparotomy prior to OLT, height, weight, standard deviation scores for height and weight, date of first OLT, serum alanine aminotransferase, asparagine aminotransferase, albumin, total bilirubin, cholinesterase activity, glomerular filtration rate, and prothrombin time. Significant independent predictors of survival after OLT were bilirubin (P=0.0024), SDS for weight (P=0.034), and albumin (P=0.039). In a subsequent discriminant analysis cut off points for these variables could be identified--i.e., bilirubin >340 micromol/L, SDS for weight <-2.2 and albumin < 33 g/L. Patients with one or more of these risk factors were grouped as urgent indication group (n=76) and those with no risk factor as elective indication group (n=42). Comparing the posttransplantation survival in these groups there is a statistically significant difference at 1 year (57% vs. 90.5%) and 4 years (49% vs. 90.5%) after OLT (P=0.0001, log rank test). It is concluded that the risk of OLT is much higher if liver function is very poor. Optimal nutritional support prior to transplantation is mandatory to optimise the clinical status of the children and to improve the results of OLT.
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PMID:Liver transplantation in children with chronic end stage liver disease: factors influencing survival after transplantation. 890 Mar 4

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

Glucose intolerance and diabetes mellitus are both prevalent in patients with chronic liver diseases. We examined the efficacy and systemic safety of therapy with an alpha-glucosidase inhibitor, acarbose, in diabetes mellitus associated with chronic liver diseases. Twenty patients with chronic hepatitis or liver cirrhosis and overt diabetes mellitus received acarbose (taken orally) for 8 weeks. The initial dosage of acarbose was 50 mg three times daily, taken before meals; this was increased to 100 mg three times daily after 2 weeks. The mean fasting plasma glucose level was 173.7 +/- 18.6 mg/dl (mean +/- SE) at entry, and was significantly decreased to 132.9 +/- 7.5 mg/dl (P < 0.05) after 8 weeks of acarbose treatment. The improved glycemic control was reflected by a significant decrease in glycosylated hemoglobin (HbA1c) from 7.2 +/- 0.3% at entry to 6.3 +/- 0.2% (P < 0.05) after 8 weeks. Serum levels of both aspartate and alanine aminotransferases fluctuated during acarbose treatment, probably due to the natural course of chronic liver diseases, but the mean values had decreased after 8 weeks of treatment. Plasma ammonia levels increased, from 61.3 +/- 10.7 micrograms/dl to 71.1 +/- 9.6 micrograms/dl after 8 weeks of acarbose treatment but the increase was not significant. Clinically significant elevation of plasma ammonia concentration was seen in 2 cirrhotic patients (121 and 124 micrograms/dl); this was asymptomatic and gradually returned to the normal range despite continuous acarbose treatment in one patient, and was reversed after the withdrawal of acarbose with the concomitant administration of lactulose in the other patient. No other blood tests results, including albumin, cholinesterase, and prothrombin time, or lipid profile and nutritional status, in terms of rapid turnover proteins, prealbumin, retinol binding protein, and transferin, were altered throughout the study period. These results indicate that diabetes mellitus associated with chronic liver diseases may be safely and effectively treated with acarbose. However, clinicians must be aware of the possibility of hyperammonemia when they prescribe acarbose for patients with diabetes mellitus and advanced liver cirrhosis.
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PMID:Safe and effective treatment of diabetes mellitus associated with chronic liver diseases with an alpha-glucosidase inhibitor, acarbose. 943 16

We have studied the levels of the MEGX test in a heterogeneous group of 50 patients with chronic liver disease and with hepatic tumours and we have compared it with the routine LFTS commonly used to assess liver function and with the Child-Pugh Classification system. Our results demonstrate a statistically significant relationship between MEGX levels and prothrombin levels, and between MEGX and alkaline phosphatase and a highly significant relationship between MEGX and cholinesterase. In the group of patients with cirrhosis we found a statistically significant difference amongst the MEGX levels in the 3 classes of the Child Classification system. The MEGX test is a good index in evaluating hepatic function and it is also quick and easy to perform and capable of determining residual liver function. The test can also be used for preoperative assessment in patients with focal hepatic lesions, especially in those with a previous history of cirrhosis, and in patients with functional hepatic disease.
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PMID:Monoethylglycinexylidide (MEGX) test in patients with different liver diseases. 971 90


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