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)

In 75 cases of histologically verified liver cirrhosis the plasma amino acids were determined by ion exchange chromatography and the results were correlated with different liver function tests as prothrombin time, pseudocholinesterase, serum albumin, GOT, bilirubin and venous ammonia. Out of these parameters prothrombin time, pseudocholinesterase and serum albumin significantly correlated with the sum of branched-chain amino acids and with the Fischer's quotient (molar ratio of branched-chain and aromatic amino acids). Methionin and aromatic amino acids inversely correlated with these parameters, additionally methionin positively correlated with bilirubin and GOT. By comparing plasma amino acid levels in cirrhotics without and with hepatic encephalopathy (grade 3 or 4) no significant differences were found. "Fischer's quotient" showed an overlap in patients with and without encephalopathy. Therefore the precipitation of hepatic encephalopathy is not fully explained by the changes in plasma amino acids. Therapeutic administrations of specially mixtures of amino acids with a high content in branched-chain and a low content in aromatic amino acids correct the plasma amino inbalance for a short time and improves hepatic encephalopathy.
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PMID:Plasma amino acids in hepatic encephalopathy. 29 Jul 44

The value of the aminoterminal procollagen-III-peptide (P-III-P) in predicting death or survival was evaluated in a group of 43 patients with proven postnecrotic or alcoholic cirrhosis. Patients were followed-up prospectively for 2 years. The prognostic value of P-III-P was compared with the Child classification, fasting and postprandial serum bile acids, and standard laboratory tests such as bilirubin, prothrombin index, pseudocholinesterase, albumin, GOT, GPT, gamma-GT, and clinical findings such as ascites, encephalopathy (assessed with the number connection test = NCT), and nutritional status. Between patients who died and those who survived the following 2 years, there were significant differences in the following parameters at the time of inclusion in the study: encephalopathy judged by NCT (p = 0.001), serum albumin (p = 0.0012), postprandial serum bile acids (p = 0.0024), fasting serum bile acids (p = 0.0025), pseudocholinesterase (p = 0.0044), GOT (p = 0.015), bilirubin (p = 0.016), and prothrombin index (p = 0.01). None of the other parameters investigated, including SP-III-P (p = 0.46), revealed any statistically significant differences between patients who died and survivors. The prognostic significance of laboratory tests and recorded clinical findings was evaluated, either alone or in combination with life-table analysis using the Cox model. SP-III-P, alone or in combination with other parameters, failed to improve prediction of mortality in patients with cirrhosis. In comparison to the Child classification (p = 0.0004) the combination of NCT and postprandial serum bile acids showed a similar ability (p = 0.0003) to predict patient survival.
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PMID:Predictive value of serum procollagen-III-peptide for the survival of patients with cirrhosis. 180 22

The aim of this prospective study was to examine the usefulness of flow-dependent dynamic liver function tests and conventional methods of evaluating liver function as predictors of pretransplant survival in patients with advanced cirrhosis. Patients who underwent orthotopic liver transplantation within the follow-up period of 365 days were excluded. One hundred one patients with histologically confirmed cirrhosis were studied. Fifty-eight patients had post-hepatitic cirrhosis, 13 had cryptogenic cirrhosis and 30 had biliary cirrhosis. During follow-up, 28 patients died of their liver diseases. At entry, we recorded indocyanine green half-life, monoethylglycinexylidide formation from lidocaine, bilirubin and albumin serum concentrations, activities of cholinesterase and alkaline phosphatase, prothrombin time, clinical complications of ascites and encephalopathy and the Pugh score. These variables were subjected as covariates to a stepwise survival analysis by use of the Cox proportional-hazards model. At the final step, Pugh score, monoethylglycinexylidide formation and indocyanine green half-life were found to be the only independent variables significantly related to 1-yr survival. The parallel combination of Pugh score and monoethylglycinexylidide test yielded the highest prognostic sensitivity (82%). The series approach combining either the Pugh score and indocyanine green test or the monoethylglycinexylidide and indocyanine green tests was associated with the highest specificity (96%/97%) and high predictive values of a positive result (81%/82%). These findings suggest that appropriate combinations of the studied flow-dependent dynamic liver function tests and the Pugh score could be useful in improving transplant candidate selection and the timing of transplantation.
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PMID:Predictors of one-year pretransplant survival in patients with cirrhosis. 195 50

Six-year survival of cirrhosis was assessed in a series of 1155 consecutive patients (751 men, 404 women). Among the men, 33% were alcoholics and 18% were HBsAg positive; corresponding figures for the women were 15% and 6% respectively. Features of decompensation at first presentation were observed in 63% of the patients. Six-year survival was 54% in compensated and 21% in decompensated patients. No significant differences in survival were found between alcoholics and nonalcoholics. Leading causes of death were liver failure (49%), hepatocellular carcinoma (22%), and bleeding (13%). The prognostic role of 21 variables was evaluated separately in compensated and decompensated patients by the Cox's regression model. The following variables were found to be significant predictors of death risk in compensated patients: male sex, HBsAg positivity, age, prothrombin time prolongation, and esophageal varices. In decompensated disease the significant indicators of death risk were: hepatocellular carcinoma, encephalopathy, hemorrhage, SGOT, esophageal varices, gamma globulins, prothrombin time prolongation, continued abuse of alcohol, HBsAg positivity, gamma glutamyl transpeptidase, and cholinesterase. A simple prognostic index based upon the relative risk coefficient of the significant variables is suggested.
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PMID:Survival and prognostic indicators in compensated and decompensated cirrhosis. 300 9

BMT has become an important therapy for many hematologic disorders. Following BMT, the recipient may develop GVHD when it appears that immunocompetent donor lymphocytes react to host antigens. Acute and chronic GVHD represent two distinct syndromes. Acute GVHD has not been associated with primary neurologic involvement. Polymyositis has been reported in 12 patients with chronic GVHD, with the most common underlying illness being aplastic anemia. The clinical, serologic, and muscle biopsy features of the myositis in GVHD have been similar to those observed in idiopathic polymyositis. Weakness was moderate to severe and responded to prednisone, sometimes with the addition of azathioprine. Prognosis depended upon the underlying disease and not on the severity of the myositis. MG occurs rarely in chronic GVHD. Most patients with MG and GVHD have had aplastic anemia; those with aplastic anemia are more likely to have anti-AchR prior to BMT. The clinical manifestations of GVHD MG have not differed from classic autoimmune MG; each patient had elevated antiacetylcholine receptor antibodies titers. All patients have responded well to cholinesterase inhibitors but have received other immunosuppressants. These observations suggest that aplastic anemia is an important host factor in the development of the autoimmune disorders seen with chronic GVHD, certainly of myositis and MG. Herpes zoster peripheral nerve infections have occurred in patients with chronic GVHD. One patient had mononeuritis multiplex. In both acute and chronic GVHD, CNS impairment is usually caused by metabolic encephalopathy or infection. Primary CNS involvement has not been recognized.
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PMID:Neurologic complications of graft-versus-host disease. 304 48

The effect of soman, a powerful organophosphorus (OP) cholinesterase inhibitor, was investigated in the central nervous system (CNS) of Wistar rats by neurohistology, histochemical mapping of acetylcholinesterase (AChE), and biochemical determination of cholinesterase (ChE) activity. Rats were poisoned by one lethal or sublethal subcutaneous (s.c.) injection or by several less strong weekly doses. When the acute cholinergic action of the OP led to severe respiratory failure and to repeated or prolonged convulsions, the surviving rats exhibited neuronal changes similar to those of hypoxic encephalopathy. In one case chronic intoxication gave rise to these symptoms and lesions after the fourth injection. The histochemical data showed that lesioned gray structures were generally poor in AChE. The enzymatic inhibition was quick and strong, but differed from one structure to another. ChE recovery was rapid until about 96 h after poisoning, the time course depending on the structure, but was incomplete even after 8 days. An attempt to correlate the initial level of ChE inhibition with the severity of the symptoms was not very conclusive. Our data suggest that the encephalopathy comes at least in part from complex hypoxic factors produced by the cholinergic crisis. The sequelae of slight hypoxic encephalopathy could account for some nervous long-term effects in men acutely poisoned by OP and surviving owing to mechanical ventilation.
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PMID:Histological and histochemical changes in the central nervous system of the rat poisoned by an irreversible anticholinesterase organophosphorus compound. 663 96

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

We compared the etiology and prognosis of liver cirrhosis in patients age 60 and older with that of patients under age 60 during the 1980s (1981-89, n = 207). Non-A, non-B hepatitis (NANB) was significantly more prevalent in the elderly (p < 0.05), and the mean age of NANB and alcoholic cirrhosis (Alc) were significantly older than those with hepatitis B virus (HBV) (p < 0.05). Evaluation using hepatitis C virus (HCV) antibody also revealed significantly higher mean age of HCV (p < 0.05). Male patient was predominant in the younger patients than in the elderly patients. (M/F = 2.94 and 1.33, respectively) The estimated 5-year survival rate was 73.1% in the younger patients and 60.2% in the elderly patients (p < 0.05). Multivariate analysis revealed that male sex, a lower serum albumin level, and the presence of the encephalopathy were significantly associated with poor prognosis in the elderly, while a lower serum cholinesterase level and a higher indocyanin green retention rate at 15 minutes (ICGR15) were significantly associated with poor prognosis in younger patients. However, causes of deaths were not significantly different between the younger patients and the elderly patients, the proportion of deaths unrelated to liver disease predominated in the elderly patients. Thus, the etiology and the prognostic factors of liver cirrhosis in elderly patients differ from those in younger patients.
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PMID:Etiology and prognosis of liver cirrhosis in elderly patients. 856 28

Approximately 25% of patients with idiopathic Parkinson's disease (IPD) later develop dementia, with the typical characteristics as detailed in ICD-10 and DSM-IV. Differential diagnosis has to exclude dementia due to Lewy bodies, subcortical vascular encephalopathy and subcortical dementia due to progressive supranuclear paralysis or corticobasal degeneration. Several studies showed promising results for cholinesterase inhibitors such as donepezile, rivastigmine and galantamine. The demented Parkinsonian patients then present with improvement in cognitive function while motor skills do not deteriorate.
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PMID:Dementia in idiopathic Parkinson's syndrome. 1567 22

The objective of the study was to describe the clinical characteristics and course of delayed-onset organophosphate (OP) poisoning. In our clinical experience, we have noticed patients with onset of deep coma 4-7 days after hospital admission, clinical features that have not been previously described. We set up a prospective observational study over 1 year to formally characterize this observation. Thirty-five patients admitted to the intensive care unit (ICU) with severe OP poisoning and treated with atropine and supportive therapy were followed up. Oximes were not administered. Three patients developed delayed-onset coma after presenting with normal or near normal Glasgow coma score (GCS). They developed altered conscious state rapidly progressing to deep coma, 5.0+/-1.0 (mean+/-S.D.) days after OP ingestion. The GCS persisted at 2T for 4.3+/-2.1 days despite the cessation of sedative drugs at the onset of coma. During this period, the patients had miosed non-reacting pupils and no clinically detectable cortical or brainstem activity. Computed tomography of the brain and cerebrospinal fluid analysis were normal. Electroencephalogram showed bihemispheric slow wave disturbances. Two patients required atropine during this period to maintain heart rate and reduce secretions. In all three patients, no metabolic, infective or non-infective cause of altered conscious state was identified. With supportive therapy the GCS improved to 10T in 8.0+/-2.0 days. All patients survived to hospital discharge. Three other patients who developed a reduction in GCS (3T-7T) by 4.7+/-1.2 days but not progressing to coma and recovering (GCS 10T) in 3.3+/-0.6 days may have manifested delayed-onset encephalopathy. Delayed-onset coma appears to have a distinct clinical profile and course with complete resolution of symptoms with supportive therapy. Although persistent cholinesterase inhibition is likely to have contributed to the manifestations, the mechanism of coma and encephalopathy need to be explored in further trials. The good outcomes in these patients suggest that therapy should not be limited in OP-poisoned patients developing profound coma or encephalopathy during hospitalization.
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PMID:Delayed-onset encephalopathy and coma in acute organophosphate poisoning in humans. 1830 42


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