Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For the evaluation of certain differences in the diminution of export proteins of the liver we examined some exactly defined groups of liver diseases with the aim of further differentiation of the pathogenetic mechanisms. We measured the activity of glutamate-oxalacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, lactate dehydrogenase, alkaline phosphatase, cholinesterase and lecithin-cholesterol acyltransferase, the Quick value, the coagulation factors I, II, V, VII, VIII, IX and X. Clotting factors were determined by a Schnitger-Gross Coagulometer. Prothrombin, antithrombin III, plasminogen, factor VIII associated antigen and activated factor XIII were measured by immunoelectrophoresis according to Laurell. Lipoprotein electrophoresis in agarose gel was performed to evaluate changes in lecithin-cholesterol acyltransferase activity. Except of the rising diminution of export proteins in the course of liver disease from acute hepatitis to cirrhosis we found also specific changes of the patterns of the plasma specific enzymes. These proteins were diminished dependent on their half life time and the inflammatory activity--measured as the height of the transaminases. Lecithin cholesterol acyltransferase and factor VIII did not participate in the general diminution of the most export proteins; some details were found to explain this differing behaviour. Results are critically discussed with regard to new aspects in the biochemistry of the damaged liver cell.
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PMID:[Correlations between the diminished secretion of export proteins from the liver and the plasmatic activity of liver cell enzymes (author's transl)]. 42 91

Part I: Immunological assays of clotting factors in the diagnosis of liver diseases. The immunological determination of Antithrombin III is a good measure of the capacity of the liver to synthesize plasma proteins. Antithrombin III concentration in serum correlated significantly with the prothrombin time and the activity of cholinesterase. The immunological determination of factor VIII related antigen seems to be important for the early recognition of the transition of an acute hepatitis into a chronic course. While following uncomplicated acute hepatitis the level of factor VIII related antigen is normal after 40 weeks, it remains high in cases which become chronic. Immunological assay of factor XIII seems to be not very useful in the diagnosis of liver diseases. Part II: Management of coagulation disturbances in liver diseases. Except cases of hepatic coma the hemostatic abnormalities in chronic liver diseases are rarely severe enough that correction is necessary. Prothrombin concentrates are considered by most of the discussants as unnecessary and potentially dangerous. Transfusion of platelets is only neccessary when the platelet count is below 40.000 and surgery is planned. It is uncertain whether patients with chronical liver disease and laboratory signs of DIC benefit from heparin therapy. Although laboratory tests may be improved, prognosis, especially in cases of acute oesophageal bleeding, seems to be not changed by this treatment.
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PMID:[Summary of work session 1: Blood coagulation in gastroenterology]. 78 39

In vitamin K deficiency or treatment with vitamin K antagonists, a precoagulant of prothrombin (Factor II) called preprothrombin has been established. We measured preprothrombin with Clarke-Freeman electrophoresis in 26 patients with acute viral hepatitis (21 HBS-AG positive) who did not suffer from vitamin K deficiency. Prothrombin and the vitamin-K dependent Factors VII, IX, and X were determined by standard coagulometric methods. Prothrombin was additionally estimated by immunoelectrophoresis according to Laurell. Three patients with acute HBS-AG positive hepatitis showed preprothrombin in their plasma. The activity of Factors II, VII, IX, and X was slightly below normal with normal concentration of Factor II in the immunoelectrophoresis. Liver parenchymal damage and cholestasis were slight; the pseudocholinesterase showed subnormal levels in all three patients. Possible causes for the appearance of preprothrombin in the peripheral blood in acute viral hepatitis and the possible connections with liver cell damage are discussed.
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PMID:[Preprothrombin in acute viral hepatitis B]. 717 63

Serum cholinesterase catalytic concentrations were estimated in 26 patients diagnosed as having systemic sepsis syndrome (septic shock) in the Intensive Care Unit (12 were admitted with the diagnosis of systemic sepsis syndrome while 14 patients developed the syndrome while in the unit) and in 66 normal, healthy subjects. The assay was performed for 7 consecutive days in the patient group. There was a very significant decrease in the level of cholinesterase in the patient group from the onset of the study as compared to the control group (P < 0.00001). This decrease remained during the course of the seven day study period, indicating hepatic dysfunction early in the diagnosis. When compared to other conventional liver function tests, serum cholinesterase seems to change earlier on in the diagnosis. Prothrombin time showed a pattern of change similar to that of serum cholinesterase. There was a significant relationship between the catalytic concentration of serum cholinesterase and the outcome of the systemic sepsis syndrome, the level being significantly lower in patients who died in comparison to those who lived. It seems that serum cholinesterase is a sensitive indicator of hepatic dysfunction in the systemic sepsis syndrome.
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PMID:Profile of serum cholinesterase in systemic sepsis syndrome (septic shock) in intensive care unit patients. 775 36