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:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five patients had amiodarone hepatotoxicity detected on routine biochemical monitoring. Symptoms attributable to hepatotoxicity were minimal or absent; reversible hepatomegaly was seen in two patients, whereas three patients had signs of nonhepatic amiodarone toxicity before or with hepatotoxicity. Serum aminotransferase levels were elevated in all patients and alkaline phosphatase levels in four; no patient had hyperbilirubinemia or prolongation of the prothrombin time. Light microscopy showed steatosis, cellular degeneration, and cellular necrosis in the biopsy samples of four patients, whereas the fifth patient's sample had a granulomatous injury pattern. Electron microscopic study of liver tissue done in two patients showed phospholipid-laden lysosomal lamellar bodies. These findings suggest that both toxic and hypersensitivity liver injury can occur in response to amiodarone. The presence of phospholipid-laden lysosomal lamellar bodies may help differentiate amiodarone hepatotoxicity from alcoholic liver disease or other causes of hepatic steatosis.
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PMID:Amiodarone hepatotoxicity. A clinicopathologic study of five patients. 394 78

Tritoqualine (TRQ) administered at doses of 100 or 200 mg/kg, perorally, had a preventive effect on the liver injury in rats induced by the treatment with CCl4 for 12 weeks consecutively. Rats subjected to this chronic treatment with CCl4 showed a decrease in body weight gain and changes in several serum parameters that are indicators of hepatic function were observed: the increase of transaminases, as a parameter of hepatocyte breakdown; the increase of alkaline phosphatase, as a parameter of biliary system abnormalities, the reduction of prothrombin time, as a marker of protein biosynthesis in the liver; and the change of lipids concentrations, reflecting liver injury. After the administration of TRQ perorally, there was a notable suppression of the increment in leaked enzymes in the serum and a marked improvement of the parameters concerning protein biosynthesis and lipid metabolism in comparison with CCl4 control rats. Marked fibrosis in the liver was observed after CCl4 treatment for 12 weeks, and the collagen content in the liver was 5 times higher than that of control rats. TRQ suppressed the increment in collagen formation and also showed improvement of the decrease of the liver function with regards to protein biosynthesis in CCl4-treated rats. Judging from these results, it was concluded that TRQ had a remarkable protecting action on the liver injury chronically induced by CCl4 treatment and was a effective compound for restoring liver function.
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PMID:[Prophylactic effect of tritoqualine (TRQ) on the CCl4-induced chronic liver injury model in rats]. 400 7

To determine the predictive value of laboratory procedures for severity of liver disease, twelve laboratory tests were evaluated in seventy-two patients with various liver disease and in nine non-liver disease hospitalized cases. A numerical score based on the number and extent of abnormal findings was developed for grading clinical and histological severity. Multiple linear regression, utilizing a forward stepwise selection procedure, was used to find the best combination of laboratory tests for prediction of disease severity. The best predictive model for both clinical and histological severity was found for lecithin cholesterol acyltransferase (LCAT), total plasma cholesterol, alkaline phosphatase and bile acids. Of the routine tests prothrombin time and albumin/globulin were useful if the four-test combination listed above was not used. There was a significant correlation (p less than 0.001) between the clinical and the histological score, confirming validity of clinical scoring. In conclusion, this study shows LCAT to rank as first in predicting severity of liver disease. Cholesterol metabolism appears to be affected by liver disease even more than prothrombin time, albumin and globulins. LCAT and bile acids have a place in routine testing of severity of liver disease.
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PMID:Predicting severity of liver disease: twelve laboratory tests evaluated by multiple regression. 405 27

T-2 toxin was given as a single intravascular dose at either 0.6 or 4.8 mg/kg to different groups of 50-kg female swine. Blood samples were taken at hourly intervals for determination of concentrations or activities of the following substances in serum or plasma: creatinine, blood urea nitrogen, inorganic phosphorus, total calcium, ultrafilterable calcium, magnesium, sodium, potassium, chloride, total protein, albumin, cholesterol, glucose, alkaline phosphatase, aspartate aminotransferase, and total bilirubin. Coagulation analyses included prothrombin time, partial thromboplastin time, activated coagulation time, and fibrin degradation products. Red blood cell, white blood cell, and platelet counts, hemoglobin concentrations, and hematocrits were determined from whole blood samples. An initial leukocytosis was followed by a leukopenia. The numbers of red cells, the hemoglobin concentration, and the hematocrit were increased. Nucleated red blood cells were seen in the blood smears. The serum concentration of bound calcium decreased, while phosphorus, magnesium, and potassium increased. Clinical screening tests detected no evidence of a coagulopathy in swine given T-2 toxin intravascularly.
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PMID:Experimental T-2 toxicosis in swine. II. Effect of intravascular T-2 toxin on serum enzymes and biochemistry, blood coagulation, and hematology. 406 62

Child-Turcotte classification (CTC) is an empirical but widely accepted approach for assessment of severity of cirrhosis. However, it is not known to what extent CTC reflects accurately the degree of impairment of hepatic function. In this study we compared CTC, standard liver tests and intrinsic hepatic clearance (IHC) of indocyanine green as means of assessing hepatic function in 63 cirrhotic patients. As compared to 10 control patients, IHC was significantly decreased in the cirrhotic group: (mean +/- SD) 0.270 +/- 0.141 l/min vs 1.227 +/- 0.312 l/min (P less than 0.001). Serum bilirubin (SB), prothrombin time (PT) and serum albumin were significantly correlated with the degree of IHC impairment while alkaline phosphatase, ALAT and clinical criteria of CTC were not. Multivariate analysis showed that SB and PT were the only 2 variables that significantly explained the impairment of IHC. The model which best explained IHC impairment was Z = 21.77 + 4.78 PT - 1.25 SB. The rate of IHC variance explained by this model, as determined by multiple correlation coefficient square (R2), was 42.6%. These results suggest that CTC provides only gross information about the degree of impairment of liver function in cirrhosis. To evaluate the role of liver function in the prognosis or in the response to treatments, it should therefore be preferable to employ direct measurement of liver function using a clearance technique.
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PMID:Intrinsic hepatic clearance and Child-Turcotte classification for assessment of liver function in cirrhosis. 406 57

The clinical syndrome of "shock liver," also known as ischemic hepatitis, is characterized by sudden elevation (to more than 20 times the upper limit of normal) of SGOT and SGPT in response to cellular anoxia, followed by resolution to near normal levels within seven to ten days. In our experience with ten cases, systemic hypotension was documented in only four, but processes characterized by decreased cellular perfusion were identified in all and included cardiac failure or arrhythmia, sepsis, cerebrovascular accidents, renal failure, and chronic obstructive pulmonary disease. We were also able to document the transient rise in serum bilirubin and alkaline phosphatase levels and prolonged prothrombin time that followed the transaminase elevations by 24 to 48 hours in most cases, followed by rapid resolution. In neither of the two cases in which tissue was available by biopsy after resolution of the biochemical abnormalities did we find the classic histologic picture of necrosis in zone 3 ("centrilobular necrosis"). The clinical picture of shock liver is so characteristic and resolves so rapidly that there should be no confusion with other causes of marked elevations of transaminase levels.
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PMID:Shock liver. 407 Nov 67

The activity of certain serum enzymes ornithine carbamyl transferase (OCT), serum isocitric dehydrogenase (SIC-D), total serum lactic dehydrogenase (LDH) and its isoenzymes (LD(1) and LD(5)) was evaluated as a mean of assessing experimental hepatic necrosis on dogs treated with CCl(4). Measurement of activity levels of these enzymes, seldom carried out in veterinary clinical pathology, was made together with tests commonly used in our laboratories: serum glutamic pyruvic transaminase (SGPT), serum glutamic oxalacetic transaminase (SGOT) and serum alkaline phosphatase (SAP), cholesterol, bilirubin and prothrombin time. Measurement of the level of OCT was useful in the diagnosis of liver necrosis. The SIC-D level was important during the first four days of the experiment, but on subsequent days, the enzymatic activity was practically normal. Because of the wide variations of LDH serum levels in normal animals and since many factors influence its activity, the measurement of this enzyme and its isoenzymes was not a good index in the diagnosis of canine liver necrosis. The evaluation of cholesterol and bilirubin was judged of secondary importance because these metabolites are not specific to hepatic problems.A small battery of tests must be used to establish a precise diagnosis and a clear prognosis. To the routine tests like those for SGOT, SGPT and SAP, should be added the evaluation of OCT and SIC-D.
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PMID:[Serum enzymes for the diagnosis of experimental acute hepatic necrosis]. 424 68

A case report of cholestatic jaundice in a 25 year old woman, who had had jaundice at age 4 years, and had taken Stediril (a combined oral contraceptive) for 1 month, implicates either the pill or a possibly hereditary hyperlipidemia. The jaundice developed in 2 weeks with vomiting, epigastric pain, anorexia, then discolored urine and feces, and intense pruritus. On hospitalization the patient had moderate bilirubinemia (56 mg/1), low alkaline phosphatase (13 U.K.) and slightly high serum glutamate pyruvate transaminase (270 U.W.). There were elevated serum cholesterol (3 gm/1), triglycerides (2.05 gm/1), total lipids (10.6 gm/1), and a definitely increased pre-beta lipoprotein, suggesting hyperlipidemia type IV (Frederickson classification). Liver biopsy showed fibrosis of the portal spaces lymphocytic infiltration, canalicular and intrahepatocytic thrombi. On laparoscopy the liver had a regular lower border, normal volume color and surface. Albumin, prothrombin and flocculation tests were normal. The patient's jaundice lasted about 1 month, then liver function slowly improved, although pruritus remained intense. Probably this jaundice was due to oral contraceptives, in a patient predisposed either by jaundice in childhood or endogenous hyperlipidemia.
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PMID:[Cholestatic icterus due to oral contraceptives]. 426 76

Serum aluminum levels twice to three times those in controls were found in 30 of 36 workers in a factory in an atmosphere of alumina dust. Inorganic phosphate and total alkaline phosphatase levels were within normal range, with no clinical evidence of phosphate depletion syndrome. Serum intestinal alkaline phosphatase, acid phosphatase and adenosine triphosphate levels were significantly reduced in the group with high levels of aluminum. The finding that the mean prothrombin time was significantly prolonged is of particular interest with respect to beneficial antithrombogenic effect.
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PMID:Increased prothrombin time and metabolic changes with high serum aluminum levels following long-term exposure to Bayer-process alumina. 433 26

Liver damage in a woman who had taken an overdose of paracetamol and dextropropoxyphene was assessed by monitoring serum prealbumin concentrations and by routine plasma enzyme determinations. The plasma aspartate aminotransferase returned to normal levels after 3 days, alkaline phosphatase was slow to show increases in activity, and serum albumin concentration was in the normal range throughout. Prothrombin-time, although initially very high, returned almost to normal as a result of the administration of plasma. In contrast, serum prealbumin concentration decreased significantly after 36 h and continued to decrease, showing the course of failing liver function, until the patient's death 15 days after presentation. Prealbumin, a functional plasma protein synthesised in the liver, has a short half-life, is a true index of liver function, and seems to be a more reliable indicator of liver function in drug overdose than plasma enzymes, prothrombin-time, or plasma drug concentration.
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PMID:Prealbumin as an index of liver function after acute paracetamol poisoning. 610 95


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