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)

1 The free fraction of azapropazone in the plasma of 37 healthy volunteers ranged from 0.0027 to 0.0070 (0.0044 +/- 0.0009, mean +/- s.d.). The principal binding protein was found to be albumin. 2 In 27 patients with various degrees of renal failure the free fraction values of azapropazone were markedly enhanced (0.0260 +/- 0.0239, mean +/- s.d.) and increased more than tenfold in some patients. There was a weak correlation (r = 0.46, P less than 0.05) between the free fraction and the clearance of endogenous creatinine. Such correlation was not found for serum creatinine, serum albumin, serum uric acid and serum urea nitrogen. 3 In 32 patients with chronic liver disease the free fraction values of azapropazone were also markedly higher (0.0210 +/- 0.0242, mean +/- s.d.) than in healthy subjects. There were statistical significant correlation between free fraction values and the prothrombin complex activity in the plasma (r = 0.40, P less than 0.05) and the total bilirubin concentration in the plasma (r = 0.90, P less than 0.001), respectively. Such correlation was not found for serum albumin, serum glutamic oxalacetic transaminase, serum gamma-glutamyl transpeptidase and serum alkaline phosphatase. 4 In patients with kidney and liver disease the free fraction values of azapropazone correlated well with those of the anticoagulant drug phenprocoumon (r = 0.93, P less than 0.001). However, the binding of the latter drug was less impaired. Bilirubin, when added in vitro, displaced both drugs from plasma proteins but this displacing effect was much smaller than the binding changes observed in patients with liver disease. 5 Kidney and liver disease caused a marked impairment of the plasma protein binding of azapropazone. In patients with kidney disease the degree of impairment of azapropazone binding cannot or only poorly (creatinine clearance) be predicted from the biochemical parameters of kidney function whereas in patients with chronic liver disease the total bilirubin concentration in the plasma may serve as an index of the binding defect.
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PMID:Plasma protein binding of azapropazone in patients with kidney and liver disease. 725 29

Hippurate-synthesizing ability was investigated in patients with jaundice with percutaneous transhepatic biliary drainage (PTBD) in relation to hepatic metabolic capacity. In 16 patients with PTBD because of obstructive jaundice and 11 patients without hepatic disease, 1.77 grams of sodium benzoate was injected and the amount of hippurate synthesized and excreted in the urine collected at 30, 60, 120 and 180 minutes was measured (hippurate test). In patients with jaundice and patients in the control group, an almost linear increase was observed in the level of urinary hippurate after benzoate loading. However, the values of the patients with jaundice at one and two hours after the benzoate loading were significantly lower than those of the patients in the control group. Serum levels of glutamate oxaloacetic transaminase, glutamate pyruvate transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, total bilirubin and direct bilirubin were significantly decreased during PTBD (p < 0.05). Bilirubin levels were closely correlated with hippurate test values (r = 0.567, p < 0.05). Values were also correlated with the period of PTBD before the hippurate test was performed (r = 0.632, p < 0.05). Recovery in hippurate synthesizing ability was observed when the total bilirubin levels decreased to less than 5 milligrams per deciliter or PTBD was maintained for more than three weeks. Because hippurate synthesis is dependent on adenosine triphosphate supply in the hepatic mitochondria, the value of the hippurate test reflects the metabolic viability of the liver in relation to energy metabolism. It is also suggested that the steady maintenance of PTBD for three weeks or more with a decrease in total bilirubin level less than 5 milligrams per deciliter is necessary for full recovery of the metabolic capacity of the jaundiced liver.
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PMID:An assessment of percutaneous transhepatic biliary drainage in the correction of the metabolic capacity of the jaundiced liver by hippurate-synthesizing test. 832 55

The influence of biochemical parameters of hepatic function on vancomycin pharmacokinetics was retrospectively evaluated in 76 adult patients (age 18 to 81 years), from biochemistry data gathered during routine therapeutic drug monitoring. All subjects had normal serum creatinine levels. Vancomycin concentrations were determined by fluorescence polarization immunoassay in 101 paired serum samples. All data for vancomycin concentration versus time were fitted to a one-compartment model using the bayesian approach. Bilirubin, transaminases (n = 101), gamma-glutamyl transferase (n = 97), alkaline phosphatase (n = 95), albumin (n = 92) and lactate dehydrogenase (n = 42) were determined. No strong correlation was seen between any of the pharmacokinetic and biochemistry parameters studied. In patients with hyperbilirubinaemia, the mean Vss and t1/2 were increased (Vss: 0.75 +/- 0.31 versus 0.92 +/- 0.42 1.kg-1, p = 0.020; t1/2 5.93 +/- 3.30 versus 7.48 +/- 4.44 hr, p = 0.049). When liver function was evaluated according to hepatic profile (normal, mildly altered and severely altered), no significant differences were observed in vancomycin pharmacokinetics among the groups. In conclusion, vancomycin pharmacokinetics are only weakly influenced by the biochemistry parameters of liver function.
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PMID:Influence of biochemical parameters of liver function on vancomycin pharmacokinetics. 887 46

Abnormal liver tests, as well as morphological changes in the liver, are frequent among obese patients. Other frequent disturbances are visceral fat accumulation, insulin resistance, non-insulin-dependent diabetes mellitus (NIDDM), hypertriglyceridemia, and hypertension; these are set of aberrations known as the metabolic syndrome. In order to investigate a possible relationship between the metabolic syndrome and impaired liver status we examined associations between liver tests, metabolic variables (insulin, glucose, and triglycerids), body composition and nutrition in 1,083 men (BMI 28.8-63.8 kg/m2) and 1,367 women (BMI 26.7-68.0 kg/m2) in the ongoing intervention study of Swedish Obese Subjects (SOS). Standard biochemical techniques were used to assess liver status and metabolic variables. Lean body mass (LBM) and masses of visceral and subcutaneous adipose tissue (AT) were estimated by means of computed tomography (CT) calibrated anthropometric equations. In both genders aspartate aminotransferase and alanine aminotransferase were, or tended to be, positively correlated to fasting serum insulin, visceral AT (women), and alcohol intake. In women, the aminotransferases were also correlated with fasting blood glucose. In both genders alkaline phosphatase was, or tended to be, positively associated with visceral AT, insulin (women), and glucose. Bilirubin was negatively correlated to insulin and visceral AT in men and women. Additional multivariate analyses indicated that alcohol had less explanatory power than serum insulin for the examined liver tests, especially among women. These results suggest that pathological liver tests in the obese may represent an expression of the metabolic syndrome.
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PMID:Are elevated aminotransferases and decreased bilirubin additional characteristics of the metabolic syndrome? 911 45

A prospective study of 74 consecutive HIV patients (mean age, 34 years) at a public hospital in Mumbai, India, found evidence of hepatitis B and C virus, hepatic tuberculosis, and other liver disease. Clinical evaluation, liver function tests, ultrasonography, radioisotope liver scan, hepatitis B and C virus markers, and liver histology were performed. 34 patients (45%) were classified as chronic alcoholics on the basis of a history of consumption of at least 80 g of alcohol daily for at least 5 years and test findings. 59 (80%) had a history of multiple sex partners or encounters with commercial sex workers. 12 patients (16%) were hepatitis B surface antigen-positive and 22 (30%) were positive for hepatitis C virus antibody. Bilirubin, transaminases, and alkaline phosphatase were elevated in 13%, 13%, and 24%, respectively. Liver cirrhosis was present in 5 patients. Hepatitis B virus was detected in 4 patients and dual hepatitis B and C infection was found in another patient. Finally, 5 patients had liver tuberculosis. The mean absolute lymphocyte count was 2521/cu. mm; only 20 had a count indicative of immunosuppression (2000/cu. mm). These findings confirm that hepatic effects are a major feature of HIV infection in India.
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PMID:Spectrum of liver diseases in HIV infection. 935 1

The increasing availability and use of automatic analysers in clinical chemistry have revealed a number of endogenous interferences. We evaluated the effect of bilirubin, haemolysis and lipaemia on the Falcor-600 analytical system (Menarini Diagnostics) and the Dax-48 (Bayer Diagnostic). We studied the potential endogenous interferences in the measurement of serum glucose, urea, creatinine, cholesterol, triacylglycerols, total bilirubin, total protein, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyltransferase on both analysers; and albumin, direct bilirubin, uric acid, inorganic phosphorus, iron, calcium, magnesium, chloride, sodium, potassium, alkaline phosphatase, amylase, lactate dehydrogenase and creatine kinase on the Dax-48. We followed the guidelines of the Spanish Society of Clinical Biochemistry and Molecular Pathology. Bilirubin samples were prepared using bovine bilirubin, and studied in the concentration range of 20 to 400 mumol/l. For haemolysis, the pool was spiked with a diluted haemolysate of human red cells to achieve a concentration range of 10 to 120 mumol/l of haemoglobin. Lipaemia was studied using samples spiked with Intralipid, a fat emulsion, at concentrations from 1 g/l to 6 g/l (3 to 18 mumol/l of triacylglycerols).
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PMID:Potential interfering substances on Falcor-600 and Dax-48 analytical systems. 936 98

Seven hundred clinical laboratories in all over 27 provinces in Indonesia participated the Indonesian External Quality Assurance Scheme (Program Nasional Pemantapan Kualitas Laboratorium Kesehatan bidang Kimia Klinik). Among those laboratories, the government laboratory account for 288 (41%), and the rest 412 (59%) are private laboratories. Automatic analyzer was used by approximately 22% of the participating laboratories. Seventeen analytes were included in the program: bilirubin, cholesterol, creatinine, glucose, total protein, urea, uric acid, triglycerides, AST, ALT, calcium, albumin, alkaline phosphatase, gamma-GT, sodium, potassium, and chloride. Using WHO scoring system, median overall VIS of 128 was obtained. It means that the all over performance was fairly good . Bilirubin got the best median VIS (33). Sodium (median VIS 177), potassium (162) and chloride (209) got the worst VIS compared to the other parameters.
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PMID:Country report: Clinical chemistry in Indonesia. 1092 52

The hepatoprotective effect of the boiled and non-boiled aqueous extracts of Pistacia lentiscus, Phillyrea latifolia, and Nicotiana glauca, that are alleged to be effective in the treatment of jaundice in Jordanian folk medicine, was evaluated in vivo using carbon tetrachloride (CCl(4)) intoxicated rats as an experimental model. Plant extracts were administrated orally at a dose of 4 ml/kg body weight, containing various amounts of solid matter. Only total serum bilirubin level was reduced by treatment with non-boiled aqueous extract of N. glauca leaves, while the boiled and non-boiled aqueous extracts of the N. glauca flowers were non effective. Bilirubin level and the activity of alkaline phosphatase (ALP) were both reduced upon treatment with boiled aqueous extract of P. latifolia without reducing the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aqueous extract of P. lentiscus (both boiled and non-boiled) showed marked antihepatotoxic activity against CCl(4) by reducing the activity of the three enzymes and the level of bilirubin. The effect of the non-boiled aqueous extract was more pronounced than that of the boiled extract.
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PMID:Evaluation of hepatoprotective effect of Pistacia lentiscus, Phillyrea latifolia and Nicotiana glauca. 1241 19

ALTHOUGH THE LIVERS OF RATS TREATED WITH AGENTS KNOWN TO SUPPRESS BILIRUBIN TRANSPORT APPEARED RELATIVELY NORMAL ON ROUTINE HISTOLOGICAL SECTIONS, CYTOCHEMICAL AND ELECTRON MICROSCOPIC PREPARATIONS REVEALED MARKED CHANGES IN: (a) levels of alkaline phosphatase and apparent ATPase activities of the cell membrane at the sinusoids, bile canaliculi, and between adjacent cells; (b) morphology of the bile canaliculi such as dilatation, fragmentation, vesiculation and reduced numbers of microvilli; (c) the number of lysosomes and their distribution within the cell. Similar changes in the cytochemistry of the liver cell were induced by extrahepatic obstruction.
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PMID:Cytochemical and electron microscopic studies of rat liver with reduced capacity to transport conjugated bilirubin. 1389 61

Here we report on the impact of completely unpurified islet transplantation on the portal vein pressure (PVP) and the hepatic biochemistry in the peritransplant period and on follow-up. Type I diabetic patients underwent simultaneous kidney and islet transplantation. Islets were not purified from the acinar tissue to prevent loss of endocrine mass. Each patient received a mean 521,846 +/- 201,539.4 islet equivalents (7812.1 islet equivalents/kg/recipient). Immunosuppression and peritransplant medication were given according to the Giessen protocol. The islets were injected into the left hepatic lobe through the umbilical vein. PVP was recorded at time 0 and every 5 min throughout cell infusion. Liver function was assessed daily for the first 10 days, and on follow-up. Basal, peak, and final PVP were 12 +/- 3.8, 25.1 +/- 7.9, and 19.5 +/- 6.2 mmHg, respectively (basal vs. final, p < 0.05). Bilirubin, alkaline phosphatase, prothrombin time, and APTT stayed within normal range. Peak aspartate aminotransferase (AST), alanine aminotransferase (ALT), and serum amylase were 109.4 +/- 61.2 IU/L (basal vs. peak, not significant), 79.5 +/- 56.9 IU/L (basal vs. peak, not significant), and 887.5 +/- 153.6 IU/L (basal vs. peak, p = 0.02), respectively. In all cases AST, ALT, and amylase normalized within 6 days posttransplant and remained so on follow-up (longest control, 33 months posttransplant). Although the intrahepatic infusion of unpurified pancreatic islets affects both the portal vein pressure and the hepatic biochemical profile, this effect is transient and does not compromise the safety of the procedure.
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PMID:Effect of the embolization of completely unpurified islets on portal vein pressure and hepatic biochemistry in clinical practice. 1504 Jun 6


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