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)

Adult cystic fibrosis (CF) patients are increasingly diagnosed with hepatic cirrhosis, cholecystitis, and cholelithiasis. A continuing diagnostic problem is the early detection of cirrhosis prior to diffuse liver involvement. Sonography has been used in evaluating the pancreas, gallbladder, liver, and spleen in cystic fibrosis patients. We used a real-time mechanical sector scanner to study the portal veins in adult CF patients randomly selected from our CF population and correlated the portal vein diameters with liver function studies. A measurement greater than 12 mm was interpreted as a probable sign of portal hypertension. Of 21 patients studied, 14 had portal veins that measured greater than 12 mm, and 12 patients had (although not necessarily at the time of the exam) elevated serum alkaline phosphatase levels. Three patients had associated splenomegaly and thrombocytopenia, and 10 patients also exhibited cholelithiasis and abnormal gallbladders on sonography. Initial results indicate that portal vein measurement may be a sensitive indicator of early portal hypertension. Sonography may, thus, isolate patients at high risk for possible future complications. Serial sonograms can be performed easily in evaluating the progress of liver disease.
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PMID:Portal vein measurement by ultrasonography in patients with long-standing cystic fibrosis: preliminary observations. 354 Feb 61

Two hundred twenty-eight patients from a total of 466 (49%) receiving renal allografts under cyclosporine/prednisone (CsA/Pred) immunosuppression experienced at least one episode of posttransplant hepatotoxicity. All patients were documented to have normal serum bilirubin, serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), lactic acid dehydrogenase (LDH), and alkaline phosphatase (AP), as well as negative results of biliary ultrasound and upper gastrointestinal contrast examinations prior to transplantation. Hepatotoxic episodes usually were self-limited (82%), and generally occurred during the very early posttransplant period (76%). Liver function abnormalities included hyperbilirubinemia (48% of patients), elevated SGOT (47%), SGPT (73%), LDH (84%), and AP (59%). The CsA serum trough radioimmunoassay (RIA) was relatively high among hepatotoxic patients with a mean value of 225 +/- 17 ng/ml. Pharmacokinetic parameters, including bioavailability and drug clearance, were significantly altered among this group of patients. The management strategy of CsA dose reduction was effective; however, 11 patients (2.4%) developed biliary calculous disease posttransplant while under CsA/Pred immunosuppression. Seven patients had cholelithiasis, and two patients underwent choledochoduodenostomy because of primary choledocholithiasis. The results contrast with 279 renal transplant recipients from an overlapping nonrandomized group treated with azathioprine (Aza)/Pred in whom cholelithiasis was not identified. Pancreatic abnormalities were relatively common, but clinical pancreatic disease occurred in only six patients. There were two episodes of acute pancreatitis, three patients developed pancreatic abscess, and one patient developed a pancreatic pseudocyst. The apparent proclivity of CsA-treated patients to develop biliary calculous disease, and the occurrence of serious pancreatic complications in a small percentage of patients did not affect the majority of CsA-treated patients. They may, however, represent important problems associated with the use of this immunosuppressive agent.
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PMID:Hepatobiliary and pancreatic complications of cyclosporine therapy in 466 renal transplant recipients. 354 20

Estimation of alkaline phosphatase activity is a sensitive and specific test for biliary tract inflammation. The enzyme penetrates into bile from biliary tract epithelium. Activation of the enzyme was noted in cholelithiasis, while the maximal level of alkaline phosphatase activity was detected in patients with chronic cholecystitis. Inflammation of gall bladder may result in deterioration of its epithelium functions, which appears to be responsible for conversion of stable bile colloidal phase into precipitates.
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PMID:[Alkaline phosphatase of the bile as a criterion of biliary tract inflammation]. 376 95

The pre-operative diagnosis of choledocholithiasis, or common bile-duct stones, is important in patients with cholelithiasis. Intraoperative cholangiography or choledochoscopy followed by exploration of the common bile duct could be limited to those patients with stones, if an adequate pre-operative diagnosis could be made. Many clinicians use pre-operative total alkaline phosphatase level alone or in combination with bilirubin level to determine the presence or absence of choledocholithiasis. Predictive value theory was used to analyze data reported by others to assess the value of alkaline phosphatase level alone or in combination with bilirubin level in identifying patients with choledocholithiasis. The authors conclude that alkaline phosphatase level is not useful either alone or in combination with bilirubin level in determining the presence of common bile duct stones in patients with cholelithiasis.
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PMID:Alkaline phosphatase in the assessment of choledocholithiasis before surgery. 390 62

To further clarify the relationship between physical-chemical characteristics of bile acids and biliary lipid secretion, we investigated the effect of ursocholic acid, the 7 beta-hydroxyepimer of cholic acid, on bile lipid secretion and composition. The study included acute duodenal infusion (1 g/h for 5 h) of ursocholic acid contrasted with a less hydrophilic bile acid, ursodeoxycholic acid, in 3 T-tube patients and short-term oral administration (2 wk) of ursocholic acid (10-15 mg/kg X day) to 10 gallstone patients. Following acute infusion, ursocholic acid, similarly to ursodeoxycholic acid, accounted for greater than 80% of the biliary bile acids. However, ursocholic acid induced (per micromole of secreted bile acid) a significantly lower (p less than 0.01) secretion of cholesterol (0.013 mumol) and phospholipids (0.054 mumol) than that induced by ursodeoxycholic acid (0.034 mumol of cholesterol and 0.138 mumol of phospholipids). Biliary alkaline phosphatase activity during ursocholic acid administration was significantly lower (p less than 0.01) than during ursodeoxycholic acid administration. After short-term oral administration, ursocholic acid, undetectable before treatment, constituted 20.50% +/- 8.60% of the biliary bile acids. The percentage of deoxycholic acid increased from 32.35% +/- 18.79% to 47.53% +/- 16.19% (p less than 0.05). Mean saturation index decreased from a pretreatment value of 1.23 +/- 0.22 to 0.99 +/- 0.17 (p less than 0.05), but only in 4 of 10 subjects did bile become undersaturated. It is concluded that ursocholic acid, due to its higher hydrophilicity, stimulates a lower cholesterol and phospholipid output than ursodeoxycholic acid. Consequently, despite the low enrichment of the biliary bile acids with ursocholic acid, oral administration of ursocholic acid induces a reduction of bile cholesterol saturation.
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PMID:Effect of ursocholic acid on bile lipid secretion and composition. 394 16

The development of peritonitis in hospitalized patients, especially those with significant associated illness, can be a difficult and delayed diagnosis. To ascertain the clinical presentation of acute cholecystitis in this group, a retrospective analysis was performed. Over a 10-year period 18 patients were identified who developed either posttraumatic or postoperative acute cholecystitis. The condition occurred in 12 patients admitted for some form of trauma and in six patients after elective surgery. Fever and right upper quadrant pain and tenderness were present in most. These physical findings were generally accompanied by leukocytosis (average = 16,200), hyperbilirubinemia (average = 4.2), and elevated alkaline phosphatase (average = 214). At laparotomy gangrenous cholecystitis was found in the majority, reflecting delayed diagnosis. Eleven patients had acalculous disease, and seven patients calculous cholecystitis. Three patients died, yielding a 17 per cent mortality. The majority with acalculous disease had significant underlying illness. Shock, multiple transfusions, or infection preceded acute cholecystitis in this group. Those with calculous cholecystitis were usually not as ill prior to its development. The morbidity of acute cholecystitis in previously hospitalized patients can be reduced by an awareness of the predisposing factors in those with acalculous disease. Emphasis should be placed on signs and symptoms rather than laboratory values to ensure early diagnosis and treatment of acute cholecystitis in hospitalized patients regardless of the presence or absence of gallstones.
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PMID:Posttraumatic and postoperative acute cholecystitis. 395 69

A 4-year-old cat was examined because of anorexia and lethargy. The cat became icteric within 3 days of admission. Values for aspartate transaminase, alanine transaminase, total bilirubin, alkaline phosphatase, and cholesterol were higher than normal. Radiography revealed hepatomegaly, with loss of detail in the cranioventral portion of the abdomen. Further diagnostic procedures were not permitted, and the cat was euthanatized. At necropsy, cholecystitis, cholangitis, and numerous choleliths were found. Cholelithiasis is a rare cause of obstructive jaundice in the cat.
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PMID:Cholelithiasis in a cat. 397 77

Although, in suitable patients, oral chenodeoxycholic acid (CDCA) dissolves gallstones, the results of recent animal studies suggest that it might be hepatotoxic. Liver function was therefore studied in patients with gallstones before and during treatment with CDCA and liver biopsies were carried out both in patients with cholelithiasis given bile acid therapy and in those who had been given no medical treatment. In 25 patients treated with 0.5-1.5 g CDCA/day (7-20 mg kg body weight(-1) day(-1)) there was no significant change in serum bilirubin, albumin, globulin, transaminase, isocitric dehydrogenase, alkaline phosphatase, and gamma glutamyl transpeptidase levels before and at monthly intervals during six months' treatment. The kinetics of bromsulphthalein (BSP) clearance and its apparent transport maximum were not significantly changed during CDCA therapy. The mean fasting serum bile acid concentrations of 18.0 +/- SEM 1.2 mumoles/litre before and 20.0 +/- 3.5 mumoles/litre during treatment were both significantly greater than control values. Liver histology was not appreciably different in 11 patients treated with CDCA from that in eight patients with untreated cholelithiasis and in three patients who had received CDCA three to four months before biopsy. These results suggest that in doses of 0.5 to 1.5 g/day CDCA is not hepatotoxic in man.
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PMID:Liver structure and function in cholelithiasis: effect of chenodeoxycholic acid. 415 91

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the enzyme catalyzing the rate-limiting step in cholesterol biosynthesis, exists in one active (dephosphorylated) and one inactive (phosphorylated) form in liver microsomes obtained from several animal species. The present study was undertaken in order to determine a) whether the human enzyme also exists in active and inactive readily interconvertible forms; b) whether the large inter-individual variation in HMG-CoA reductase activity observed in normal man can be explained by variations in the activation state of the enzyme; and c) to characterize the reactivity of antibodies raised against rat liver HMG-CoA reductase with the intact human microsomal enzyme. HMG-CoA reductase activity, assayed in microsomes prepared in the presence of 50 mM NaF, was only 17 +/- 3% of the activity observed in microsomes prepared from the same liver in the absence of fluoride. Preincubation of microsomes prepared in NaF with alkaline phosphatase resulted in a tenfold increase of enzyme activity, while the activity of microsomes prepared without fluoride was increased also (by about 45%) with this treatment. On the other hand, the activated enzyme could be inactivated by incubation of microsomes with Mg-ATP. In eleven normal weight, normolipidemic gallstone patients, the HMG-CoA reductase activity determined in microsomes prepared without NaF ("standard procedure") reflected well both the "expressed" activity (in microsomes prepared with NaF) and the "total" (fully activated) enzyme activity; correlation coefficients were +0.80 and +0.84, respectively. Preincubation of human liver microsomes with rabbit antiserum against partially purified HMG-CoA reductase from rat liver resulted in a 72 +/- 6% inhibition of enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:3-hydroxy-3-methylglutaryl coenzyme A reductase in human liver microsomes: active and inactive forms and cross-reactivity with antibody against rat liver enzyme. 608 40

According to current concepts, soluble phosphatidic-acid phosphatase, converting phosphatidic acid into a diglyceride, is a rate-limiting enzyme in the hepatic biosynthesis of triglycerides. The present paper is the first report on this enzyme in human liver. The enzyme activity was assayed in ammonium sulphate precipitates of cytosol obtained from human liver biopsies. The activity was stimulated by preincubation with alkaline phosphatase and inhibited by Mg-ATP, suggesting that phosphorylation-dephosphorylation may be of some importance for the expression of the activity of the enzyme. When assayed under optimal conditions, the activity obtained in liver biopsies from normal-weight gallstone patients averaged 12.8 +/- 2.0 nmol min-1 (mg protein)-1 (mean +/- SEM) (n = 17). The enzyme activity was slightly higher in liver biopsies from morbidly obese subjects 16.4 +/- 2.8 nmol min-1 (mg protein)-1 (n = 14). The difference between the two groups of subjects was probably in part sex-dependent and was not statistically significant. A similar small and insignificant difference between the two groups of subjects was found when the enzyme activity was assayed in the maximally stimulated state--i.e. after incubation with alkaline phosphate. These findings suggest that an increased capacity of the soluble phosphatidic-acid phosphatase is not of major importance for the increased triglyceride synthesis known to occur in obesity. Other factors (i.e. availability of substrate and cofactors) may be of greater importance.
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PMID:Triglyceride metabolism in human liver: studies on hepatic phosphatidic-acid phosphatase in obese and non-obese subjects. 608 51


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