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)

Urinary alkaline phosphatase has been measured and an investigation has been undertaken involving starch gel electrophoresis after treatment of the enzyme with antisera raised against various human tissues. Urine was obtained from patients with bone and liver disease as well as pregnant women and normal persons. The enzyme level in urine in disease and pregnancy was raised above the normal but considerable overlap occurred. After electrophoresis the most usual finding was a single zone of activity although occasionally very minor zones were also present. Antiserum to kidney had the greatest affinity for the urinary enzyme. Decreasing affinity was found with intestinal and placental antiserum. No affinity was found with liver antiserum.
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PMID:Immunological identity of urinary alkaline phosphatase in health and disease. 48 5

Serum bile acid measurements now available by radioimmunoassay have proven to be the most sensitive procedure developed to date to assess diseases of the hepatobiliary system in both adult and pediatric liver disease. Their clinical utility appears to hold particular promise in establishing the early diagnosis of liver disease when conventional liver function test such as SGOT, alkaline phosphatase, bilirubin and albumin are still normal. Serum bile acid determinations have been shown to be particularly useful in the diagnosis of alcoholic liver disease, drug-induced liver disease, viral hepatitis and cholestasis of intra- and extrahepatic origin. In infants, serum bile acid measurements can be used to establish the diagnosis of biliary atresia. When serum bile acids are determined post-prandially, they are the most sensitive indicator of liver dysfunction developed to date.
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PMID:Serum bile acids (a new advance in the diagnosis of liver disease). 49 9

We have selected for this study a well-defined group of patients with moderately advanced but compensated alcoholic cirrhosis. They were well-nourished and had no ascites, varices, azotemia, or encephalopathy. Liver biopsy showed little or no necrosis and inflammation despite wide-spread fibrosis. Serum bilirubin, transaminase, alkaline phosphatase, albumin and globulins were essentially normal. Biochemical evidence for liver disease was restricted to modest elevation of BSP retention, gamma GTP, serum bile acid concentrations, and urinary bile acid excretion. Except for changes in the interrelationships among the three biliary lipids, they were generally spared the abnormalities of sterol metabolism described in other patients with more advanced, more active liver disease. Thus, striking abnormalities in the metabolism of cholesterol and bile acids probably require severe reductions in functioning hepatocellular mass, major portal-systemic shunting, high disease activity, or all three to become manifest.
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PMID:Cholesterol and bile acid metabolism in moderately advanced, stable cirrhosis of the liver. 49 6

The chronic pancreatitis population of Wadsworth VA Hospital over the past five years was screened for two-fold or greater alkaline phosphatase elevation at any time during their course, as a marker for either distal common bile duct stenosis or other hepatobiliary disease. Forty-seven of 207 patients screened met this criterion and are reviewed in detail. Of the 16 patients with persistent alkaline phosphatase elevation (group B), 15 had proven common bile duct stenosis, demonstrating a clear pathophysiologic role of partial bile duct obstruction in their liver disease. Three had developed secondary biliary cirrhosis, marking this entity the commonest cause of secondary biliary cirrhosis at our hospital. Of the remaining 31 patients with transient alkaline phosphatase elevation (group A), only 4 had proven duct abnormalities which may resolve during recovery. Alcoholic liver disease was demonstrated with normal extrahepatic ducts in the remainder in group A adequately studies. Persistent greater than two-fold alkaline phosphatase elevation in pancreatitis thus represents a reliable marker of distal common bile duct stenosis, whose sequelae may include cholangitis and secondary biliary cirrhosis and which requires operative intervention in these cases. When a persistent alkaline phosphatase elevation greater than two-fold is encountered in a chronic pancreatitis patient, adequate cholangiography and liver histology are both necessary to confirm and grade this frequent and treatable complication.
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PMID:Common bile duct stenosis from chronic pancreatitis: a clinical and pathologic spectrum. 51 65

Eighty-eight patients with a non-alcoholic and 105 patients with an alcoholic liver disease were warned against alcohol consumption. On three consecutive ambulatory visits, serum ethanol was measured and compared with patients' admission of alcohol intake. None in the non-alcoholic group had a positive serum ethanol test, whereas 60 samples from 40 patients with alcoholic liver disease were positive. The serum ethanol values were higher in women than in men. Continuation of drinking was unrelated to sex, age, or type of alcoholic liver disease. Twenty-seven of the 40 patients with ethanol in serum denied alcohol consumption. The reliability of the patients was unrelated to sex, age, or type of alcoholic liver disease. Serum ethanol was more valuable than aspartate aminotransferase, alkaline phosphatase, bilirubin, and coagulation factors in pointing out the patients who continued drinking.
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PMID:Serum ethanol estimations in the control of alcohol abstinence in patients with liver disease. 53 8

A systematic prospective survey of 100 outpatients with rheumatoid arthritis revealed that 45 had biochemical evidence of liver disease. In most cases this was due to increases in total serum alkaline phosphatase (ALP) and/or gammaglutamyl transpeptidase (GGT). Examination of serum ALP isoenzyme profiles in 50 of the patients showed that the liver isoenzyme was the sole or major component in 44 patients, including many with normal total ALP levels. 18% had raised serum liver ALP together with raised GGT, suggestive of an underlying hepatobiliary lesion. No correlation could be detected between raised serum levels of liver enzymes and the age or sex of the patient, duration or severity of arthritis, and drug or alcohol history. However, there was a significant correlation between raised serum ALP and lacrimal or salivary gland dysfunction. It is suggested that immunological mechanisms may be involved in the development of hepatic abnormalities in rheumatoid arthritis.
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PMID:Studies on the frequency and pathogenesis of liver involvement in rheumatoid arthritis. 53 42

The authors studied total serum alkaline phosphatase (E.C. 3.1.3.1) activity and its isoenzyme spectrum 1) in relation to the activity of liver diseases, 2) in relation to cholestatic and non-cholestatic liver diseases. The isodistribution of the alkaline phosphatase isoenzymes (the bone, liver and intestinal fraction) in the serum was studied by the heat inactivation and inhibition method and by electrophoretic separation on agar gel. The results showed that alkaline phosphatase had a close diagnostic bearing not only on cholestatic forms of hepatobiliary diseases, but also on the activity of liver disease. The main source of elevated serum alkaline phosphatase activity in the serum of patients with hepatobiliary diseases is the liver isoenzyme. In the serum alkaline phosphatase isoenzymogram, an abnormally large proportion of this isoenzyme is found more frequently than elevation of total alkaline phosphatase activity.
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PMID:The source and clinical significance of alkaline phosphatases in liver diseases. 61 67

Stauffer's syndrome represents a paraneoplastic liver disorder associated with renal cell carcinoma and is characterized by elevation of the serum alkaline phosphatase, increased bromsulphthalein retention, hypalbuminaemia, elevation of alpha-2-globulin and hypoprothrombinaemia, as well as hepatosplenomegaly. Two cases are reported in which this syndrome was the presenting feature and operation was undertaken on the basis of suspected primary biliary tract disease. The aetiology of the typical findings of Stauffer's syndrome are discussed. As they may be the only symptoms of an otherwise occult renal cell carcinoma, their presence should guide the diagnostic efforts in the right direction. Moreover, the possibility of predicting the postoperative course by follow-up control of the liver function tests is stressed.
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PMID:[Stauffer's syndrome. Reversible hepatic dysfunction in renal cell carcinoma (author's transl)]. 63 40

A chemical inhibition procedure suitable for the routine determination of alkaline phosphatase (AP) isoenzymes in serum has been adapted for use with a fast kinetic analyzer, System Olli 3000. The results of this procedure are compared with the electrophoretic separation of alkaline phosphatase isoenzymes. The comparison of the results obtained indicates that the AP-urea/AP ratio can be used to differentiate between patients with bone and liver disease and that it is possible to estimate the relative bone and liver isoenzyme activities from this ratio quickly using two simple equations.
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PMID:Comparison of alkaline phosphatase isoenzymes determined by an inhibition method and by electrophoresis. 64 73

The urinary excretion of D-glucaric acid, a catabolite of glucuronic acid, is considered to be a reliable index of the state of hepatic microsomal enzyme activity. Because enzyme activity may be altered in liver disease, we examined the effect of liver disease on the excretion of this metabolite and its correlation with liver function tests. We studied 89 patients with nonhemolytic jaundice, 39 with viral hepatitis, 33 with obstructive jaundice, six with cirrhosis, and 11 patients with jaundice of mixed etiology. Glucaric acid excretion was significantly increased in all these patients as compared to controls, most pronounced in the obstructive jaundice group. No correlation was found between glucaric acid excretion and concentrations of bilirubin, albumin, globulin, aspartate aminotransferase, alkaline phosphatase, cholesterol, or gamma-glutamyltransferase in serum, even though the concentrations of these analytes did vary with the type of liver disease. We suggest that this increase in glucaric acid excretion is an indication of normal or even increased glucuronidation (UDP-glucuronosyltransferase activity), which occurs in liver disease.
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PMID:Increased D-glucaric acid excretion by jaundiced patients. 69 85


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