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)

Pancreatic juice gamma-glutamyltransferase (GGT, EC 2.3.2.2) has been proposed as a marker of pancreatic disease. We have collected pancreatic juice endoscopically from 24 control patients and 43 patients with a variety of hepatic, pancreatic, and biliary disorders. Pancreatic juice GGT, alanine transaminase (ALT, EC 2.6.1.2), and alkaline phosphatase (ALP, EC 3.1.3.1) were measured and found to be present in all samples. GGT was significantly higher in patients with pancreatic cancer (range 21-1175 IU/liter, P less than 0.005) compared with controls (range 2-52 IU/liter). Of 17 patients with pancreatic juice GGT concentrations greater than 52 IU/liter, eleven had definite pancreatic disease (seven pancreatic cancer, four chronic pancreatitis) and, in the remaining six, pancreatitis was possible although not proven. Pancreatic juice ALT and ALP provided no useful diagnostic criteria. GGT in pancreatic juice seems to be a nonspecific marker of pancreatic disease and merits further study.
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PMID:Pancreatic juice gamma-glutamyltransferase, alanine transaminase, and alkaline phosphatase in pancreatic disease. 610 99

Common bile duct (CBD) strictures associated with chronic pancreatitis may cause significant hepatobiliary disease. Nine patients with chronic alcohol-related pancreatitis and CBD obstruction requiring operative biliary or pancreatobiliary decompression are reported. Alkaline phosphatase was the most specific biochemical indicator of cholestasis. Abnormal CBD anatomy was delinated accurately in 89 per cent of cases with percutaneous transhepatic cholangiography (PTC) and endoscopic retrograde cholangiopancreatography (ERCP). All strictures were localized to the intrapancreatic portion of the distal CBD. Pancreatic pseudocysts (PPC) were identified in six (67%) cases. All nine patients underwent biliary decompression. Simultaneous PPC drainage or pancreatic duct decompression (Peustow procedure) was performed in eight cases (89%). No perioperative mortality occurred, and all patients reported subjective improvement in symptoms. Biliary tract strictures sufficient to cause clinical or biochemical cholestasis are a poorly recognized complication of chronic pancreatitis. Cholangiography (PTC or ERCP) should be obtained in order to delineate radiographic features, and extent and severity of the biliary stricture because there is no predictable correlation between levels of serum alkaline phosphatase and liver histopathology. A percutaneous biopsy is requisite to document changes in hepatic morphology. In order to prevent potential hepatobiliary complications such as cholangitis and secondary biliary cirrhosis, biliary strictures should be managed surgically even in anicteric and otherwise asymptomatic patients. Simultaneous treatment of associated pancreatic pathology can be performed if necessary with little added morbidity.
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PMID:Common bile duct strictures associated with chronic pancreatitis. 661 52

Fifty-one patients with chronic pancreatitis manifested distal common duct obstruction from fibrosis of pancreatitis. The cause of the pancreatitis was alcohol in most patients. An elevated serum alkaline phosphatase level was the most frequent abnormal laboratory finding. The serum bilirubin level elevation was never progressive; a rising and falling pattern was most often encountered. Percutaneous transhepatic cholangiography and endoscopic retrograde cholangiopancreatography are the most useful diagnostic tests. An operation was performed on 47 patients and included choledochoduodenostomy in 16 patients, choledochojejunostomy in 19 patients, cholecystenteric anastomosis in seven patients, common bile duct exploration with T-tube drainage in three patients, and sphincteroplasty in two patients. Abdominal pain was lessened after operation in 40 of 44 patients who survived surgery. Two patients with T-tube drainage and two with cholecystenteric anastomosis required conversion operations to choledochoduodenostomies. Identification of associated pancreatic duct obstruction and dilatation, pseudocysts, and duodenal obstruction is important.
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PMID:The spectrum of biliary tract obstruction from chronic pancreatitis. 671 75

Fibrosis of chronic pancreatitis can cause obstructive jaundice by compressing the intrapancreatic portion of the common bile duct. The frequency and clinical manifestations of common bile duct stricture from symptomatic chronic pancreatitis have been evaluated in 26 patients undergoing lateral pancreaticojejunostomy for intractable pain between 1974 and 1980. Four patients (15%) had a stricture with partial obstruction of the common duct in addition to pancreatic duct obstruction. Three of the four strictures were identified prior to operation by ERCP. The fourth developed biliary obstruction six months after pancreaticojejunostomy. Slight elevation of alkaline phosphatase was common and occurred in 12 of 22 patients with chronic pancreatitis without biliary obstruction. Alkaline phosphatase was elevated greater than four times normal in three of the four patients with a biliary stricture. Elevation of total and direct serum bilirubin occurred only in patients with stricture of the distal common duct. A waxing and waning picture of jaundice was seen in these four patients. When a fixed smooth stricture of the common duct is demonstrated in a patient with symptomatic chronic pancreatitis, drainage of the biliary tree should be combined with pancreatic duct drainage in order to prevent cholangitis, biliary cirrhosis, diagnostic confusion with pancreatic carcinoma, and persistence of pain.
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PMID:common duct obstruction in patients with intractable pain of chronic pancreatitis. 711 5

The liver histopathology in 40 liver biopsies from 24 patients with verified chronic common bile duct stenosis due to chronic alcoholic pancreatitis has been reviewed code-blinded. This represents an 8% prevalence of this complication in approximately 300 patients with alcoholic pancreatitis screened biochemically for alkaline phosphatase greater than two-fold for less than 1 month. The majority were anicteric with no symptoms other than from acute exacerbations of chronic pancreatitis. Biliary obstructive liver histopathology of varying severity was diagnosed in 19 patients (79%), seven of whom (29%) had secondary biliary cirrhosis. In 3 of these 7 cases, progression to biliary cirrhosis was documented with sequential biopsies. The remainder demonstrated this histologic picture when first diagnosed, supporting this insidious nature of this process. Stromal edema of the portal tracts, increased portal connective tissue, and marked proliferation of interlobular bile ducts and ductules were the most striking histologic features. Histologic cholangitis, although frequent, was generally mild or absent, reflecting the incomplete nature of the duct obstruction. Features of alcoholic liver disease were observed in only two cases. The results indicate that (1) chronic alcoholic pancreatitis with incomplete duct obstruction frequently causes secondary biliary cirrhosis, (2) significant alcoholic liver disease very infrequently coexists with persistent common bile duct stricture from alcoholic pancreatitis, and (3) surgical biliary decompression should be considered in any patient with documented persistent common bile duct stenosis from alcoholic pancreatitis.
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PMID:Liver histopathology in chronic common bile duct stenosis due to chronic alcoholic pancreatitis. 728 90

Common bile duct stricture secondary to chronic pancreatitis is difficult to detect clinically. Surgical bypass is necessary if complications from biliary obstruction develop. In 21 patients operated on between 1968 and 1979, the earliest typical biochemical finding was a persistently elevated serum alkaline phosphatase level. The SGOT level was minimally elevated in seven patients, but did not correlate with changes in the stricture. An increased bilirubin level was noted either during an acute exacerbation of pancreatitis or late in the course of the stricture development, when obstruction was almost complete. Operative cholangiograms taken in 12 of these patients and transhepatic cholangiograms taken in nine demonstrated a stricture of the intrapancreatic bile duct more than 2 cm long. Operations were performed for treatment of obstructive jaundice (11), ascending cholangitis (three), suspected pancreatic cancer (three), and progressive biliary cirrhosis (two). Sphincteroplasty, initially attempted in four patients, uniformly failed to relieve the obstruction due to the length of strictured duct. Satisfactory drainage was obtained for up to ten years with choledochoduodenostomy (12), choledochojejunostomy (three), and cholecystojejunostomy (six).
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PMID:Common duct stricture from chronic pancreatitis. 737 60

In the course of alcoholic chronic pancreatitis, increased serum alkaline phosphatase level is usually caused by common bile duct stenosis but may also be due to alcoholic liver disease. The aims of this prospective study were to investigate whether clinical, biochemical and radiological factors could predict liver histopathological appearance. The study comprised 48 patients with chronic alcoholic pancreatitis, common bile duct stenosis and increased serum alkaline phosphatase levels; clinical, biochemical, radiological and histological data were recorded in all cases. Liver biopsy examination (surgical [n = 45] or intercostal [n = 3]) showed (a) biliary obstructive liver abnormalities (n = 33), which were severe in 20 cases (biliary fibrosis in 15, secondary biliary cirrhosis in 3, secondary sclerosing cholangitis in 2) and moderate in 13 cases; (b) alcoholic liver disease in 9; and (c) normal liver in 6. Clinical, biochemical and radiological data were not statistically different between patients with biliary obstructive liver disease and those with alcoholic liver disease. Forty-five patients underwent surgery; two patients with alcoholic hepatitis died after surgery, at the beginning of this study. We conclude that in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase levels, clinical, biochemical and radiological data cannot be used to predict the type of liver lesions. Therefore liver biopsy is warranted to identify (a) alcoholic hepatitis, which increases operative risk; and (b) biliary obstructive liver disease, frequent and often severe, in which surgical biliary decompression should be considered.
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PMID:Factors predictive of liver histopathological appearance in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase. 822 11

Very late activation (VLA) receptors mediate cell adhesion to extracellular matrix, mainly by acting as adhesion receptors to fibronectin, collagen, and laminin as well as to other cells. These interactions not only regulate normal cell-extracellular matrix contact, but also are thought to be involved in metastasis and invasive tumor growth. Using immunohistochemistry [the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique] we compared the expression and distribution of VLA receptors in normal pancreatic tissue, chronic pancreatitis, and ductal pancreatic adenocarcinoma. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, whereas centroacinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Similarly, pancreatic carcinoma showed an intensive staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak and lost in about 50% of the cells. As our results suggest, cell-basement membrane interaction in ductal and acinar pancreatic cells is primarily mediated through VLA alpha 2 and VLA alpha 6, whereas VLA alpha 3 and VLA alpha 5 are the major VLA receptors on centroacinar cells. In pancreatic carcinoma a loss (VLA alpha 5) or redistribution (VLA alpha 2, VLA alpha 6) of VLAs was observed. This redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to randomly interact with extracellular matrix structures during invasion and metastasis.
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PMID:Expression and distribution of VLA receptors in the pancreas: an immunohistochemical study. 825 85

The aim of this study was to examine bone mineral density (BMD) and bone metabolism in patients with chronic pancreatitis to determine if increased severity of the disease would correlate with increased bone loss. Between October 1999 and September 2000, we investigated 42 patients with an average age of approximately 53 years suffering from chronic pancreatitis, as well as 20 healthy male controls with an average age of 49 years. Dual energy x-ray absorptiometry (DEXA) was performed on patients and controls, and serum levels of parathyroid hormone (PTH), osteocalcin (OC), carboxy-terminal propeptide of type I procollagen (CICP), bone-specific alkaline phosphatase (BAP), 1,25(OH)(2) vitamin D(3) and 25(OH) vitamin D(3), as well as fecal elastase 1 were also determined. The severity of chronic pancreatitis in patients was determined via endoscopic retrograde cholangiopancreatography (ERCP) and assigned to 1 of 3 grades based on the Cambridge classification. BMD of patients with chronic pancreatitis was markedly decreased compared to controls (means in patients: DEXA lumbar vertebra anterior/posterior (LV ap) 96.8% +/- 4.2%, DEXA Ward's triangle (WARD) 92.2% +/- 5.2%; controls: DEXA LV ap 98.7% +/- 3.7%, DEXA WARD 97.1% +/- 3.1%; P <.05 and P <.0001) and correlated with the various Cambridge-grades (DEXA LV ap and DEXA WARD, P <.01). Fecal elastase 1 showed sensitivities of 14%, 87%, and 95% for the Cambridge-grades I, II, and III, respectively, and correlated with this classification of severity of chronic pancreatitis (P <.01). Furthermore, fecal elastase 1 of patients correlated the same way with both D(3)-vitamins (P <.01), as well as with parameters of BMD (P <.01). If fecal elastase 1 in patients was below 200 micro g/g, then the BMD and vitamin D(3) values were also significantly decreased compared to those with fecal elastase 1 above 200 micro g/g. In patients with Cambridge grades II and III 1,25(OH)(2)D(3) was markedly decreased (26.7 +/- 7.7 pg/mL and 27.6 +/- 9.0 pg/mL) compared to those with Cambridge grade I (38.0 +/- 10.5 pg/mL; between I and II, P =.027; between I and III, P =.033). 25(OH)D(3) was not significantly different within the various Cambridge groups (P =.07). Compared to controls, both D(3) vitamins, as well as fecal elastase 1, were extremely low (means in patients: fecal elastase 1, 140.7 +/- 75.7 micro g/g; 1,25(OH)(2)D(3), 29.9 +/- 9.5 pg/mL; 25(OH)D(3), 26.7 +/- 9.7 nmol/L; controls: fecal elastase 1, 694.9 +/- 138.6 micro g/g; 1,25(OH)(2)D(3), 67.5 +/- 4.3 pg/mL; 25(OH)D(3), 69.5 +/- 13.5 nmol/L). A significant correlation was observed between increased severity of chronic pancreatitis based on both endoscopic retrograde cholangiopancreatography and levels of fecal elastase 1, with decreased circulating levels of vitmain D(3) and decreased BMD. This supports a connection between the inflammatory destruction of the pancreas (Cambridge classification), exocrine pancreatic insufficiency (fecal elastase 1), altered levels of vitamin D metabolites, and loss of skeletal mass.
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PMID:Alterations of bone mineral density and bone metabolism in patients with various grades of chronic pancreatitis. 1275 87

Biliary stricture and duodenal obstruction have been increasingly recognized as complications of chronic pancreatitis. The anatomical relationship of the distal common bile duct and the duodenum with the head of the pancreas is the main factor for their involvement in chronic pancreatitis. In hospitalized patients with pancreatitis, the incidence of biliary stricture and duodenal obstruction is reported to be about 6% and 1.2%, respectively. For patients requiring an operation for chronic pancreatitis the incidence increases to 35% for biliary stricture and 12% for duodenal obstruction. Fibrosis around the distal common bile duct can cause stenosis with obstruction of bile flow. Clinically, the presentation of these patients ranges from being asymptomatic with elevated alkaline phosphatase or bilirubin, or both, to being septic with cholangitis. Jaundice, cholangitis, hyperbilirubinemia, and persistent elevation of serum alkaline phosphatase occur more frequently in patients with pancreatitis with a biliary stricture. A twofold elevation of alkaline phosphatase is a marker of possible common duct stenosis in patients with chronic pancreatitis. The incidence of both biliary cirrhosis and cholangitis in these patients is about 10%. ERCP reveals a characteristic long, smoothly tapered stricture of the intrapancreatic common bile duct. In duodenal obstruction, the factors that convert self-limiting edema to chronic fibrosis and stricture formation are unknown, but ischemia superimposed on inflammation may be the major cause. These patients present with a prolonged history of nausea and vomiting. Barium studies typically show a long constricting lesion of the duodenum, and endoscopy reveals reactive inflammatory changes in a narrowed duodenum. Operation is indicated in patients with common bile duct strictures secondary to chronic pancreatitis when there is evidence of cholangitis, biliary cirrhosis, common duct stones, progression of stricture, elevation of alkaline phophatase and/or bilirubin for over a month, and an inability to rule out cancer. The operation of choice is either choledochoduodenostomy or choledochojejunostomy. A cholecystoenterostomy is less favored because of its higher failure rate (23%). Endoscopic stenting plays a role in patients who are unfit for surgery, but it is not recommended as definitive therapy. For duodenal obstruction, failure to resolve the obstruction with 1-2 weeks of conservative therapy is an indication for bypass. The operation of choice is a gastrojejunostomy. Not uncommonly, combined obstruction of the pancreatic duct, common bile duct, and duodenum will develop. Combined drainage procedures or resection are used to manage these problems.
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PMID:Management of biliary and duodenal complications of chronic pancreatitis. 1453 24


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