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)

Choledochal cysts in adults is a rare condition. The present study describes our experience with this abnormality of the biliary tree. During a 16-year period (1978-1993) eight adults with type I choledochal cyst were treated surgically in our departments. They were 4 men and 4 women with a mean age of 38.9 years (range 20-84). Symptoms, clinical findings and abnormalities in laboratory investigations included pain in all patients, history of cholangitis (n = 3), cholangitis (n = 2), acute pancreatitis (n = 1), palpable mass (n = 2), abdominal tenderness (n = 4), leucocytocis (n = 2), and increased levels of serum total bilirubin (n = 4), SGOT (n = 2), and serum alkaline phosphatase (n = 4). Diagnosis was established by intravenous cholangiography in one case, by CT-scanning in one, by ultrasonography in 5 and by intraoperative cholangiography in one. All the patients were treated surgically. Three of them underwent a Roux-en-Y choledochocystojejunostomy and one a choledochocystoduodenostomy. The other 4 patients were treated with cyst excision and Roux-en-Y hepaticojejunostomy. There were no deaths among our patients. The mean follow-up period was 6.7 years (range 1-17). So far, five episodes of mild ascending cholangitis have occurred in the patient treated with choledochocystoduodenostomy. One patient in whom a Roux-en-Y choledochocystojejunostomy was performed had 2 episodes of right upper quadrant colic pain and one episode of cholangitis. Both these patients were treated conservatively. The other 6 patients had no episodes of pain cholangitis or jaundice. In conclusion, the primary treatment of choledochal cyst type I is the excision of the cyst with Roux-en-Y hepaticojejunostomy. The Roux-en-Y choledochocystojejunostomy is indicated in cases where, for various reasons, the cyst can not be safely removed.
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PMID:Long-term results of management of type I choledochal cysts in adults. 907 38

A 1.5-year-old domestic shorthair cat was examined because of vomiting and icterus. Clinicopathologic abnormalities included high alanine transaminase, alkaline phosphatase, and gamma-glutamyltransferase activities and high total bilirubin concentration. During abdominal ultrasonography, the left limb and body of the pancreas appeared hypoechoic, and a small quantity of peritoneal effusion was seen. The liver was diffusely hyperechoic, with echogenicity similar to that of the spleen, indicating hepatic lipidosis. Feline trypsin-like immunoreactivity was high, suggesting that the cat also had pancreatitis. The cat was treated with crystalloid fluids and was fed a protein-restricted diet via a percutaneous endoscopically placed gastrostomy tube. The cat's condition continued to deteriorate despite medical treatment, and it was euthanatized. Necropsy confirmed the clinical suspicion of acute pancreatitis and hepatic lipidosis. This case suggests that measurement of trypsin-like immunoreactivity may be useful in cats suspected of having pancreatitis.
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PMID:High feline trypsin-like immunoreactivity in a cat with pancreatitis and hepatic lipidosis. 929 Aug 12

It's well known that patients was acquired immunodeficiency syndrome (AIDS) can develop various kinds of hepatobiliopancreatic diseases, for causes related to AIDS and for causes not related to HIV infection. The authors describe a case to their attention due to a suspected acute pancreatitis. The patient presented with abdominal pain, increased serum alkaline phosphatase and amylase levels. Serological test and stool concentration didn't show any opportunistic infection (Cytomegalovirus, Cryptosporidium). Abdominal ultrasonography showed enlargement of the head of the pancreas, gallbladder with biliary sludge, and a little dilatation of the biliary tree. The patient didn't feel better despite the medical treatment, so considering the probability of the migration of calculus, the patient underwent cholecystectomy. After the operation the patient felt better quickly. This case confirms the presence in HIV patients of pancreatitis for causes unrelated to AIDS like cholelithiasis as we showed, alcoholism, hypercalcemia, and the importance of an opportune surgical treatment that was resolutive.
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PMID:[Acute pancreatitis and AIDS]. 932 71

Dibutyltin dichloride (DBTC; 6 mg/kg body weight, i.v.) induced acute interstitial pancreatitis in rats. The course of the pancreatitis was examined within 28 days by light and electron microscopy as well as by pathobiochemistry (amylase, lipase, alkaline phosphatase, and bilirubin in serum; tin concentration in biliopancreatic juice, tissue, and concretions). The pathogenesis of the DBTC-induced pancreatitis in rats was studied by different experimental designs (in intact animals, after bile duct ligation, after surgical bypass of the bile duct). DBTC caused toxic necrosis of the biliopancreatic duct epithelium, which is then shed into the duct and forms obstructing plugs in the distal common bile duct. Interstitial pancreatitis occurred during the first 4 days, accompanied by significantly increased activities of serum alpha-amylase and lipase. After 7 days extensive infiltration of the pancreatic interstitium with mononuclear cells was observed. Twenty-eight days after administration of DBTC one-third of the rats showed periductal and interstitial fibrosis as well as an active inflammatory process in the pancreas. The findings suggest a twofold pathogenesis of the DBTC-induced pancreatitis: first, the cytotoxic effects on the biliopancreatic duct epithelium lead to epithelial necrosis with obstruction of the duct, subsequent cholestasis, and interstitial pancreatitis; and second, the hematogenic DBTC effects cause direct injury of pancreatic cells (mitochondrial damage, autophagy, cell necrosis) followed by interstitial edema and inflammation. Both processes lead to this special type of DBTC-induced acute pancreatitis with a tendency to a chronic course, when the obstruction of the duct and cholestasis persist.
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PMID:Acute interstitial pancreatitis in rats induced by dibutyltin dichloride (DBTC): pathogenesis and natural course of lesions. 936 Oct 94

In conclusion, our study showed that serum G.G.T rises in cholestasis, and the rise is significantly higher in extraphepatic cholestasis as compared to intrahepatic cholestasis. Serum G.G.T has not shown any superiority over alkaline phosphatase in the evaluation of cholestatic liver disease. However, two considerations must caution against the use of serum G.G.T. alone for evaluation of hepatobiliary disease. The first of these is the lack of specificity for hepatobiliary disease. Serum G.G.T. activity can be elevated in some non-hepatic disorders such as acute pancreatitis, congestive cardiac failure, myocardial infarction, diabetes mellitus and alcoholism. Determination of serum G.G.T. in these patients is of no value. Second, the possibility that changes in serum G.G.T. activity results from drug administration in man.
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PMID:"Significance of serum gamma glutamyl transpeptidase in cholestatic jaundice". 949 80

Overproduction of tumor necrosis factor (TNF-), interleukin-1beta (IL-1beta), and nitric oxide (NO) is believed to be detrimental during the progression of acute pancreatitis, yet little is known about the hepatic production of these mediators and their role in mediating pancreatitis-induced hepatic dysfunction. Rats were randomized to receive a single intraperitoneal injection of the macrophage-pacifying compound, CNI-1493 (1.0 mg/kg), or vehicle 1 hour before the induction of retrograde bile salt pancreatitis. Sham-operated animals served as controls. Animals were killed 18 hours later, with serum and livers harvested to determine the degree of hepatocellular injury and the induction of TNF-, IL-1beta, and inducible nitric oxide synthase (iNOS). In addition, serum TNF- and nitrites (end-product of NO breakdown) were determined in each group to assess the mechanism of action of CNI-1493. TNF-, IL-1beta, and iNOS gene expression (by reverse-transcription polymerase chain reaction) as well as aspartate transaminase (AST), alanine transaminase (ALT), and lactic dehydrogenase (LDH) (but not alkaline phosphatase [ALP]) increased following the development of pancreatitis (all P < .05). Macrophage pacification significantly prevented the induction of TNF- and IL-1beta mRNA (but not iNOS), resulting in lessened serum AST, ALT, and LDH (all P < .05). Serum TNF- protein and nitrites correlated with gene induction in that both were increased following the onset of pancreatitis, and TNF- protein production was significantly attenuated in animals receiving CNI-1493. Hepatocellular, but not bile duct, injury occurs during experimental pancreatitis that is associated with hepatic TNF-, IL-1beta, and iNOS mRNA gene induction, as well as TNF- protein and nitrite production. Preventing the production of TNF- and IL-1beta by macrophage pacification attenuates the hepatocellular damage, suggesting that these mediators play a role in pancreatitis-induced hepatic injury.
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PMID:Macrophage pacification reduces rodent pancreatitis-induced hepatocellular injury through down-regulation of hepatic tumor necrosis factor alpha and interleukin-1beta. 979 13

There is no golden standard for the diagnosis of acute pancreatitis (AP). The diagnosis is currently based on clinical presentation, measurement of released pancreatic enzymes and imaging studies. Serum/urinary amylase, lipase and trypsinogen-2 dipstick are the most applicable methods in the clinical practice largely because of their simple, rapid, inexpensive and readily available assay methods. In addition to the clinical picture, inflammatory markers (CRP) or contrast enhanced CT can be used to assess the severity of acute pancreatitis. Multifactorial scoring systems (Ranson's prognostic signs, APACHE II, MOF-score) may be too cumbersome for clinical practice. Patient history, determination of AST, bilirubin and alkaline phosphatase levels as well as imaging studies such as ultrasonography and ERCP can be used to distinguish between biliary and non-biliary origin of the disease.
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PMID:Diagnosis of acute pancreatitis. 982 62

A six-year-old, spayed female Shetland sheepdog was presented with acute onset of anorexia and vomiting. An inflammatory leukogram and elevated serum amylase, lipase, alkaline phosphatase, alanine transferase, and triglycerides supported a diagnosis of severe acute pancreatitis. An enlarged, hypoechoic pancreas was visualized on abdominal ultrasonography. The patient clinically responded to medical therapy consisting of nothing per os, total parenteral nutrition, and supportive care. She presented again three weeks later with anorexia and vomiting. A large, anechoic mass was seen in the left limb of the pancreas on ultrasonographic examination of the abdomen. Differentials for this mass included abscess, focal peritonitis, and pancreatic pseudocyst. Clinical signs resolved with supportive care. The mass failed to resolve. Sterile fluid (35 ml) was removed via ultrasonographic-guided centesis 42 days after initial presentation. Ultrasonographic appearance, biochemical analyses, and fluid examination with negative cultures suggested pancreatic pseudocyst. The pseudocyst gradually resolved over the next seven months postcentesis.
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PMID:Resolution of a pancreatic pseudocyst in a dog following percutaneous ultrasonographic-guided drainage. 982 89

In this study we examined the effects of continuous calcium channel blocker (CCB) infusion on pancreatic duct-ligated acute pancreatitis (AP) in rabbits. Thirty rabbits were used for this study. Animals in group 1 (n = 10), which served as a control group, underwent dummy operations and received 0.5 microliter/h normal saline via the internal jugular vein. Animals in group 2 (n = 10) with artificially-induced pancreatitis received the same dosage of saline in the same manner. Animals in group 3 (n = 10) with artificially-induced pancreatitis received 180 micrograms/kg/h CCB (Verapamil) via the jugular vein starting from just before pancreatic duct ligation. AP histology score, plasma amylase levels and liver function tests were measured after 48 h. Verapamil infusion did not prevent the rise in plasma amylase levels, nor did it prevent pancreatic inflammation and damage. Serum levels of serum glutamate pyruvate transaminase, serum glutamate oxalacetate transaminase and alkaline phosphatase were significantly elevated in group 2 and significant reductions were seen in the Verapamil treated animals (group 3). The findings in this study imply that a continuous 180 micrograms/kg/h dose Verapamil infusion does not ameliorate the pathogenesis of pancreatitis induced by ligation of pancreatic duct but do not rule out a dose-dependent protective effect. Meanwhile, the lowering of liver function test scores should be considered the beneficial effect of CCBs, and this should be investigated in further studies.
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PMID:Continuous calcium channel blocker infusion in experimentally induced acute pancreatitis: effects on pancreas and liver function. 987 64

Acute pancreatitis in rats caused by cooling of the pancreas with chloroethyl is characterized by the development of focal necrosis and activation of lipid peroxidation in the liver, activation of blood aminotransferase and acid and alkaline phosphatase, and increase in total and indirect bilirubin concentrations.
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PMID:Liver damages during experimental acute pancreatitis. 1168 43


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