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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of bilirubin, alkaline phosphatase (AP), and glutamic oxaloacetic transaminase (GOT) were measured during 122 attacks of acute pancreatitis in 114 patients, on the day of admission to hospital and 2 days after admission. Concentrations in 74 attacks associated with gallstones were compared with concentrations in 31 attacks in which no stones were found. 24 attacks were severe by clinical criteria. On the day of admission plasma GOT concentrations of more than 60 IU/l were found in 88% of attacks associated with gallstones, but in no attacks without gallstones. Plasma concentrations of more than 25 mumol/l bilirubin and more than 14 King-Armstrong units AP were found in 62% and 66% respectively, of attacks associated with gallstones, and 5% and 10%, respectively, of attacks without stones. In attacks associated with gallstones plasma concentrations of GOT and bilirubin usually fell over the first 48 h of admission. No correlation was observed between these biochemical values and the severity of the attack. In the absence of a history of excessive alcohol consumption, increases in plasma GOT on the day of admission to hospital suggest that gallstones are responsible for the pancreatitis.
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PMID:Biochemical prediction of gallstones early in an attack of acute pancreatitis. 8 54

The authors report 3 cases and report the diagnostic usefulness of two signs of minor cholestasis described by one of them in 1966. A relative increase, in the absence of obvious virus hepatitis or cirrhosis, of the serum bilirubin, cholesterol, lipids and alkaline phosphatase, together with B.S.P. excretion. suggest minor cholestasis. The sign of "metacritical aggravation" when there is some suspicion of minor cholestasis, the supervision of the course of the disease, or a retrospective inquiry, permit, in the presence of minor symptoms, such as, pain, fever, jaundice, or pruritus, one to make the diagnosis of minor cholestasis. The latter is due either to the presence of small gall stones in the common bile duct, or to inflammation of the ampulla of Vater, or sphincter of Oddi, a Vaterian ampulloma, pancreatitis, or following damage to the common bile duct. In practice, liver biopsy confirms the diagnosis, and intravenous cholangiography, by the perfusion method, is usually able to demonstrate obstruction of the common bile duct.
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PMID:[Relative increase and metacritic aggravation in the diagnosis of anicteric cholestasis]. 16 83

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

Ten episodes of massive transaminase increase with hepatic necrosis were observed in 7 patients after infusion of megluminioglycamide (Biligram). The patients were 3 men and 4 women aged 49 to 65 years with biliary tract disease (n = 1), recurrent pancreatitis (n = 1), hyperlipidaemia and minimal toxic liver damage (n = 1), pyelonephritis (n = 1), , arteriitis (n = 1), and pseudo-LE (n = 1). In 6 patients there was an increase of the alkaline phosphatase without icterus before the investigation and a slight increase of transaminases in 3 patients. After infusion of 100 ml of Biligram in 5 patients and of 200 ml in 2 patients there was an abrupt increase of GPT (98-2202 U/l) with a lesser increase of GOT. The alkaline phosphatase activity remained unchanged. Three patients showed symptoms such as upper abdominal pain, fever erythema, or conjunctivitis. Histologically all patients showed centrolobular necroses. Transaminases should be checked 2 days after intravenous cholangiograms. In patients with a definite increase reexposure should be avoided.
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PMID:[Hepatic necroses after infusion cholangiography (author's transl)]. 63 57

Twenty patients with longstanding alcoholism and biopsy-proven alcoholic liver disease presented with marked elevation of serum alkaline phosphatase (in excess of four times the upper limit of normal). None had a past or present history to suggest pancreatitis or biliary tract disease, nor had any of these patients recently taken medication which could be implicated in cholestatic jaundice. Thirteen (65%) of this group either had radiologic or post mortem confirmation of nonobstructed biliary systems. The histologic findings in this group of patients were compared with those of a group of patients with alcoholic liver disease and normal or only mild elevation of serum alkaline phosphatase. Significantly more hepatocellular necrosis (P less than 0.05), alcoholic hyaline (P less than 0.02), and cholestasis (P less than 0.002) were noted in the severely hyperphosphatasemic group. Minimal degrees of steatosis were found in both groups. These data indicate that intrahepatic cholestasis occurs in patients with alcoholic liver disease, and this may often be secondary to alcoholic hepatitis. Overemphasis has previously been given to alcoholic fatty liver as a cause of this syndrome.
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PMID:Alcoholic liver disease presenting with marked elevation of serum alkaline phosphatase. A combined clinical and pathological study. 73 13

This is a report of our experience with 13 patients who had a distal common duct stricture associated with chronic relapsing pancreatitis. All patients, when first seen, had an elevated alkaline phosphatase level; eight of 13 patients also had an elevated serum bilirubin level. Five of the jaundiced patients had a febrile course; a preoperative diagnosis of acute cholangitis was made in four of these. Eight of the 13 patients have had a choledochoduodenostomy for relief of biliary obstruction; seven of these patients are living and well; one died of continued alcoholism and pancreatitis. One patient had a loop cholecystojejunostomy; decompression was inadequate and death due to septicemia secondary to ascending cholangitis ensued. Four patients have not yet had an operation. Two are symptomatic, but elective operation has been refused. Two have been lost to follow-up. We recommend investigation of the biliary tract in patients known to have chronic relapsing pancreatitis who also have persisting abdominal symptoms and an elevated alkaline phosphatase. If a stricture of the distal common bile duct is identified in the absence of acute pancreatitis, choledochoduodenostomy should be performed.
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PMID:Chronic pancreatitis: a cause of biliary stricture. 88 95

Ten cases of pancreatitis with elevated serum alkaline phosphatase (SAP) levels are reported. Patients with chronic or relapsing pancreatitis may at times develop increased SAP levels, either with or without definitive biochemical evidence of pancreatic disease. SAP estimation may assist in establishing a clinical diagnosis in cases of abdominal pain in which pancreatitis is suspected.
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PMID:Elevated serum alkaline phosphatase level may aid in the diagnosis of pancreatitis. 90 83

Comparison of a group of patients with acute alcoholic pancreatitis with a group with gallstone pancreatitis has established the serum amylase level on admission as one of the most useful laboratory tests in aiding to differentiate the two entities. A serum amylase level greater than 1,500 IU was most often due to gallstone pancreatitis, as was elevation of the serum bilirubin and alkaline phosphatase levels.
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PMID:Diagnostic considerations in acute alcoholic and gallstone pancreatitis. 96 8

This study characterizes a syndrome of partial common bile duct obstruction and marked elevation in serum alkaline phosphatase in 6 male alcoholic patients with calcific pancreatitis. In each patient, a marked elevation in serum alkaline phosphatase was associated with minimal, if any, elevation in serum bilirubin. In all cases, the alkaline phosphatase was hepatic in origin, and intravenous or operative cholangiography showed a dilated common bile duct. Liver biopsy showed canalicular bile stasis in 4 patients and bile duct proliferation in 2 patients. This study demonstrates that calcific pancreatitis may cause partial bile duct obstruction which differentially increases serum alkaline phosphatase without altering bilirubin or bromsulphthalein excretion.
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PMID:Marked alkaline phosphatase elevation with partial common bile duct obstruction due to calcific pancreatitis. 124 86

Marked elevations of serum amylase, unexplained despite extensive evaluation in patients with acquired immunodeficiency syndrome (AIDS), prompted this retrospective review of 85 patients to determine the prevalence of hyperamylasemia and identify any associated demographic and etiologic factors. Of 39 patients who had amylase determinations, 54% had hyperamylasemia (2/3 pancreatic, 1/3 salivary) and 31% had pancreatitis. Biliary tract disease, alcohol intake, and opportunistic infections were similar in hyperamylasemic and normoamylasemic subjects. Non-Caucasian race, intravenous drug abuse, renal dysfunction, alkaline phosphatase elevation, and pentamidine use were more prevalent in patients with hyperamylasemia (p less than 0.001, p less than 0.001, p less than 0.01, p less than 0.05, and p less than 0.05, respectively). However, by stepwise deletion multiple regression analysis, only non-Caucasian race, pentamidine use, and Mycobacterium avium-intracellulare infection were significant, independent predictors of hyperamylasemia (R2 = 0.65). Followed over time, in a historical prospective manner, case fatality rates (66.6% and 61.1%) and median survival times (101 and 84 days) were similar in the hyperamylasemic and normoamylasemic groups. We conclude that, although pancreatitis occurs frequently in AIDS, hyperamylasemia is often of salivary origin and clinical outcome is unaffected. Certain demographic factors are strongly associated with hyperamylasemia in AIDS patients, but multiple, concurrent, etiologic factors are probably operative in these patients.
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PMID:Hyperamylasemia in patients with the acquired immunodeficiency syndrome. 137 38


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