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

An oral pancreatic function test (PFT) using the synthetic peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid can assess pancreatic exocrine function, since urinary recovery of the ingested dose is an indirect index of chymotryptic activity. We have studied 34 subjects using this oral PFT, which correctly distinguished the control group (8 subjects) from the pancreatitis group (10 patients), results correlating well with Lundh test findings. However, the test was falsely abnormal on 9 out of 16 occasions in patients with bowel or liver disease. We therefore conclude that the present test cannot distinguish small-bowel disease from pancreatic disease, which is often the diagnostic problem, and is also frequently falsely abnormal in the presence of chronic liver disease.
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PMID:The diagnostic value of the oral pancreatic function test. 31 36

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
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PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

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

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.
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PMID:Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis. 60 90

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.
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PMID:Associated liver disease in alcoholic pancreatitis. 68 26

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

The diagnostic yields of intravenous cholangiography (IVC) and 99mTc-diethyl-IDA cholescintigraphy (CS) were compared in 50 patients; 19 had acute cholecystitis, 5 pancreatitis, 4 obstructive disease of the common bile duct, 5 chronic gallbladder disease, 6 parenchymal liver disease and 11 had other intra-abdominal diseases. The comparison of IVC and CS covered three aspects: the definition of the biliary tract structures, their morphologic changes and an assessment of bile flow through the cystic duct and the common bile duct. The definition of the main intrahepatic bile ducts was better with IVC; that of the common bile duct and the gallbladder was better with CS. Morphologic details such as calculi or local changes in duct calibre were detected only in IVC. Measurements of common bile duct calibre obtained from operative cholangiograms correlated better with those from the IVCs than with those from the CSs. CS was more sensitive in the diagnosis of cystic duct obstruction. Bile flow in the common bile duct was estimated in the cases where the gallbladder did not fill. Delayed emptying of the common bile duct was revealed in IVC in 1 and in CS in 3 out of 6 cases with disturbed bile flow. The morphologic findings in IVC gave indication of the obstructive condition in the 1 case with retarded flow and in 2 additional cases. CS provided functional information for which the concentration of the tracer was sufficient except in one case. IVC provided morphologic and functional information, but the excretion of the contrast medium was insufficient for a morphologic assessment of the common bile duct in 16 cases and for a functional assessment in 11 cases.
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PMID:Intravenous cholangiography and cholescintigraphy in the diagnosis of hepatobiliary disease. 73 87

Tests on 100 alcoholic patients revealed increased lipoprotein levels in 24%. Type IV was the most frequently ecountered (80%), followed by type II or V. The average plasma triglyceride level of the alcoholic group was significantly increased in comparison with a control population. The causal mechanism of alcoholic hyperlipoproteinemia remains poorly understood. The combination of a genetic defect of lipid metabolism, nutritional factors and acute alcohol excess may have an essential bearing on the incidence of hyperlipoproteinemia. Acute excessive intake of alcohol was significantly increased in comparison with alcoholic subjects wihtout hyperlipoproteinemia. The critical dose may be a daily ethanol consumption of about 200 gm. There appeared to be no correlation between acute pancreatic injury or active liver disease and serum lipid elevation. On the other hand, the observation was confirmed that alcoholic patients with hepatic cirrhosis usually do not develop hyperlipoproteinemia. Ethanol-induced hyperlipoproteinemia may be a risk factor for the development of atherosclerosis and pancreatitis.
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PMID:[Alcohol-induced hyperlipoproteinemia]. 91 92

Isoenzymes of amylase were studied in serum from 72 persons by means of polyacrylamide gel electrophoresis and a direct saccharogenic assay for amylase activity. In 37 normal individuals, there were two major peaks of amylase actvity with mobilities similar to pancreatic and salivary amylases. In 11 patiets with acute pancreatitis, the area of activity corresponding with pancreatic amylases increased disproportionately. Electrophoretic patterns of amylase activity in normal and pancreatitis urine were almost identical to the respective serum patterns from the same persons. In contrast, a prominent slower-moving peak of amylase activity occurred in the serum of 8 of 12 patients who had hyperamylasemia associated with various liver diseases. Traces of this third peak were identifiable in one-third of normal serum specimens, but no increases in its activity were observed in any specimen from 11 patients with pancreatitis or from 12 other patients with hyperamylasemia unassociated with liver disease. The slower-moving peak was absent from the urine of patients whose serum contained it. The origin of the slower-moving serum amylase appearing in patients with liver disease is not established by these studies. It is possible either that a hepatic amylase is liberated from damaged liver cells or that the metabolism of an amylase not originating in the liver is altered as a result of liver dysfunction.
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PMID:Electrophoretic identification of an isoenzyme of amylase which increases in serum in liver diseases. 125 41

Splenic hematomas are infrequent complications of acute pancreatitis. In some cases, local factors that may play a role in the pathogenesis of the hematoma (thrombosis of the splenic artery or veins, intrasplenic pseudocysts, perisplenic adhesions, enzymatic digestion) are found. In the absence of local factors, the etiology of splenic hemorrhage remains unknown. We report two cases of splenic hematoma occurring during an acute necro-hemorrhagic pancreatitis associated with renal failure that required renal replacement therapy (hemodialysis and continuous arteriovenous hemodialysis). In both cases, more than half of splenic parenchyma was affected by multiple infarctions. No local factors responsible for the splenic abnormalities were detected in either case. Thrombosis of the splenic arterial microcirculation and a coagulation disorder consistent with disseminated intravascular coagulation was detected in one patient. In the second patient, coagulation disorders secondary to either liver disease, pancreatitis and its septic complications, or extracorporeal circuit heparinization for renal replacement therapy were present. Coagulation disorders should be considered whenever a splenic hematoma is found in a patient with acute pancreatitis. Disseminated intravascular coagulation may be the etiology of a splenic hematoma in acute pancreatitis.
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PMID:Splenic hematoma in acute pancreatitis. Role of coagulation disorders. 141 37


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