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

Human pure pancreatic juice (PPJ) and serum were analyzed for free fatty acids (FFAs) to study whether the damage to pancreatic cell membranes in pancreatitis is reflected as abnormal FFAs concentration and composition. Patients consisted of 13 normal controls, 7 patients with acute pancreatitis (AP) in remission, and 27 with chronic pancreatitis (CP). PPJ was collected at 2-min intervals after secretin and then cholecystokininpancreozymin stimulation by endoscopic cannulation of the pancreas. The following results were obtained: (a) serum FFAs concentration and composition showed no significant difference between the three groups. (b) FFAs concentration in PPJ was significantly raised in CP through all secretory phases. The rise was significant only in "secretin phase" in AP. In many of the cases with raised FFAs concentration in PPJ, the FFAs composition was similar to that in serum. (c) Arachidonic acid, undetected in normal PPJ, was disproportionately high in concentration and composition in PPJ of eight patients with CP. Two mechanisms were proposed to explain these abnormalities: transudation of serum FFAs into the pancreatic duct and local production of arachidonic acid as a result of the damage to pancreatic cell membranes.
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PMID:Free fatty acids in human pure pancreatic juice. 337 30

Levels of CA 19-9 in the serum and duodenal juice of nine patients with pancreatic adenocarcinoma (PC), ten patients with chronic calcifying pancreatitis (CCP) and ten healthy volunteers (C) were determined by immunoassay. Duodenal juice was obtained by duodenal intubation during the secretin caerulein test. Elevated CA 19-9 levels in the serum were significantly more frequent in PC than in CCP patients, but two PC patients gave levels only slightly above the cut-off value of 37 U/ml. CA 19-9 levels in duodenal juice were significantly higher in PC than in CCP patient, but there was some overlap between them; no overlapping was seen between PC or CCP group and controls. Two PC patients with duodenal juice CA 19-9 levels overlapping those of CCP were the same who showed only a slight rise in serum CA 19-9 levels. The CA 19-9 to total protein ratio in duodenal juice did not permit better discrimination between PC and CCP. We conclude that CA 19-9 assay in duodenal juice can differentiate healthy subjects from patients with pancreatic diseases, but it cannot improve the differential diagnosis between CCP and PC patients with a slight rise of CA 19-9 levels in serum.
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PMID:Value of CA 19-9 assay in serum and duodenal juice in the differential diagnosis of pancreatic disease. 348 62

Large pharmacological doses of ceruletide administered to conscious dogs by intravenous (i.v.) infusion uniformly induce a severe acute necrotizing pancreatitis within 4 h. High-dose i.v. secretin administered for a period of 24 h after cessation of ceruletide infusion resulted in a significant amelioration of the acute pancreatitis compared to non-secretin-treated dogs with acute pancreatitis. Light microscopy of the pancreas in secretin-treated dogs revealed a significant decrease in edema, polymorphonuclear leukocyte infiltration, cell necrosis and acinar cell vacuolization. Serum amylase levels in secretin-treated dogs were significantly decreased compared to non-secretin-treated dogs. The results of this study suggest that high-dose i.v. secretin exerts a beneficial effect on pre-established, ceruletide-induced acute pancreatitis in dogs.
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PMID:Ceruletide-induced acute pancreatitis in the dog and its amelioration by exogenous secretin. 369 75

During clinical withdrawal treatment, a disturbed exocrine pancreas function was found in 28 per cent of 72 alcohol addicts, which occurred in connection with an alcohol-induced pancreatitis. The clinical course was mainly quiescent. Altered bicarbonate concentrations and enzyme dissociations were found as a result of the secretin pancreozymin test. In alcohol addicts, the maximum activity of the amylase output was reached as early as 20 minutes and that of bicarbonate, trypsin and chemotrypsin not until 40 minutes post stimulationem. The sums of the logarithmically transformed 40-minute output of bicarbonate, amylase and trypsin displayed significant differences between the alcohol-addict and control groups. The degree of severity of the disturbed exocrine pancreas function was essentially a function of the daily amount of alcohol taken by the addict and of the age of the patient. The dysfunction was most evident in the 30-to-50-year-old patients. Chronic consumption of alcohol is assumed to give rise to a selective effect on the hydro-kinetic and ecbolic pancreas function.
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PMID:[Relations between disordered exocrine pancreas function, alcohol consumption and age in alcoholics]. 371 63

Pancreas divisum is a congenital variant of pancreatic duct drainage in which the dorsal duct dominates, most likely due to the failure of the two independent pancreatic ductal systems to fuse embryologically. Although 5 to 10 percent of the population have this congenital variation, few demonstrate symptoms related to their pancreaticobiliary ductal systems. However, patients may present with symptoms referable to this system, and the diagnosis is difficult. In this series, endoscopic retrograde cholangiopancreatography with cannulation and radiographic injection of the dorsal duct demonstrated this abnormality in 30 of 32 patients, and results of morphine-prostigmine testing were positive for symptoms, chemical enzyme elevation, or both in three fourths of the patients tested, but other maneuvers were not as helpful. The surgical approach has been to perform a sphincteroplasty of both the main and accessory ampullas and to excise the gallbladder when it is present. Pathologic study of the gallbladders showed nearly all of them to have been diseased, whereas histologic study of the ampullas was not as conclusive. In general, this condition should be suspected as part of the postcholecystectomy syndrome or in patients who present with idiopathic pancreatitis and whose conditions cannot be identified by all other diagnostic methods. Preoperative screening may be carried out with noninvasive techniques such as the morphine-prostigmine test, or by use of the secretin-stimulated ultrasonographic visualization of the ductal system. The primary tool for making the diagnosis is endoscopic retrograde cholangiopancreatography. The goal of surgical treatment should be the opening of the main and accessory ducts, since this offers the best chance for long-term relief of the patient's symptoms.
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PMID:Pancreas divisum: stenosis of the dorsally dominant pancreatic duct. A surgically correctable lesion. 371 5

In a model of acute pancreatitis which requires that pancreatic enzymes leak from a permeable duct, we studied the role of intravenous enterokinase (195,000 daltons) in pancreatic enzyme activation. Anesthetized cats were given intravenous 16,16-dimethyl prostaglandin E2 to increase pancreatic blood flow and microvascular permeability. In some animals the permeability of the pancreatic duct was increased by perfusion of the duct with glycodeoxycholic acid (7.5 mM). Endogenous enzyme secretion was stimulated by IV CCK and secretin. Some cats also received enterokinase intravenously. Those animals that received PGE2, glycodeoxycholate, and enterokinase all developed pancreatitis. When any of these agents were not given the pancreases appeared normal. These findings were consistent with the hypothesis that intravenous enterokinase leaked from small pancreatic blood vessels into the pancreatic parenchyma and/or ducts where activation of pancreatic enzymes occurred. The development of pancreatitis appeared to require an increase in both microvascular and ductal permeability.
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PMID:Pancreatic duct and microvascular permeability to macromolecules. The relation to acute pancreatitis. 385 17

The diagnostic accuracy of the measurement of CA 19-9 in the serum, pure pancreatic juice, and aspirated pancreatic fluid in the diagnosis of pancreatic tumors was assessed in 32 patients with malignant pancreatic tumors and 19 patients with pancreatitis. Pure pancreatic juice was collected from the pancreatic duct by endoscopic cannulation with a duodenofiberscope after intravenous administration of secretin. Pancreatic material was obtained by percutaneous fine-needle aspiration biopsy under ultrasonic guidance. Abnormally high CA 19-9 levels in the serum were significantly more frequent in patients with malignant pancreatic tumors than in those with pancreatitis: they were elevated in 71.9% of the patients with pancreatic tumors. High CA 19-9 levels were found primarily in patients with a tumor of the head of the pancreas, in those with a tumor greater than 3 cm in its greatest diameter, and in those with an unresectable cancer. Only 57.1% of seven patients with a tumor of less than 3 cm in its greatest diameter showed an increase in CA 19-9 level. The CA 19-9 levels in pure pancreatic juice were significantly higher in patients with pancreatic tumors than in patients with pancreatitis without pancreatic stone. However, it was not useful for differentiating pancreatic tumors from pancreatitis with pancreatolithiasis. The CA 19-9 level in pancreatic materials obtained by aspiration biopsy was significantly higher in patients with malignant pancreatic tumors than in those with pancreatitis. Eight patients (80%) with pancreatic tumors had values above 1000 U/ml, whereas all five patients with pancreatitis had values of less than 30 U/ml. Although CA 19-9 levels in pancreatic materials was useful only when cytologic examination did not provide any evidence of malignancy, the combination of the CA 19-9 assay and the cytologic study of specimens obtained by percutaneous fine-needle aspiration biopsy of the pancreas increased the diagnostic rate to 100%.
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PMID:Values of CA 19-9 in the serum, pure pancreatic juice, and aspirated pancreatic material in the diagnosis of malignant pancreatic tumor. 386 91

The oral (PABA) pancreatic function test (PFT), the secretin-pancreozymin test and endoscopic retrograde pancreatography (ERCP) have been carried out in 32 patients with suspected chronic alcohol induced pancreatitis (CAIP) in order to evaluate which, if any, test was most likely to confirm the provisional diagnosis. Thirty one patients had changes of minimal (n = 6) moderate (n = 7) or advanced (n = 18) chronic pancreatitis on pancreatography, whilst one patient had a pancreas divisum. Eight hour urinary PABA excretion was significantly reduced in patients with moderate and advanced structural changes (p less than 0.001) and correlated significantly with all parameters of the PFT, although eight patients with an abnormal pancreatogram and pancreatic function test had a normal PABA value. The PFT was abnormal in 23 patients, but normal in five patients with an abnormal pancreatogram and low PABA value. Most patients with minimal change pancreatitis had a normal PABA test and PFT. We conclude that pancreatography appears to be the most sensitive method for detecting chronic pancreatic damage and for confirming a clinical diagnosis of chronic alcohol induced pancreatitis. Both the PFT and PABA test are useful confirmatory tests and whilst the PFT is slightly more sensitive for assessing pancreatic exocrine function, the PABA test is well tolerated and simple to perform. It may therefore be the complementary investigation of choice for this group of patients.
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PMID:Comparison of the oral (PABA) pancreatic function test, the secretin-pancreozymin test and endoscopic retrograde pancreatography in chronic alcohol induced pancreatitis. 387 66

Ultrasonography can detect changes in pancreatic and bile duct sizes after pancreatic stimulation by secretin or morphine and prostigmine. The effects of the two pharmacologic regimens on pancreatic duct dilatation were comparable and correlated with papillary stenosis determined at surgery, but the morphine and prostigmine combination produced more false-positive responses than did secretin. After administration of intravenous secretin (1 unit/kg), the pancreatic duct dilated in 83 percent of 12 symptomatic patients found at surgery to have a stenotic sphincter of Oddi and in 72 percent of 17 symptomatic patients found to have a stenotic accessory papilla associated with the pancreas divisum anomaly. Comparable dilatation occurred in 14 percent of 14 control subjects without suspected ampullary disease and in none of 10 patients with surgically disproved stenosis (p less than 0.001). The morphine and prostigmine combination produced more false-positive results in both the pancreatic duct and bile duct. Concomitant elevation of the serum amylase level and reproduction of pain were found to be of no discriminatory value. In patients whose pancreatic duct dilated preoperatively during secretin stimulation, dilatation did not occur after surgical sphincteroplasty. A positive test result was associated with a 90 percent success rate in preventing recurrent pancreatitis and ameliorating pain. A negative test result was associated with a 29 percent success rate. Ultrasonography of the pancreatic duct with secretin stimulation may provide objective criteria to supplement clinical judgment in selecting patients for sphincteroplasty to treat stenosis of either the sphincter of Oddi or the accessory papilla in pancreas divisum.
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PMID:Objective evaluation of ampullary stenosis with ultrasonography and pancreatic stimulation. 388 Oct 57

The practical implications of the new Marseilles classification (1984) of pancreatitis are discussed and the present-day diagnostic methods critically reviewed. The new classification distinguishes between two typical long-term profiles, i.e. acute (reversible) and chronic (progressive) pancreatitis. Modern diagnostic tests such as sonography, CT, ERCP and the secretin-CCK test do not provide a "gold standard" for early chronic pancreatitis. Thus, long-term studies of function and morphology are needed to differentiate chronic pancreatitis (progressive dysfunction, calcification, ERP changes) from acute (reversible) pancreatitis. The etiology is a helpful prognostic guide since gallstone pancreatitis virtually never becomes chronic. However, alcoholic "acute" pancreatitis may not always progress to chronic pancreatitis. Drug or surgical treatment of pain is symptomatic and empirical, since the pathomechanisms of pain are poorly understood. A prerequisite for optimum therapy is exact staging of the disease into: uncomplicated early stages with short, self-limiting episodes of pancreatitis: conservative therapy, persistent pain, mainly due to pseudocysts (diagnosis by morphological tests): surgical therapy, advanced painless forms of chronic pancreatitis associated with diabetes and/or steatorrhea: diet and substitution therapy. After successful surgical drainage persistent pain subsides, but postoperative episodic recurrences of pancreatitis are common in the early stages of the disease and in association with continued alcohol intake. However, spontaneous pain relief occurs in all cases in the late stages of the disease and with progressive pancreatic dysfunction (despite continued alcohol abuse).
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PMID:[Diagnosis and therapy of chronic alcoholic pancreatitis. A critical review of the status]. 390 86


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