Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that the DU-PAN-2 antigen is elevated in approximately 70% of serum samples obtained from pancreatic adenocarcinoma patients, and within the normal range (less than 400 U/ml) in 99% of normal subjects. In this study, the DU-PAN-2 antigen level of the serum and pancreatic ductal fluid in patients with malignant pancreatic disease were compared to antigen levels in patients with benign pancreatic diseases. Six percent of patients with chronic pancreatitis and 13% of patients with severe acute pancreatitis had elevated DU-PAN-2 antigen levels in their sera. Pancreatic ductal fluid DU-PAN-2 levels were elevated in 33% (11 of 33) of patients with pancreatic adenocarcinomas, whereas 16% (5 of 31) of patients with chronic pancreatitis and 38% (8 of 21) of control patients had elevated secretion levels. Unlike DU-PAN-2, the tumor markers carcinoembryonic antigen (CEA) and carcinoma (CA) 19-9 were elevated in 90 and 100%, respectively, of secretions of patients with pancreatic adenocarcinoma. However, CEA and CA 19-9 ductal fluid levels were also elevated in patients with chronic pancreatitis (CEA: 61%; CA 19-9: 85%), and therefore these markers are not helpful in distinguishing benign from malignant pancreatic disease. The physiologic implications of elevated DU-PAN-2 serum antigen levels in patients with normal ductal fluid DU-PAN-2 levels are discussed.
Pancreas 1988
PMID:DU-PAN-2 levels in serum and pancreatic ductal fluids of patients with benign and malignant pancreatic disease. 317 10

The effects of a polyethylene glycol linked oxygen free radical scavenger enzyme, superoxide dismutase (PEG:SOD) on caerulein induced acute pancreatitis (AP) in rats were examined. Pancreas weights and serum amylase concentrations in rats given a three hour continuous intravenous infusion of caerulein (7.5 micrograms/kg/h, n = 18) for induction of AP followed by a three hour infusion of normal saline were significantly raised by approximately 25% (p less than 0.005) and 750% (p less than 0.001), respectively, compared with values obtained in control rats (n = 7) infused for six hours with normal saline alone. A single intraperitoneal injection of either 1 X 10(4) U/kg (n = 6), 2 X 10(4) U/kg (n = 5), or 4 X 10(4) U/kg (n = 5) of PEG:SOD immediately before caerulein infusion did not significantly alter pancreas weights, serum amylase content, or pancreatic histopathology compared with rats given caerulein alone. By contrast, a single intravenous bolus injection of 4 X 10(4) U/kg (n = 9) of PEG:SOD before caerulein treatment significantly reduced serum amylase content by approximately 25% (p less than 0.05) and a continuous six hour intravenous infusion of 4 X 10(4) U/kg/h of PEG:SOD (n = 5) produced significant reductions of approximately 25% (p less than 0.001), 35% (p less than 0.05), and 50% (p less than 0.01) in pancreas weights, serum amylase concentrations, and acinar cell vacuolisation (p less than 0.01), respectively, compared with values in rats given caerulein alone. In studies using bovine serum albumin linked to polyethylene glycol and infused for six hours at protein concentrations identical to high dose PEG:SOD (n = 6), no beneficial effects against caerulein induced AP were observed. These data suggest that (a) oxygen derived free radicals are involved in the early pathogenesis of caerulein induced AP in rats, and (b) the greatly extended circulating half life of polyethylene PEG:SOD ( > 35 hours in rats compared with less than six minutes for native superoxide dismutase) may make this compound more suitable than native superoxide dismutase as a potential therapeutic agent in AP.
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PMID:Evidence for a role of oxygen derived free radicals in the pathogenesis of caerulein induced acute pancreatitis in rats. 320 8

A previously unknown major protein in human pancreatic cytosol has been purified and partly characterized. The protein, designated pancreas specific protein (PASP), has a molecular weight of 44,500 and a pI of 6.9. A two-dimensional gel separation technique revealed the protein to be specific for normal pancreatic tissue. Antibodies against PASP were raised in rabbits and a radioimmunoassay was developed for the quantitation of this protein. The following concentrations of PASP (mg/kg wet weight) were found in human tissues: normal pancreas 100-1,000; pancreatic carcinoma 0.1-20; prostate 0.5-5; and 13 other tissues less than 0.5. The levels of PASP in peripheral serum were less than 0.1 mg/L in normal subjects, 0.7-3 mg/L in cases of acute pancreatitis, and less than 0.1 mg/L in cases of pancreatic carcinoma, prostatic diseases, and other abdominal diseases investigated. The high tissue specificity and the specific elevation of serum PASP levels in acute pancreatitis may indicate a use of this protein as a marker of this pancreatic condition.
Pancreas 1988
PMID:A novel serum assay for pancreatic cellular damage. II. High tissue specificity of a pancreatic protein. 322 47

Real-time ultrasonography (US), computed tomography (CT), and biochemical tests were prospectively performed to detect gallstones in 88 consecutive patients immediately after the onset of an attack of acute pancreatitis. The sensitivity of biochemical tests was 84.6% when the patients had three or more positives of five parameters [including serum bilirubin, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), alanine transaminase (ALT), and alanine transaminase-aspartate transaminase (ALT-AST) ratio]. The sensitivity, specificity, and accuracy were 71.8, 98.0, and 86.4% for US, and 52.9%, 100%, and 79.5% for CT. The sensitivity, specificity, and accuracy were improved to 82.1, 100, and 93.2% by the combination of US and CT, and 94.9, 100, and 97.7% by the combination of US and biochemical tests. Adding CT to the combination of US and biochemical tests resulted in only a slight improvement in sensitivity and accuracy. In conclusion, a combination of US and biochemical tests can provide the best noninvasive method in rapidly detecting gallstones as an etiological factor in acute pancreatitis. Computed tomography is not cost-effective. A positive result of biochemical tests despite a negative finding in US calls for an intensive search for gallstones by further investigation with endoscopic retrograde cholangiography or repeated US examinations.
Pancreas 1988
PMID:Clinical significance of ultrasonography, computed tomography, and biochemical tests in the rapid diagnosis of gallstone-related pancreatitis: a prospective study. 328 69

The serum carbohydrate antigenic determinant (CA 19-9) was assayed in patients with various diseases (87 patients with pancreatic carcinoma, 747 patients with benign diseases, and 547 patients with extrapancreatic malignant growths) and it proved to be particularly sensitive for adenocarcinoma of the pancreas (80 of 87, 92%) as compared to only 14% in the group of patients with benign diseases. Twenty-seven percent of the patients with chronic pancreatitis and 28% of the patients with acute pancreatitis showed elevated CA 19-9 concentrations of more than the upper normal value of 37 U/ml. In 38% and 32% of our cases with carcinoma of the stomach and colorectal carcinoma, respectively, CA 19-9 was estimated as being above the normal range. The preoperatively raised CA 19-9 concentration in patients with pancreatic carcinoma decreases after curative resection of the carcinoma to values within the normal range. However, in no CA 19-9 estimation following a palliative surgical intervention or in cases of inoperable carcinomas a serum concentration of less than 37 U/ml was recorded. In immunohistochemical specimens we found a difference between CA 19-9 antigen concentrations on the cell surface and secretion in pancreatic carcinoma and chronic pancreatitis.
Pancreas 1987
PMID:High sensitivity and specificity of CA 19-9 for pancreatic carcinoma in comparison to chronic pancreatitis. Serological and immunohistochemical findings. 330 67

Five patients with severe acute pancreatitis had a low contrast enhancement (CE) of the pancreas in computed tomography (CT) and underwent subtotal pancreatectomy. Microangiography and histologic studies were performed on the resected pancreases, and the findings were related to those of CE. All patients had histologically documented hemorrhagic/necrotizing pancreatitis. The more disturbed the vascular anatomy in microangiography, the more hemorrhages and necroses were found in histology. The microangiographic and histologic findings corresponded closely to the low contrast-enhanced CT of the diseased pancreas in each patient. Thus, in the early phase of severe acute pancreatitis, one can detect by noninvasive means which areas of the gland are necrotic and which edematous by a dynamic study of contrast-enhanced CT of the pancreas.
Pancreas 1988
PMID:Contrast-enhanced computed tomography and microangiography of the pancreas in acute human hemorrhagic/necrotizing pancreatitis. 336 43

Acute pancreatitis may be complicated by acute lung injury associated with increased lung vascular permeability to plasma protein. The pulmonary accumulation of the plasma protein transferrin, radiolabelled in vivo with indium-113m, was monitored using a portable probe radiation detector in sixteen patients with acute pancreatitis. Plasma protein accumulation (PPA) indices were within normal limits (less than 0.5 X 10(-3)min-1) in all survivors (n = 10) and elevated in all but one of the non-survivors. All non-survivors had severe acute pancreatitis as judged by standard criteria. Thus increased lung vascular permeability was not a constant feature of uncomplicated acute pancreatitis and was only observed in patients with multisystem failure accompanied by clinically evident acute lung injury.
Pancreas 1988
PMID:Lung vascular permeability in patients with acute pancreatitis. 337 28

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.
Pancreas 1988
PMID:Free fatty acids in human pure pancreatic juice. 337 30

Hypocalcemia frequently occurs in acute pancreatitis (AP), but its pathogenesis remains unknown. Since AP is often accompanied by acute alteration in the structure and function of cellular membranes, we investigated whether hypocalcemia associated with AP can be explained by acute translocation of Ca from extracellular to intracellular compartments. AP was induced in dogs by injection of autologous bile into the pancreatic duct, and in rats by controlled infusion of artificial bile containing Na-taurochlorate, Keflin, and trypsin into the cannulated bile duct. Plasma Ca, Mg, amylase, and PTH concentrations were determined in the serial samples. Tissue [Ca] and [Mg] were determined in pancreas, liver, kidney, and abdominal wall muscle biopsies obtained immediately before and 24 h after induction of AP in dogs or 2 h following induction of AP in rats to evaluate the temporal correlation between hypocalcemia and excessive intracellular Ca accumulation in soft tissues. Hypocalcemia (p less than 0.001) and hyperamylasemia (p less than 0.01) occurred within 6 h of AP in dogs, and persisted throughout. Plasma [Mg] was lowered and PTH activity was elevated at 6 and 18 h, and returned to a near normal level by 24 h. Concomitant with persisting hypocalcemia and lower ultrafilterable plasma [Ca2+], tissue [Ca] was significantly elevated in pancreas (71%), liver (24%), and abdominal muscle (112%), but was depleted in kidney by 25%. Pancreas biopsy following AP revealed histological signs of fulminant pancreatitis. [Mg] was depleted only in the pancreas (18%) and remained unaltered in other tissues. No significant changes were noted in the sham-operated animals. The observed temporal correlation between profound hypocalcemia and acute excessive intracellular Ca accumulation in soft tissues strongly suggests that hypocalcemia in AP may be precipitated by leaky-plasma-membrane-mediated excessive intracellular Ca accumulation. Similar data together with significantly reduced cellular energy charge (p less than 0.01) obtained from AP rats provided additional support to our hypothesis.
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PMID:Mechanism of calcium and magnesium translocation in acute pancreatitis: a temporal correlation between hypocalcemia and membrane-mediated excessive intracellular calcium accumulation in soft tissues. 339 93

Acute pancreatitis can be induced experimentally in rats by the retrograde pancreatic duct injection of deoxycholic acid. In order to evaluate if prostaglandins have a protective or therapeutic role, pancreatitis was induced with 0.03, 0.1, or 0.2 ml of 3% deoxycholic acid. Then, 16,16 dimethyl prostaglandin E2 or prostaglandin I2 were infused i.v. for 30 min before the deoxycholic acid injection or for 1 or 24 h beginning 30 min or 1 h after the injection. Deoxycholic acid, 0.1 and 0.2 ml, produced an 80-100% mortality at 24 h after the induction of pancreatitis, and prostaglandin administration had no appreciable effect. Induction of pancreatitis with 0.03 ml deoxycholic acid was associated with a 15% mortality at 24 h, and both prostaglandins significantly increased the mortality. In the experimental model of pancreatitis tested, the administration of exogenous PGI2 and 16,16 dimethyl PGE2 significantly worsened the outcome.
Pancreas 1986
PMID:Prostaglandin E2 and I2 treatment of acute experimental pancreatitis in rats. 355 Jul 89


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