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

The pathogenesis of endoscopic retrograde cholangiopancreatography (ERCP)-induced pancreatitis is poorly understood. To elucidate a role for pancreatic enzymes in ERCP-induced pancreatitis, we measured serum amylase, lipase, trypsin, and elastase in 25 patients undergoing ERCP. Serum alpha 1-antitrypsin and alpha 2-macroglobulin, two major pancreatic protease inhibitors, also were measured. All pancreatic enzymes measured rose significantly after ERCP. Pancreatic duct cannulation was associated with a greater elevation in serum amylase and lipase. Circulating alpha 2-macroglobulin was reduced by 7% (p = 0.04) 6 h after ERCP, whereas circulating alpha 1-antitrypsin increased over the same time period. Papillotomy, stent placement, or underlying disease did not influence changes any further. Three patients developed ERCP-induced pancreatitis. All three patients had circulating alpha 2-macroglobulin levels below 243 mg/dl (p = 0.03). The ERCP-induced alterations in circulating pancreatic enzymes and their inhibitors are similar to changes seen in clinical pancreatitis. Low circulating alpha 2-macroglobulin levels may predispose to ERCP-induced pancreatitis.
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PMID:The effect of ERCP on circulating pancreatic enzymes and pancreatic protease inhibitors. 171 6

From a computerized database comprising 28 pertinent items in each of a consecutive series of 664 patients with cholelithiasis, differences were studied between men and women. In 52 patients there was a documented attack of acute pancreatitis (7.8%). Twenty-five of 174 men had pancreatitis, compared with 27 of 490 women (p less than 0.0001). Men developed gallstones later in life than women, but suffered gallstone pancreatitis earlier in life and in the course of their gallstone-related disease. A history of flatulent dyspepsia, chronic cholecystitis, and biliary colic was less common in men than in women with pancreatitis (p less than 0.0001). Men with pancreatitis had fewer stones in their gallbladders than did women (p = 0.0002). The cystic duct and the common bile duct in the pancreatitic patient were more likely to be dilated (p less than 0.0001). In the nonpancreatic group, these ducts were larger in men. Pancreatic duct reflux on operative cholangiography was more common both in patients with pancreatitis 62% cf 14% (p less than 0.0001), and in men (p less than 0.001). Predisposition to pancreatitis relates to duct size rather than stone size per se. Men are more susceptible to gallstone migration at an early stage of their disease. In addition they have a larger diameter duct system and possibly a different anatomic disposition of the sphincter of Oddi, which predisposes them to a higher incidence of pancreatitis than women. The data suggest that it is cystic duct size that is critical in the pathogenesis of gallstone pancreatitis.
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PMID:Sex differences in gallstone pancreatitis. 144 54

The pathologic changes associated with human cryptosporidiosis have not been well characterized. In this report, 15 cases of cryptosporidiosis in acquired immunodeficiency syndrome patients are described. Organisms were found in autopsy tissue specimens in 13 cases, and only in antemortem stool samples in two. Gastrointestinal/hepatobiliary distribution of organisms was as follows: small intestine (13 cases), extrahepatic bile ducts (eight), intrahepatic bile ducts (seven), large intestine (six), pancreas (five), stomach (three), and esophagus (one). At all sites, infection was usually associated with nonspecific reactive epithelial changes, architectural abnormalities such as villous flattening in the small intestine, and interstitial edema with mixed inflammatory cell infiltrates. Presence of organisms and associated mucosal injury were patchy and of variable severity in the intestine. In the biliary tract, injury was commonly diffuse and severe. Pancreatic duct injury was generally mild and often limited to hyperplastic squamous metaplasia. In late-stage acquired immunodeficiency syndrome patients with cryptosporidiosis, widespread infection in the gastrointestinal and biliary systems by this coccidian was more common and severe than previously suggested. Although the mechanisms have yet to be determined, infection usually is accompanied by pathologic changes that may be causally related to pathophysiologic abnormalities, such as diarrhea and malabsorption, and may account for other clinical manifestations of pancreatitis, cholangitis, and obstructive cholestasis.
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PMID:Cryptosporidiosis in the acquired immunodeficiency syndrome: a study of 15 autopsy cases. 174 28

Increasing surgical experience with the immediate consequences of pancreatic injuries has resulted from parallel growth in the volume of motor vehicle accidents and societal violence. However, few surgeons are aware that complications may be considerably delayed following pancreatic trauma, occurring in some cases months to years after apparent recovery from the original injury. In four patients with blunt pancreatic trauma initially treated by non-operative means, stricture of the main pancreatic duct developed over a period of months as a result of progressive fibrosis at the site of ductal injury. Pancreatic duct hypertension was demonstrated to be present in the obstructed duct, and secondary changes of chronic pancreatitis developed in the obstructed segment of the gland ("upstream" chronic pancreatitis). Seven similar patients with delayed onset of chronic obstructive pancreatitis after pancreatic trauma were found in the literature. Symptoms related to these acquired ductal strictures are most commonly those of abdominal pain and recurrent episodes of acute pancreatitis. Recognition of post-traumatic chronic obstructive pancreatitis principally involves awareness that injuries to the pancreatic duct can produce remote complications. Pancreatoenteric drainage, or resection of the obstructed segment of pancreas, provides prompt and effective relief.
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PMID:Chronic obstructive pancreatitis as a delayed complication of pancreatic trauma. 177 10

Chronic "idiopathic" pancreatitis (CP) in a 7 year-old-boy, whose father has suffered from CP, and whose former grandfather had suffered from pains possibly of pancreatic origin, led us suspect a hereditary etiology. An analysis, extended in a control fashion to the relatives of the healthy spouse of the affected grandfather, surprisingly revealed 2 more proven and 3 more suspected CP, giving the overall number of 8 affected members in this 35-member 3 generation kindred and revealed a maternal heredity instead of paternal heredity (which was first thought to be apparent). We therefore recommend that in a family suspected to suffer from hereditary CP (HCP), a screening should be extended to cover even the unaffected spouse's family--the present extended study revealed for 23 new members them to belong in an affected family. Without an extensive screening advises for family planning, alcohol consumption etc. can not be given. Plain abdominal X-ray accompanied with epigastric ultrasonographic are suitable for screening, which might be extended to every individual in smaller families, but may be safely restricted to the members ever suffered from epigastric pains in the case of a huge family. Pancreatic duct anomalies, hyperlipidaemia, hypercalcaemia, aminoaciduria or hyperimmunoglobulinaemia, all of which have been seen to accompany HCP, were not present in this family. Neither was any linkage found between the penetrance of HCP and ABO/Rh blood groups or HLA haplotypes.
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PMID:Screening a family for hereditary chronic pancreatitis. 226 97

Chronic pancreatitis is associated with glucose intolerance and resultant pancreatogenic diabetes. Using the canine pancreatic duct-ligated model of pancreatitis, we serially evaluated pancreatic histology and electron microscopy, tolerance to intravenous and oral glucose, and insulin response to glucose loading. Pancreatic duct ligation caused microscopic evidence of acute pancreatitis at 1 week, progressing to acinar loss and fibrosis consistent with chronic pancreatitis at time periods up to 6 months. The islets of Langerhans showed degranulation early and appeared to be structurally preserved late. Calculated K values indicated a progressive significant deterioration in intravenous glucose tolerance, falling significantly from 3.46 +/- 0.23 basally to 1.51 +/- 0.17 at 6 months after duct ligation (p less than 0.0001). Oral glucose tolerance deteriorated significantly, with the integrated glucose response rising from 23.7 +/- 1.2 g/dl.minute basally to 32.3 +/- 2.8 g/dl.minute at 6 months after duct ligation (p less than 0.05). Integrated insulin response to both intravenous and oral glucose deteriorated with pancreatitis. Pancreatitis-induced glucose intolerance is a consistent feature of this duct-ligated model. Glucose intolerance stabilizes between 4 and 6 months after duct ligation and is associated with pancreatic acinar fibrosis and pancreatic endocrine structural preservation. While the mechanism of altered glucose tolerance may involve mechanical, neural, humoral, or vascular events, our data clearly support the conclusion that pancreatic ductal stenosis with resultant pancreatic fibrosis and chronic pancreatitis is associated with abnormal islet responsiveness leading to circulating insulin deficiency and glucose intolerance, despite histologic and ultrastructural evidence of intact islets of Langerhans.
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PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

Pancreatic duct pressure was studied by endoscopic manometry in 12 patients with chronic pancreatitis and in 9 patients with a normal pancreas (suspected biliary dyskinesia). To study the effect of increased intraduodenal concentration of pancreatic enzymes, the duct pressure was measured before and after intraduodenal enzyme infusion. The mean pancreatic duct pressure was 12 (range, 6-25) mm Hg and 18 (range, 6-38) mm Hg in the pancreatitis and 'control' groups, respectively. The occasional patient in each group who had a high duct pressure also had an elevated sphincter of Oddi pressure. A significant correlation between the two pressures was found in both groups of patients. During intraduodenal infusion of pancreatic enzymes a decrease of the pancreatic duct pressure occurred in only two patients. We conclude that an increased pancreatic duct pressure is not a frequent finding in chronic pancreatitis. An elevation of the duct pressure can also be found in patients without pancreatitis. The sphincter of Oddi pressure appears to be more important for the pancreatic duct pressure than the severity of the pancreatitis. Intraduodenal infusion of enzymes, as done in our study, had an inconsistent effect on the pancreatic duct pressure.
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PMID:Endoscopic manometry of the sphincter of Oddi and pancreatic duct in chronic pancreatitis. 372 50

The biliary tract has been prospectively studied in a consecutive series of 769 patients undergoing surgery for gallstones to determine whether differences exist between subjects with and without a history of acute pancreatitis. The incidence of acute gallstone pancreatitis (AGP) was 7.7 per cent and men with gallstones were significantly more likely to develop pancreatic inflammation. Operations on patients with AGP were accompanied by a higher mortality rate which was almost entirely due to the severity of the disease at the time of surgery. The earlier operations were performed after the onset of pancreatitis the more often stones were found in the common bile duct and at the ampulla. Patients with AGP had smaller and more numerous gallbladder stones in association with a wider cystic duct that controls. The common bile duct diameter in patients with AGP was independent of the presence of choledochal calculi implying either previous temporary obstruction to the biliary tree or a dilated duct ab initio. Pancreatic duct reflux was far more commonly observed on the cholangiograms of patients with AGP and in these patients reflux occurred into a wider pancreatic duct, at a greater angle and was associated with a longer functioning common channel. No patient developed recurrent pancreatitis following biliary surgery. These features strongly support the concept of gallstone migration and suggest that patients with gallstones who develop acute pancreatitis have essential differences in their biliary tree which mechanically facilitate migration of calculi.
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PMID:The biliary tract in patients with acute gallstone pancreatitis. 401 39

Endoscopic manometry was used to measure pancreatic duct, common bile duct, pancreatic duct sphincter and bile duct sphincter pressures in 43 healthy volunteers and 162 patients with a variety of papillary, pancreatic and biliary disorders. Common bile duct pressure was significantly raised after cholecystectomy, with common bile duct stones and papillary stenosis but pancreatic duct pressure only in papillary stenosis. After endoscopic sphincterotomy mean common bile duct pressure fell from 11.2 to 1.1 mmHg and pancreatic duct pressure from 18.0 to 11.2 mmHg. Distinct pancreatic duct sphincter and bile duct sphincter zones were identified as phasic pressures of 3-12 waves/minute on pull-through from pancreatic duct and common bile duct to duodenum. Pancreatic duct sphincter pressures were higher with common bile duct stones and stenosis whereas bile duct sphincter pressures were higher in pancreatitis and stenosis. Bile duct sphincter activity was present in 60% of patients after surgical sphincteroplasty but 21% of patients after endoscopic sphincterotomy. Endoscopic manometry facilitated the diagnosis of papillary stenosis, has allowed study of papillary pathophysiology and has shown a functional inter-relationship between the two sphincteric zones.
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PMID:Endoscopic pancreatic and biliary manometry in pancreatic, biliary, and papillary disease, and after endoscopic sphincterotomy and surgical sphincteroplasty. 650 Mar 63

Haemorrhage via the pancreatic duct, a rare cause of upper gastrointestinal bleeding (GIB), often poses a diagnostic dilemma. We analysed our experience with 10 patients (8 men, 2 women; mean age 44 years, range 34-62) treated during a 12 year period. All had a history of alcohol abuse and presented with major upper GIB requiring a median of 8 units (range 2-40) blood transfusion. Nine had upper abdominal pain at the time of admission and nine had a history of pancreatitis. Upper gastroduodenal endoscopy (median 4; range 1-9), was diagnostic in only one. Side-viewing endoscopy showed bleeding from the pancreatic duct in 7 of 8 patients. Visceral aneurysms were demonstrated in 7 of 9 patients in whom coeliac angiography was carried out: (splenic artery 4, gastroduodenal artery 2, and pancreaticoduodenal artery 1). Two of 4 selective embolisations were successful. Six patients underwent distal pancreatectomy, 1 had gastroduodenal artery ligation and 1 died of coagulopathy following a total pancreatectomy. Pancreatic duct haemorrhage should be considered in patients with unexplained recurrent upper GIB, alcohol abuse and epigastric pain, particularly in those with established chronic pancreatitis. Selective angiography is essential for diagnosis and management. For bleeding sites in the head of the pancreas, embolisation should be attempted to avoid major resection. Distal pancreatectomy is preferred for splenic artery lesions.
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PMID:Diagnostic pitfalls and therapeutic strategies in the treatment of pancreatic duct haemorrhage. 929 83


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