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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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 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

Stool screening for gallstones and ultrasound monitoring of diameter changes of the biliary and pancreatic duct were performed in 129 patients with choledocholithiasis. Gallstone migration was found in 44 patients, all of whom were operated on electively. At surgery, acute pancreatic lesions were found in 16 patients; in the remaining 28 there was no evidence of pancreatic inflammation. There were no significant differences among patients in both groups regarding sex, age, stone size, shape or number found in stools, interval between admission and migration, or the presence of a dilated pancreatic duct before migration. Pancreatic duct reflux, however, was significantly more frequent in cholangiograms of patients with acute pancreatitis, implying that a common channel may be a major factor relating to acute pancreatitis in patients with migrating gallstones.
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PMID:Risk factors for acute pancreatitis in patients with migrating gallstones. 281 83

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

Twenty-four cases of primary sclerosing cholangitis (PSC) and 17 cases of acute or chronic pancreatitis associated with ulcerative colitis (UC) reported in Japan were reviewed. Most of PSC cases revealed intra- and extra-hepatic bile duct involvement. Symptoms of the 22 cases disappeared by predonisolone (PSL) and/or salazosulfapyridine (SASP). Ursodeoxycholic acid was effective in 4 patients. One case received liver transplantation, but currently his liver is biliary cirrhotic 11 years after operation. Another case received total colectomy and pyoderma gangrenosum was cured. Twelve cases had acute pancreatitis, and 5; chronic. Pancreatic duct of 9 patients on ERCP was stenotic and dilated; pancreas was swelling in 3; and normal, in 2. SASP and/or PSL for UC and pancreatitis in 16 patients were effective. Gabexate mesilate and/or urinastatin was used in 10 patients. Only one patient with jaundice received pancreatoduodenectomy. When UC is well controlled, PSC and pancreatitis may be remitted.
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PMID:[Hepatobiliary and pancreatic complications in patients with ulcerative colitis]. 1057 29

Acute pancreatitis is a common complication of endoscopic retrograde cholangiopancreatography (ERCP). Pancreatic duct stent insertion after ERCP has been widely accepted as the standard of care for the prevention of this complication in high-risk patients. Unfortunately, the placement of pancreatic stents requires higher level of endoscopic expertise and is not always feasible due to anatomic considerations. Therefore, effective non-invasive pharmacologic prophylaxis remains appealing, particularly if it is inexpensive, easily administered, has a low risk side effect profile and is widely available. There have been multiple studies evaluating potential pharmacologic candidates for post-ERCP pancreatitis (PEP) prophylaxis, most of them yielding disappointing results. A recently published large, multi-center, randomized controlled trial reported that in high risk patients a single dose of rectal indomethacin administered immediately after the ERCP significantly decreased the incidence of PEP compare to placebo.
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PMID:Indomethacin for post-endoscopic retrograde cholangiopancreatography pancreatitis prophylaxis: is it the magic bullet? 2291 38

This guideline presents recommendations for the management of patients with acute pancreatitis (AP). During the past decade, there have been new understandings and developments in the diagnosis, etiology, and early and late management of the disease. As the diagnosis of AP is most often established by clinical symptoms and laboratory testing, contrast-enhanced computed tomography (CECT) and/or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically. Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed. Patients with organ failure and/or the systemic inflammatory response syndrome (SIRS) should be admitted to an intensive care unit or intermediary care setting whenever possible. Aggressive hydration should be provided to all patients, unless cardiovascular and/or renal comorbidites preclude it. Early aggressive intravenous hydration is most beneficial within the first 12-24 h, and may have little benefit beyond. Patients with AP and concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP) within 24 h of admission. Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients. Routine use of prophylactic antibiotics in patients with severe AP and/or sterile necrosis is not recommended. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis may be useful in delaying intervention, thus decreasing morbidity and mortality. In mild AP, oral feedings can be started immediately if there is no nausea and vomiting. In severe AP, enteral nutrition is recommended to prevent infectious complications, whereas parenteral nutrition should be avoided. Asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts do not warrant intervention regardless of size, location, and/or extension. In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed, preferably for 4 weeks, to allow the development of a wall around the necrosis.
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PMID:American College of Gastroenterology guideline: management of acute pancreatitis. 2459 57

The patient was a 30-year-old female who had undergone excision of the extrahepatic bile duct and Roux-en-Y hepaticojejunostomy for congenital biliary dilatation at the age of 7. Thereafter, she suffered from recurrent acute pancreatitis due to pancreaticobiliary maljunction and received subtotal stomach-preserving pancreaticoduodenectomy. She developed a pancreatic fistula and an intra-abdominal abscess after the operation. These complications were improved by percutaneous abscess drainage and antibiotic therapy. However, upper abdominal discomfort and the elevation of serum pancreatic enzymes persisted due to stenosis from the pancreaticojejunostomy. Because we could not accomplish dilation of the stenosis by endoscopic retrograde cholangiopancreatography, we tried an endoscopic ultrasonography (EUS) guided rendezvous technique for pancreatic duct drainage. After transgastric puncture of the pancreatic duct using an EUS-fine needle aspiration needle, the guidewire was inserted into the pancreatic duct and finally reached to the jejunum through the stenotic anastomosis. We changed the echoendoscope to an oblique-viewing endoscope, then grasped the guidewire and withdrew it through the scope. The stenosis of the pancreaticojejunostomy was dilated up to 4 mm, and a pancreatic stent was put in place. Though the pancreatic stent was removed after three months, the patient remained symptom-free. Pancreatic duct drainage using an EUS-guided rendezvous technique was useful for the treatment of a stenotic pancreaticojejunostomy after pancreaticoduodenectomy.
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PMID:Pancreatic duct drainage using EUS-guided rendezvous technique for stenotic pancreaticojejunostomy. 2396 56