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

There are no experimental models which mimic the most common causes of human acute pancreatitis, i.e. gallstones and alcohol abuse. However, existing models can reproduce the morphology and physiological derangements of certain phases of the illness. Current models have been useful in elucidating the earliest events involved in the initiation and progression of pancreatitis. However, very few animal studies demonstrate effective therapeutic intervention when treatment is given after the induction of experimental pancreatitis. Since immediate intervention is unachievable in human disease, most experimental therapies have not been successfully applied to clinical disease.
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PMID:Experimental models of acute pancreatitis and their relevance to human disease. 886 63

A 40-year-old man with diabetes mellitus, congestive heart failure, alcoholic cirrhosis, and chronic pancreatitis had an exacerbation of pancreatitis due to alcohol abuse. His condition deteriorated rapidly with development of apparent sepsis; cultures were negative. He slowly improved with multiple antibiotic therapy and total parenteral nutrition. Serial imaging of the pancreas revealed edematous pancreatitis that evolved initially into a phlegmon and later into multiple pseudocysts. Intermittent fever prompted computed-tomography-directed percutaneous aspiration of the largest pancreatic fluid collection, yielding purulent material that grew only Candida albicans. Subsequently, disseminated candidiasis developed. Despite therapy with amphotericin B and aggressive supportive care, the patient died from multiple organ system failure.
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PMID:Infection of a pancreatic pseudocyst due to Candida albicans. 890 99

The authors draw attention to the rising incidence of acute pancreatitis, based on their own observations. They present very briefly the last version of the classification of acute pancreatitis, the so-called Atlanta classification of 1992. They summarise methods of conservative treatment of acute pancreatitis which they used as a basis for elaborating their own therapeutic pattern. In the presented group in 1995 19 patients with the diagnosis of acute pancreatitis were treated which was diagnosed based on the clinical condition, biochemical results, US and CT examination of the pancreas. CT examination is considered most important. In three instances acute non-complicated pancreatitis was involved, seven times acute accumulation of fluid in the pancreas and eight times acute necrosis of the pancreas. In 13 men and 6 women the mean age was 54.3 years. As to the aetiology, acute pancreatitis was 9 times of biliary origin, 6 times due to alcohol abuse, twice due to ERCP, once after chemotherapy and in one case the cause was not revealed. All patients with acute necrosis of the pancreas were operate by laparostomy, zip closure was used and repeated surgical revisions were made. Of 19 patients 8 died (all with acute necrosis of the pancreas). In antibiotic prevention of secondary infection of the pancreas in acute pancreatitis cefazoline proved most useful. Aprotinine administration to inhibit proteases is according to the authors effective only during the first 48 hours after the onset of the disease.
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PMID:[Acute pancreatitis--the need for an active approach. Experience in our department]. 896 39

Normal pancreatic ageing is characterized by functional and morphological changes of the pancreatic parenchyma and of the ductal system, which, however, do not interfere with normal exocrine pancreatic function. It can be speculated that 'pancreatic lithiasis in the aged' as well as the 'senile idiopathic chronic pancreatitis', two conditions of chronic pancreatitis in the elderly, may represent more extreme forms of these normal age-related changes in pancreatic structure and function. In elderly people, acute and chronic pancreatitis are only rarely related to alcohol abuse, in contrast to the situation in a younger patient population. The presence of gallstones represents the most frequent cause of acute pancreatitis in the elderly. In most aged patients with acute biliary pancreatitis, endoscopic sphincterotomy is the treatment of choice, even when bile duct stones cannot clearly be demonstrated at ERCP. Endoscopic sphincterotomy has been shown to reduce morbidity as well as mortality rates in acute biliary pancreatitis. This technique can even be considered as treatment of choice in elderly patients with an increased operative risk. An elective laparoscopic cholecystectomy should be performed in elderly patients with an acceptable operative risk.
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PMID:[Acute and chronic pancreatitis in the elderly patient]. 896 46

Ethanol abuse is a well known association of pancreatitis. Research into the pathogenesis of alcoholic pancreatitis has generally followed two directions. Firstly, factors which may predispose alcoholics to pancreatitis have been examined. To date, these studies have been negative and the predisposing factor(s) remain unknown. The second approach has involved studies on the constant metabolic effects of ethanol on the pancreas which may render the acinar cell susceptible to digestive enzyme induced injury. Recently developed models of experimental pancreatitis have implicated intracellular activation of digestive enzymes by lysosomal enzymes as an early event. Using the Lieber-DeCarli model of ethanol administration to rats, a number of changes have been described in pancreatic acinar cells which may predispose the gland to autodigestion. These changes include: (1) increased glandular content of digestive enzymes as a result of increases in mRNA levels for these enzymes; (2) increased glandular content of the lysosomal enzyme cathepsin B (known to be capable of activating trypsinogen); (3) increased fragility of lysosomes possibly mediated by cholesteryl esters and fatty acid ethyl esters; and (4) increased fragility of zymogen granules. These effects of ethanol constitute a "primed" setting (the "Drinker's Pancreas") for autodigestion. Triggering factors for autodigestion in this setting have not yet been identified.
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PMID:Ethanol induced acinar cell injury. 897 57

Alcohol abuse and gallstones are the most important factors in the pathogenesis of acute pancreatitis. Other factors are less frequent, and in some patients one is unable to identify any risk factor. Even in the most frequent forms of alcoholic or biliary pancreatitis little is known about the cellular and molecular mechanisms which lead to severe pancreatitis. New experimental studies have shown that many biochemical and morphological events are similar in different experimental models of pancreatitis as well as in human disease. These changes include intracellular premature activation of trypsin, blockade of luminal enzyme secretion and appearance of intracellular vacuoles. Although activated trypsin triggers the activation of other proteases, it is not trypsin but other proteases (e.g. elastase, chymotrypsin and phospholipase) which damage the pancreatic acinar cell. These pathogenetic findings may lead to the development of inhibitors which more effectively inhibit the latter cell-toxic proteases and may thereby help to improve the therapy.
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PMID:[Current aspects in the pathogenesis of acute pancreatitis]. 917 94

Interleukin 10 (IL-10) recently emerged as an antiinflammatory cytokine that inhibits the secretion of proinflammatory cytokines by monocytes and/or macrophages and the release of free oxygen radicals. It has been reported that treatment with IL-10 decreases the severity of experimental pancreatitis, mainly by inhibiting cellular necrosis. The aim of this study was to evaluate the behavior of serum IL-10 in patients with acute pancreatitis and to explore the possibility of a relationship between this cytokine and severity of the disease. Forty-five patients with acute pancreatitis were studied. Acute pancreatitis was of biliary origin in 30 patients, due to alcohol abuse in 10, due to pancreas divisum in 1, and of unknown origin in the remaining 4. According to the Balthazar criteria, 19 patients had scores of A, B, or C and 25 had scores of D or E. Twelve healthy subjects were also studied as controls. Serum IL-10 was determined in all subjects on admission, and in acute pancreatitis patients also daily for the following four days using a commercial kit. Healthy subjects had no detectable serum levels of IL-10. In acute pancreatitis patients, serum IL-10 levels were increased on the first day of the disease and then progressively decrease in the following days. On the first day of the acute pancreatitis, patients with the mild disease had serum levels of IL-10 significantly higher than those with severe disease, whereas in the following days, no statistically significant difference was observed between the two groups. The elevation of IL-10 on the first day of the illness is more marked in patients with mild acute pancreatitis than in those with the severe form of the disease. The finding of low values of serum IL-10 in severe acute pancreatitis suggests that there may be altered down-regulation of the immune system response in these patients.
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PMID:Serum interleukin-10 in human acute pancreatitis. 924 48

While alcohol abuse and biliary disease can result in the development of pancreatitis, the factors that contribute to the idiopathic form of the disease are not well understood. I propose that coxsackievirus infections account for a subset of cases of pancreatitis of unknown etiology. Evidence to support this concept is derived from serological studies, case reports and animal models. In reviewing the available data, it is obvious that the relationship between coxsackievirus infection and the development of pancreatitis is not a simple one. Many elements contribute to the development of the disease including the strain of the infecting virus, the genetic predisposition of the host and additional environmental factors that maintain the disease process. Studies that show an association between coxsackievirus infection and acute pancreatitis in humans are given additional support by the extensive data from mouse studies demonstrating that some serotypes (B4,B3) are tropic for the exocrine pancreas. Some viral strains may cause limited pancreatic tissue injury which is compatible with tissue repair followed by full restoration of pancreatic function. Other viral strains may cause more extensive tissue damage giving rise to chronic pancreatitis which, on a genetic background that predisposes to autoimmunity, may result in an autoimmune chronic pancreatitis. A multi-disciplinary approach is required to increase our understanding of the complex relationship between coxsackievirus infection and pancreatic diseases. Such studies should address the biology of viral replication, the immune response to infection, the role of viruses in the development of autoimmunity, the biology of pancreatic tissue injury and the underlying repair process.
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PMID:Coxsackieviruses and pancreatitis. 925 48

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

We examined the feasibility of the lipase-amylase (L/A) ratio to differentiate alcoholic from nonalcoholic acute pancreatitis in a large prospective series of patients with acute pancreatitis. One hundred fifty-eight consecutive patients with acute pancreatitis were studied. The pancreatitis was of biliary origin in 112 patients, due to alcohol abuse in 26, due to other causes in 8, and of unknown origin in 12. For all patients, serum, amylase, and lipase levels were determined simultaneously, and the L/A ratio was calculated using the amylase and lipase serum levels expressed as multiples of the respective upper normal limit. The ratios in patients with alcoholic acute pancreatitis ranged from 0.3 to 8 and in patients with nonalcoholic acute pancreatitis from 0 to 19.9. A value of 2.2 for the serum L/A ratio was found to be the best cutoff value for differentiating alcoholic from nonalcoholic acute pancreatitis. Using this limit, the sensitivity, specificity, and diagnostic accuracy of the L/A ratio in determining the alcoholic form of acute pancreatitis were 54%, 82%, and 77% respectively. Our study showed that the L/A ratio is not useful in distinguishing alcoholic from nonalcoholic acute pancreatitis.
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PMID:Lipase-amylase ratio does not determine the etiology of acute pancreatitis. Another myth bites the dust. 949 61


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