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

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

In the period of 1984-1996, 569 patients were treated for acute pancreatitis and 37 of them (6.5%) developed infected pancreatic necrosis (IPN). All these patients were submitted to repeated laparotomies according to Bradley's procedure. The IPN was caused by: bile duct stones--in 11 cases, alcohol abuse-14, ERCP-6, trauma-1, in 6 cases the etiology was cryptogenic. The accuracy of imaging tests was: USG-62%, CT-100%. Sepsis was present in all cases, and multiorgan insufficiency-in 25 patients. Hospital mortality was 30% (11 patients). The most frequent reason of death was multiorgan insufficiency. The actuarial survival was 26 patients (70%).
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PMID:[Repeated laparotomy for acute necrotizing pancreatitis]. 942 32

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

Acute pancreatitis is only rarely the first presentation of a cystic neoplasm of the pancreas. Mucinous cystadenomas have not been reported to be a cause of acute pancreatitis; however, we present two cases of mucinous cystadenoma of the pancreas which have caused acute pancreatitis. Both patients (female) presented acute abdominal pain, with serum amylase elevation and ultrasound scan (US) and computed tomography (CT) evidence of moderate pancreatitis, which resolved with medical treatment; fluid collection in the distal pancreas had been misinterpreted as a pseudocyst. There was no history of alcohol abuse or gallstone disease. After distal pancreatectomy the diagnosis of mucinous cystadenoma was confirmed; in one case a large pseudocyst was associated with this diagnosis. Pre-operative differential diagnosis between inflammatory and neoplastic cysts is difficult, especially when the patient's first presentation is due to an episode of acute pancreatitis. A neoplastic cyst should be considered when acute pancreatitis attacks occur in non-alcoholic women, who do not have gallstone disease.
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PMID:Mucinous cystadenoma of the pancreas as a cause of acute pancreatitis. 995 36

The available morphologic data on ACP are consistent with the view that ACP evolves from acute pancreatitis. How alcohol abuse triggers pancreatic injury and which factors are responsible for the progression to chronic pancreatitis remain to be clarified, however.
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PMID:Progression from acute to chronic pancreatitis. A pathologist's view. 1047 Mar 28

Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
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PMID:[Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis]. 1049 50

Acute pancreatitis is a disorder that has numerous causes and an obscure pathogenesis. Bile duct stones and alcohol abuse together account for about 80% of acute pancreatitis. Most episodes of biliary pancreatitis are associated with transient impaction of the stone in the ampulla (that causes obstruction of the pancreatic duct, with ductal hypertension) or passage of the stone though and into the duodenum. Other causes of acute pancreatitis are various toxins, drugs, other obstructive causes (such as malignancy or fibrotic sphincter of Oddi), metabolic abnormalities, trauma, ischemia, infection, autoimmune diseases, etc. In 10% of cases of acute pancreatitis, no underlying cause can be identified; this is idiopathic pancreatitis. Occult biliary microlithiasis may be the cause of two thirds of the cases of "idiopathic" acute pancreatitis. Intra-acinar activation of trypsinogen plays a central role in the pathogenesis of acute pancreatitis, resulting in subsequent activation of other proteases causing the subsequent cell damage. Ischemia/reperfusion injury is increasingly recognized as a common and important mechanism in the pathogenesis of acute pancreatitis and especially in the progression from mild edematous to severe necrotizing form. Increased intracellular calcium concentration also mediates acinar cell damage. Oxygen-derived free radicals and many cytokines (e.g., interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor-alpha, platelet activating factor) are considered to be principal mediators in the transformation of acute pancreatitis from a local inflammatory process into a multiorgan illness.
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PMID:Etiology and pathogenesis of acute pancreatitis: current concepts. 1087 61

Acute pancreatitis usually occurs as a result of alcohol abuse or bile duct obstruction. A careful review of the patient's history and appropriate laboratory studies can help the physician identify the etiology of the condition and guide management. Serum amylase and lipase levels are still used to confirm the diagnosis of acute pancreatitis. Although not routinely available, the serum trypsin level is the most accurate laboratory indicator for pancreatitis. Ultrasonography, computed tomography and endoscopic retrograde cholangiopancreatography are additional modalities that can help the family physician choose the best treatment approach. Prompt identification of patients who need intensive care referral or subspecialty consultation is crucial. The APACHE II and the multiple organ system failure scales provide prognostic information at the time of admission and may be repeated daily to monitor disease progression. Therapies such as nasogastric suctioning, anticholinergics and histamine H2-receptor blockers have not been shown to decrease symptoms or hospital stays in patients with acute pancreatitis. Systemic antibiotics have been found to improve outcome in patients with severe disease. With supportive care, most patients have a good clinical outcome.
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PMID:Diagnosis and management of acute pancreatitis. 1147 69


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