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Query: UMLS:C1389183 (autodigestion)
 317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The exocrine pancreas secretes into the gut on demand more than 20 proteins that are indispensable for digestion. In-vivo autodigestion is prevented by an array of natural safeguards. In acute pancreatitis, inappropriate intrapancreatic activation and release of pancreatic hydrolases occur, but the pathogenetic mechanism of autodigestion is unclear. The release of proteases, lipase and colipase, phospholipase A, vasoactive peptides, and other agents probably accounts for the edema, tissue destruction, fat necrosis, metabolic abnormalities, and complications. Ethyl alcohol abuse, gallstones, trauma, and other common and rare conditions can induce pancreatitis. The patient's outcome can be predicted by certain prognostic signs. Ultrasonography and computerized tomography are invaluable diagnostic tools and magnetic resonance imaging appears promising. Hemodynamic monitoring, intensive care with colloid and crystalloid infusions, correction of electrolyte abnormalities, judicious use of antibiotics, peritoneal lavage, drainage of pancreatic exudation fluids, and surgical intervention require a team approach, especially in patients with multiple complications. Additional research is needed into the pathogenetic mechanism of autodigestion and the design of specific therapies.
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PMID:Acute pancreatitis. 389 Jun 60

Acute pancreatitis is a disease in which there are still considerable difficulties of etiologic, diagnostic and therapeutic nature due to a lack of knowledge of the mechanism responsible for the pancreatic autodigestion process. With the objective of evaluating the diagnostic criteria and therapeutic options, with particular emphasis on surgical treatment, we undertook a prospective clinical study of 153 cases of acute pancreatitis, over a period of 66 months (January 1986-June 1991) based on a specially prepared computerised register. The analysis of the results we obtained allows us to emphasise the following: a) the most common etiology was the alcoholism, closely followed by cholelithiasis, with values of approximately 40% for both; b) abdominal ultrasonography allowed the diagnosis of acute pancreatitis in 51.2% and the diagnosis of associated pathology in 56.7%, particularly cholelithiasis (41.7%); c) abdominal CT diagnosed acute pancreatitis in all 15.7% of the cases on which it was performed; d) medical therapy alone was performed in 43.1%, associated with the peritoneal lavage in 10.5% and with surgical therapy in 46.4%; e) indication for surgical therapy was a doubtful diagnosis in 32.4%, clinical-laboratory deterioration in 8.5%, treatment of associated biliary pathology in 47.9%, pancreatic abscess in 5.6% and pancreatic pseudocyst also in 5.6%; f) surgical treatment of the biliary tract was performed in 67%, with an operative mortality of 2.1%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The diagnosis and treatment of acute pancreatitis]. 765 1

The theory of pancreatic gland autodigestion by pancreatic enzymes assumed by Chiari 1886 as the crucial moment in the pathogenesis of acute pancreatitis (AP) remains accepted so far. The appearance of mutations of cationic trypsinogen gene on the 7th chromosome in several families with hereditary AP, supports the significance of trypsin in the initiation of AP. The generally recognized etiologic factors of AP include the biliary tract disease and alcohol. Opie in his "Common Channel theory" assumed that the impacted gallstone in the ampulla of Vater could cause a permanent obstruction and subsequently AP. Later clinical studies have confirmed that a short-term block of the common pancreatic duct caused by migrating gallstones is associated with onset of AP. Chronic consumption of alcohol evokes subclinical pancreatic disturbances already prior to the onset of AP. PAP (pancreatic associated protein) being the marker of pancreatic inflammation was significantly increased in chronic alcoholism without signs of AP. Many pathophysiological concepts and effective therapeutic procedures which were successful in the animal studies have not turned out to be appropriate in man. The destruction of both cellular structure and cellular connections is an early event in the development of experimental AP. There is much evidence that free oxygen radicals and the disturbances of microcirculation determine the severeness of AP. The roles of NO (nitric oxide) and kinins remain to be clarified cytokins a interleukin 2 (IL2) and interleukin 10 (IL10) had a protective effect in experimental AP. In humans the antagonist of PAF (platelet activating factor) had reduced the occurrence of organ failure. There is hope, that this knowledge, will lead to new therapeutic possibilities.
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PMID:[Etiology and pathogenesis of acute pancreatitis]. 972 65

Acute pancreatitis is an acute disease of the pancreas due to the organ autodigestion. The disease is still burdened with numerous complications and quite frequently with lethal outcome, in spite of the sophisticated diagnostic and therapeutic methods currently available. The disease has a benign course in a majority of patients (80%), however, in the remaining 20% it assumes a malignant course with the development of massive necroses of the pancreatic and peripancreatic tissues, infection, hemorrhage, and endogenous intoxication with lesions of the lungs, kidneys, heart and liver. The biliary tract disease plays the major role in the etiology of acute pancreatitis (80%), followed by alcoholism (10% to 15%). This differs from the experience acquired at the Zabok General Hospital, where an almost identical incidence of biliary and ethylic etiology was recorded. Other, less common causes include post-traumatic, postoperative, infective and hormonal (hyperparathyroidism) etiology. In some cases, the cause of acute pancreatitis remains unknown. The disease shows a female predominance, which results from the higher prevalence of cholelithiasis in women than in men. Anatomically, there are two main forms of acute pancreatitis, interstitial or edematous form, and hemorrhagic necrotizing form. The interstitial or edematous form of acute pancreatitis is characterized by edema (exudation) of the pancreatic interstitium. The hemorrhagic necrotizing form of acute pancreatitis is characterized by autodigestion of a minor or major portion of the pancreas and peripancreatic tissues. The diagnosis of acute pancreatitis may initially pose a considerable problem. Decision on the mode of treatment should primarily be based on the clinical picture and supported by relevant laboratory parameters and other diagnostic procedures (ultrasonography, computed tomography). Conservative therapy is indicated for the edematous form of acute pancreatitis, whereas operative treatment is as a rule used for the necrotizing form of acute pancreatitis. Secondary bacterial contamination of the necrotic foci with the development of septic complications occurs in more than 50% of patients with the necrotizing form of acute pancreatitis, and is an absolute indication for surgical intervention. The modes of treatment used in 57 patients admitted for acute pancreatitis during the 1996-1999 period are described. Cholelithiasis was the cause of acute pancreatitis in 28 (49.1%), and alcoholism in 29 (50.9%) patients. Conservative treatment was used in 41 (72%) patients. Sixteen (28%) patients underwent operative treatment. Explorative laparotomy and drainage were performed in four patients, and explorative laparotomy, necrectomy, sequestrectomy and drainage with two or more drains in 11 patients. Cholecystectomy and T drainage along with necrectomy and drainage were performed in one patient. There were 12 (21%) patients with the most severe form of acute pancreatitis. Nine of these patients were operated on (necrectomy drainage) between day 6 and 10 of the disease. Two of these patients had to be reoperated on within a month, due to necrosis and abscess recurrence. Three of the 12 patients with the severe form of acute pancreatitis received conservative therapy. Fifteen patients were operated on 8-10 weeks after acute pancreatitis had subsided. Pseudocysts developed in three patients. These patients were operated on 6-8 weeks from the onset of disease, with internal drainage via isolated small intestine flexure performed in all of these patients. The mean duration of intensive care unit stay for all patients with acute pancreatitis was 20.6 days. Four of 57 patients hospitalized for acute pancreatitis died. The mortality rate in the group of patients with the severe form of acute pancreatitis (n = 12) was 33%. Complications developed in 50% of operatively treated patients.
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PMID:Acute pancreatitis in the Zabok General Hospital. 1150 33

Acute pancreatitis (AP) is characterized by edema, acinar cell necrosis, hemorrhage, and severe inflammation of the pancreas. Patients with AP present with elevated blood and urine levels of pancreatic digestive enzymes, such as amylase and lipase. Severe AP may lead to systemic inflammatory response syndrome and multiorgan dysfunction syndrome, which account for the high mortality rate of AP. Although most (>80%) cases of AP are associated with gallstones and alcoholism, some are idiopathic. Although the pathogenesis of AP has not yet been elucidated, a common feature is the premature activation of trypsinogen within pancreatic tissues, which triggers autodigestion of the gland. Recent advances in basic research suggest that etiologic factors including cyclooxygenase-2, substance P, and angiotensin II may have novel roles in this disease. Basic research data obtained thus far have been based on animal models of AP ranging from mild edematous pancreatitis to severe necrotizing pancreatitis. In view of this, an adequate selection of experimental animal models is of paramount importance. Notwithstanding these animal models, it should be emphasized that none of these models mimic the clinical situation where varying degrees of severity usually occur. In this review, commonly used animal models of AP will be critically evaluated. A discussion of recent advances in our knowledge about AP risk factors is also included.
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PMID:Acute pancreatitis: animal models and recent advances in basic research. 1719 79