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

Pancreatic regeneration involves two pathways; proliferation and differentiation of pancreatic progenitor cells, which probably exist in pancreatic ductal epithelium, and replication of pre-existing differentiated acinar, islet, and ductal epithelial cells. During pancreatic development, differentiated cells arise from the ductal progenitor cells expressing the pancreatic/duodenal homeobox-1 (PDX-1) homeodomain transcription factor. The aims of this study were to characterize cell proliferation and differentiation during regeneration after acute necrotizing pancreatitis and to evaluate the role of PDX-1-positive stem cells. Necrotizing pancreatitis was induced in rats by retrograde intraductal infusion of sodium taurocholate. Cell types were classified into five categories: main, large, and small ductal epithelial cells, tubular complexes and acinar cells. Each category was scored using a 5-bromo-2'-deoxyuridine (BrdU) labelling index (LI) at various time points after induction of pancreatitis. Tissue sections were also immunostained for PDX-1 to determine the source of pancreatic stem cells. Acinar necrosis was observed at 24 h after induction of pancreatitis and most lobules were filled with tubular complexes on day 5. Subsequently, newly formed acinar cells were observed on day 7, but the lobular architecture returned to normal appearance on day 28. Proliferation started in the main and large ducts at 24 h; marked mitotic activity was evident in small ductal epithelial cells and tubular complexes on day 3, and in acinar cells on day 7. At 24 h after induction of pancreatitis, epithelial cells of the main duct with PDX-1-positive nuclei were greatly increased, simultaneously with the peak LI of BrdU. These results suggest that regeneration after necrotizing pancreatitis involves proliferation and differentiation of pancreatic progenitor cells, and that ductal epithelial cells with PDX-1-positive nuclei may contribute to the differentiation of pancreatic stem cells in the main duct.
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PMID:Induction of PDX-1-positive cells in the main duct during regeneration after acute necrotizing pancreatitis in rats. 1221 84

The authors define pathogenetics correlations as a acute necrotizing pancreatitis complicated by infection and bacterial translocation. Acute necrotizing pancreatitis infection occurs for gastrointestinal bacterial translocation due to structural and functional modifications of intestinal mucosa. These modifications are results of mucosa ischemic-reperfusion system caused by systemic emodynamic instability in micro- and macro-circulation of splanchnic district. Emodynamic systemic instability has a central role in different multiple physiopathologic phenomena (ipovolemic shock; pancreatic shock, SIRS), which is caused by acute pancreatic necrosis and carries to common way established by severe systemics emodinamics modifications; these changes promote growth of adverse events which conduce by means of process previously described to bacterial translocation and infection of acute pancreatic necrosis. Indeed, emodynamic systemic instability of any etiology, can determine for one way bacterial translocation and on the other acute ischemic pancreatitis; both phenomena concur lead to cause beginning of acute necrotizing pancreatitis complicated by infection. The authors confirm that improved knowledge of acute pancreatic necrosis complicated by infection and own pathogenetic correlations with bacterial translocation, allows the realization of therapeutic measures aimed to prophylaxis of infection of acute pancreatic necrosis. Central emodynamic stability regularization of splanchnic perfusion and antibiotic prophylaxis, have a central role in prophylaxis of infection of acute pancreatic necrosis. Antibiotic is given by systemic (imipenem e.v.) and selective decontamination of gastrointestinal tract (SDD). SDD provides for oral antibiotic prophylaxis (PTA protocol) and systemic antibiotic prophylaxis (cefotaxime and gentamicin), in addition to microbiologic and gastrointestinal monitoring. If on the one hand the role of SDD about mortality reduction is not clear, however, on the other it is well recognized capacity of reduction the intercurrents and pulmonary infections. Other Authors think that SDD is insignificant on early mortality, whereas, is a good option to reduce late and overall mortality of acute pancreatic necrosis complicated by infection.
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PMID:[Acute pancreatic necrosis complicated by infection and gastro-intestinal translocation: pathogenesis correlation and therapeutic implication]. 1282 May 85

The influence of experimental pancreatitis on bowel motility was measured in vivo with the propulsion technique and in vitro as contractility of isolated ileum muscle strips. In edematous pancreatitis, propulsion was reduced but contractility was normal. Both, propulsion and contractility were reduced in necrotizing pancreatitis. The intravenous saline infusion normalized propulsion in edematous pancreatitis but was of no benefit in necrotising pancreatitis. These results indicate that extraintestinal (neuroendocrine) regulation pathways were effected in edematous pancreatitis. Necrotising pancreatitis appears to have an additional profound influence on the intrinsic, intramural regulation of motility.
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PMID:[Different mechanisms in intestinal paralysis in edematous and necrotizing pancreatitis of the rat]. 1451 87

The effectiveness of continuous arterial infusion of Gabexate Mesilate (FOY-007) on experimental acute pancreatitis was investigated. Acute necrotizing pancreatitis was induced by an injection of 10% Na-taurocholate (1ml/kg) into the main pancreatic duct of mongrel dogs. Animals were divided into three groups; Group A: non-treated control, Group B: after the induction of pancreatitis, injected with FOY-007 intravenously (5mg/kg/hr), Group C: after the induction of pancreatitis, injected with FOY-007 via the celiac artery. The changes in the values of amylase and lipase in serum and ascites etc. were examined. A histological examination was done and the FOY-007 concentration of the pancreas was measured. In both groups B and C, the serum levels of amylase and lipase reached significantly to low levels compared with those in group A. The extents of pancreatic parenchyma necrosis in each group were 36.1, 25.3 and 19.5%, respectively, and were significantly improved in group C. In addition, the FOY-007 levels in pancreas specimens in the intraarterial infusion group exceeded those in the intravenous infusion group by 32 times. The results suggest that continuous FOY-007 arterial infusion therapy is useful as a local treatment for severe acute pancreatitis.
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PMID:The effect of continuous arterial infusion of gabexate mesilate (FOY-007) on experimental acute pancreatitis. 1546 Sep 5

Gabexate mesilate is a synthetic protease inhibitor. The effectiveness of gabexate mesilate in patients with acute pancreatitis is controversial. Proinflammatory cytokines are associated with systemic inflammatory response syndrome (SIRS) in acute pancreatitis. A compensatory anti-inflammatory response occurs in parallel with SIRS. We investigated the effects of gabexate mesilate on acute necrotizing pancreatitis in rats, emphasizing the changes in serum levels of proinflammatory and anti-inflammatory cytokines. Acute necrotizing pancreatitis was induced by retrograde infusion of sodium taurodeoxycholate into the pancreatobiliary duct in rats. The rats were divided into three groups. Group I was given gabexate mesilate 2 mg/kg/h i.v. continuously 1 h before the induction of acute pancreatitis. Group II was given gabexate mesilate the same dose immediately after the induction of acute pancreatitis. Group III was given normal saline as the controls. Serum levels of amylase, lipase, tumor necrosis factor alpha, interleukin-6, and interleukin-10, pancreatic histopathology and hemodynamics were examined at 5h after the induction of acute pancreatitis. Gabexate mesilate significantly reduced serum levels of amylase, lipase, tumor necrosis factor alpha and interleukin-6 at 5 h. Serum levels of interleukin-10 significantly increased in Group I, as compared with Groups II and III. The severity of pancreatic histopathology, the reduction of mean arterial pressure, the volume of ascites and pancreatic wet weight/body weight ratios were also significantly improved by the administration of gabexate mesilate. The beneficial effects of gabexate mesilate on acute pancreatitis may be, in part, due to the modulation of inflammatory cytokine responses.
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PMID:Effects of gabexate mesilate on serum inflammatory cytokines in rats with acute necrotizing pancreatitis. 1647 21

Acute necrotising pancreatitis is a dramatic and often life-threatening disease with a high rate of mortality, varying between 30-70% and necessitating heavy medical care. The surgical attitude regarding acute necrotising pancreatitis is disputed between the supporters of drainage with closed abdomen and the supporters of laparatomy with open drainage. The goal of this study is the evaluation of the number of intervention required, the timing of the interventions and the mortality and morbidity in a group of patients with necrotising pancreatitis. The studied group consists in 112 patients with necrotising pancreatitis, treated in Surgical Clinic of Caritas "Prof. Dr. N. Cajal" Clinical Hospital, Bucharest during 1983-2005. Infection of pancreatic necrosis supervened in 55,35% of patients in this group, not any pancreatic necrosis becomes infected. Infected necrosis is not synonymous for abscessed of necrosis, in the same patient pancreatic necrosis, infected pancreatic necrosis and abscessed necrosis may coexist. Clinical and biological criteria are the decisive factors in the indication for surgical treatment, the radiology being decisive in the choice of the laparotomy approach. In the study group 50,89% of patients necessitated only one surgical intervention. Implicitly, more than half of the patients would have been suffered multiple useless planned staged relaparotomies. The mortality in our study group treated by the method of closed drainage was 25,89%.
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PMID:[Surgical approach in acute necrotising pancreatitis]. 1692 12

In acute pancreatitis, local as well as systemic organ complications are mediated by the activation of various inflammatory cascades. The role of complement in this setting is unclear. The aim of the present study was to determine the level of complement activation in experimental pancreatitis, to evaluate the interaction of complement and leukocyte-endothelium activation, and to assess the effects of complement inhibition by soluble complement receptor 1 (sCR1) in this setting. Necrotizing pancreatitis was induced in Wistar rats by the combination of intravenous cerulein and retrograde infusion of glycodeoxycholic acid into the biliopancreatic duct; edematous pancreatitis was induced by intravenous cerulein only. In control animals, a sham operation (midline laparotomy) was performed. Complement activation, leukocyte sequestration, and pancreatic as well as pulmonary injury were assessed in the presence/absence of sCR1. Increased levels of C3a were found in necrotizing but not in edematous pancreatitis. When complement activation in necrotizing pancreatitis was blocked by sCR1, levels of C3a and total hemolytic activity (CH50) were decreased. Leukocyte-endothelial interaction, as assessed by intravital microscopy, and pancreatic as well as pulmonary organ injury (wet-to-dry weight ratio, MPO activity, and histology) were ameliorated by sCR1. As a result of the present study, necrotizing but not edematous pancreatitis is characterized by significant and early complement activation. Based on the interaction of complement and leukocytes, complement inhibition by sCR1 may be a valuable option in the treatment of leukocyte-associated organ injury in severe pancreatitis.
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PMID:Interaction of complement and leukocytes in severe acute pancreatitis: potential for therapeutic intervention. 1703 Aug 99

Necrotizing pancreatitis is a severe form of pancreatitis and is associated with substantial morbidity and mortality. We report a case of necrotizing pancreatitis that developed following combined hepatitis A and B vaccination. No other causes of pancreatitis could be determined. Although confirming the diagnosis is challenging, 3 main factors suggest a possible link to the vaccine: the chronology of the events, the patient's human leukocyte antigen genotype and the incongruent immune response to the vaccine components. This report serves to alert physicians to the possible development of necrotizing pancreatitis after vaccination.
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PMID:Severe necrotizing pancreatitis following combined hepatitis A and B vaccination. 1726 31

Necrotizing pancreatitis is the most severe form of acute pancreatitis associated with high morbidity and mortality. Percutaneous CT-guided catheter drainage is an important treatment option that can be effective whether used alone, or as an adjunct to operation. Existing literature describing the role of percutaneous catheter drainage of necrotizing pancreatitis is limited. This update reviews techniques, indications, outcomes, and complications of CT-guided percutaneous treatment of acute necrotizing pancreatitis.
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PMID:Acute necrotizing pancreatitis: role of CT-guided percutaneous catheter drainage. 1750 82

Necrotizing pancreatitis continues to challenge clinicians, and few other medical subjects currently elicit as much debate. Host characteristics or underlying differences in pathophysiology that lead to pancreatic necrosis remain poorly understood. Severe pancreatitis follows a two-phase clinical course. The early first phase manifests the features of the systemic inflammatory response syndrome, and the second late phase is characterized by infectious complications. This article presents a multidisciplinary literature-based approach to the treatment of patients with necrotizing pancreatitis.
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PMID:Necrotizing pancreatitis. 1753 81


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