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Objective: The aim of this study was to investigate the clinical progression of patients who had severe acute pancreatitis (AP) and a stay in hospital of more than a month., Methods: A total of 24 patients (median age: 57 years) were included in this eight-year retrospective study. Cure was defined as the restoration of the pancreatic parenchyma, and the disappearance of all pseudocysts and pancreatic fistulae. Data including the duration of hospital stay, disease severity and pancreatic sequelae were also collected., Results: The median total duration of the hospital stay was 67 days. The overall mortality rate was 20.8%, whereas the mortality rate due to AP was 12.5%. The average healing period was 7.7 months. On univariate analysis, patients who also had respiratory diseases, chronic alcoholism, necrotizing superinfection, pseudocyst, food intolerance and/or hospital-acquired infection took significantly longer to heal. After cure, we observed pancreatic and/or hepatic duct stenoses in 50% of cases, and the onset or aggravation of diabetes in 25%., Conclusion: In patients hospitalized for more than one month because of necrotizing AP, the rate of mortality is around 20%, with a final hospital stay of two months and a healing period of more than seven months. In addition, half of the patients presented with pancreatic or biliary sequelae.

Introduction: Treatment of pancreatic postoperative collections are usually managed with a multidisciplinary team. Different managements are possible: abstention, external drainage, endoscopic treatment or surgery., Methods: We report on a case series of five patients with a postoperative pancreatic collection, endoscopically managed. Patients underwent all a CT scan associated or not with endoscopic ultrasonography., Results: An endoscopic cystenterosotomy was performed in all the cases, with two double pig tail stents sometimes associated with nasocystic drainage for clearing the cyst lumen and with transpapillary drainage in one case. All the procedures were successful and patients healed in all the cases with the disappearance of the radiological image within a 33 days to three months range with one complication due to superinfection of the drained cyst, endoscopically managed with a nasocystic catheter., Conclusion: Therapeutic endoscopy, with a multidisciplinary approach, is a promising way to manage postoperative pancreatic collections.

Pancreatic hydatid cysts represent 0.1 to 1% of all hydatidoses. A 12 year-old-boy, with a previous history of abdominal pain, was admitted for acute cholangitis. Laboratory investigations showed cholestasis, cytolysis and eosinophilia. Serum amylase levels were normal. Abdominal ultrasound and CT scan revealed a 100 mm hydatid cyst, located in the head of the pancreas. The biliary and pancreatic ducts were markedly dilated. Exploratory laparotomy confirmed the diagnosis. A pancreatic fistula was discovered. Subtotal excision of the cyst and external drainage of the pancreatic fistula were performed. Laboratory tests were normal post-operatively. The pancreatic fistulae persisted for two months. Hypercaloric and hyperprotidic feeding resulted in occlusion in three weeks. The rest of the postoperative course was uneventful and the size of the biliary and pancreatic ducts was normal. The authors discuss the diagnostic features of pancreatic hydatid cyst and discuss therapeutic modalities.

Background and Aim: Recent clinical data suggest that pancreatitis could be an extraintestinal manifestation of inflammatory bowel disease. However, no experimental data support such a clinical relationship. The aim of this study was to investigate the presence of pancreatic damages in mice with TNBS-induced colitis., Methods: Colitis was induced in Balb/C mice by intrarectal instillation of TNBS. Control mice received either intrarectal instillation of NaCl saline solution or 50% ethanol. Presence of colitis was assessed by macroscopic and microscopic examination, extent of mucosal damage being evaluated by the scoring systems of Wallace and Ameho in 8 mice with TNBS-induced colitis and in 4 controls. Pancreatic samples from the same mice underwent morphological examination after standard coloration. Intrapancreatic expression of the pancreatitis-associated protein (PAP), a marker of pancreatic inflammation, was monitored by automated immunohistochemistry using specific antibodies. In addition, quantification of TNFalpha mRNA by competitive PCR and semi-quantification of PAP, IL-10 and IL-1B mRNAs were performed on pancreas in 10 mice with TNBS-induced colitis and in 10 control mice., Results: All mice treated with TNBS and none of the controls had colitis. Macroscopic and microscopic examination of the pancreas of the 4 control mice was normal, whereas in 5 out of the 8 TNBS-treated mice histological changes were observed, with inflammatory infiltrate and fibrin aggregates at the periphery of the gland. PAP immunohistochemistry was negative in all control mice and positive in all mice with TNBS-induced colitis, with a patchy distribution of staining. PAP immunolocalized to the cytoplasm of acinar cells, duct cells and islets of Langherans being negative. PAP and IL-1B mRNA levels in the pancreas were significantly increased but the increase in TNFalpha mRNA level did not reach statistical significance (P=0.06). IL-10 mRNA levels did not show any significant modification., Conclusion: PAP overexpression in pancreas demonstrates that inflammatory stress early occurs in the mouse pancreas during the course of TNBS-induced colitis. The concomitant pancreatic overexpression of IL-1B and, to a lesser extent, of TNFalpha, two proinflammatory cytokines also associated with the intestinal lesions of colitis, supported a pancreatic inflammatory mechanism mediated by cytokines.