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Acute Pancreatitis (acute + pancreatitis)
Kinds of Acute Pancreatitis Selected AbstractsDOES MATRIX METALLOPROTEINASE ACTIVITY PREDICT SEVERITY OF ACUTE PANCREATITIS?ANZ JOURNAL OF SURGERY, Issue 9 2006Murat Aynaci Background: Matrix metalloproteinases (MMP) modulate end-organ complications of acute pancreatitis, but the correlation between increased MMP production and histological severity of disease remains unclear. We examined the role of MMP and pancreas histology on experimental acute pancreatitis. Methods: Forty male Wistar albino rats were subjected to cerulein-induced pancreatitis (8, 16, 24 and 32 h groups) or sham treatment. The animals were killed at different time points and pancreatic tissues were harvested to assess MMP (1, 2 and 9) activity and inflammatory changes. Results: Compared with other groups, 8 h group had decreased tissue MMP-1 concentrations. MMP-9 concentrations were lower in 24-h and 32-h groups, as were histological severity scores. MMP-2 activity did not differ among groups. Pancreatitis was prominent in 8-h, 16-h and 24-h groups by means of histology. Conclusion: Induction of pancreatitis by cerulein altered pancreatic MMP levels in the early phase of inflammation. Inhibition of MMP-2 and MMP-9 paralleled histological scores. Therefore, MMP may have a predictive value to assess histological severity. [source] COELIAC ARTERY TRUNK THROMBOSIS IN ACUTE PANCREATITIS CAUSING TOTAL GASTRIC NECROSISANZ JOURNAL OF SURGERY, Issue 4 2006Chinnappan Kumaran No abstract is available for this article. [source] New-Onset QT Prolongation and Torsades De Pointes Accompanied by Left Ventricular Dysfunction Secondary to Acute PancreatitisPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2003PIROOZ S. MOFRAD A 70-year-old woman presented with acute pancreatitis and new-onset QT prolongation with subsequent torsades de pointes. Coronary catheterization was performed and was unremarkable. After persistent QT prolongation, despite temporary atrial pacing, a permanent dual chamber cardioverter defibrillator was implanted. In addition to the QT prolongation, significant depression in the left ventricular function was noted. Both resolved once the pancreatitis abated. (PACE 2003; 26:1765,1768) [source] COMPARING BALLOON DIAMETER ON PERFORMING ENDOSCOPIC PAPILLARY BALLOON DILATATION WITH ISOSORBIDE DINITRATE DRIP INFUSION FOR REMOVAL OF BILE DUCT STONESDIGESTIVE ENDOSCOPY, Issue 4 2004Hiroshi Nakagawa Background:, Endoscopic papillary balloon dilatation (EPBD) is one of the methods to remove bile duct stones. EPBD might preserve the function of the sphincter of Oddi despite the potential risk of acute pancreatitis. There are only a few reports of EPBD reducing the risk of acute pancreatitis and, at same time, preserving the function of the sphincter of Oddi. Methods:, We performed EPBD for bile duct stone removal in 60 patients using two balloons with different diameters. Patients were randomized to EPBD with a 6 mm balloon (n = 30) or an 8 mm balloon (n = 30). In both groups, isosorbide dinitrate (ISDN) was infused in a rate of 5 mg/h while low pressure EPBD were being performed. The pressure of the sphincter of Oddi was observed before and after the EPBD procedures. Also, serum amylase level after EPBD was observed for both groups. Results:, Serum amylase level of the 6 mm group was signi,cantly higher than that of the 8 mm group (P < 0.05). Acute pancreatitis occurred in two patients ( 6.7%) in the 6 mm group whereas no case was observed for the 8 mm group. The rates of duct clearance were 93% in the 6 mm group and 100% in the 8 mm group. Stone removals were dif,cult in seven cases with 6 mm balloon dilatations due to the narrow ori,ces of the papilla. In the 6 mm group, there was no signi,cant difference between the basal sphincter of Oddi pressure (BSOP) and the phasic sphincter of Oddi pressure (PSOP) before and after EPBD. However in the 8 mm group, the BSOP observed after the EPBD procedure was signi,cantly higher than BSOP before the treatments. Within this group, BSOP values after EPBD were preserved by approximately 80% of the BSOP values before the treatments. In contrast, there was no signi,cant difference in PSOP before and after the treatments. Regarding the stone numbers, no signi,cant difference was observed in BSOP before and after the treatments for the 6 mm group with less than two stones. Also, as for stone size, no signi,cant difference was observed in BSOP before and after the treatments for the 6 mm group with stones of less than 6 mm in diameter. Conclusion:, We are now conducting EPBD with ISDN infusion using a 6 mm balloon for a patient who has less than two stones with size not exceeding 6 mm in diameter. An 8 mm balloon is used for a patient with more than two stones or a stone greater than 6 mm in size. [source] Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitisHPB, Issue 5 2007ANDRE S. MATHEUS Abstract Objective. Acute pancreatitis is one the important causes of systemic inflammatory response syndrome (SIRS). SIRS results in gut barrier dysfunction that allows bacterial translocation and pancreatic infection to occur. Indomethacin has been used to reduce inflammatory process and bacterial translocation in experimental models. The purpose of this study was to determine the effect of inhibition of prostaglandin E2 (PGE2) production on pancreatic infection. Materials and methods. An experimental model of severe acute pancreatitis (AP) was utilized. The animals were divided into three groups: sham (surgical procedure without AP induction); pancreatitis (AP induction); and indomethacin (AP induction plus administration of 3 mg/kg of indomethacin). Serum levels of interleukin (IL)-6 and IL-10, PGE2, and tumor necrosis factor (TNF)-, were measured 2 h after the induction of AP. We analyzed the occurrence of pancreatic infection with bacterial cultures performed 24 h after the induction of AP. The occurrence of pancreatic infection (considered positive when the CFU/g was >105), pancreatic histologic analysis, and mortality rate were studied. Results. In spite of the reduction of IL-6, IL-10, and PGE2 levels in the indomethacin group, TNF-, level, bacterial translocation, and pancreatic infection were not influenced by administration of indomethacin. The inhibition of PGE2 production did not reduce pancreatic infection, histologic score, or mortality rate. Conclusion. The inhibition of PGE2 production was not able to reduce the occurrence of pancreatic infection and does not have any beneficial effect in this experimental model. Further investigations will be necessary to discover a specific inhibitor that would make it possible to develop an anti-inflammatory therapy. [source] Role of diclofenac in reducing post-endoscopic retrograde cholangiopancreatography pancreatitisJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7pt2 2008Manouchehr Khoshbaten Abstract Background and Aims:, Acute pancreatitis following endoscopic retrograde cholangiography presents a unique opportunity for prophylaxis and early modification of the disease process because the initial triggering event is temporally well defined and takes place in the hospital. We report a prospective, single-center, randomized, double-blind controlled trial to determine if rectal diclofenac reduces the incidence of pancreatitis following cholangiopancreatography. Methods:, Entry to the trial was restricted to patients who underwent endoscopic retrograde pancreatography. Immediately after endoscopy, patients were given a suppository containing either 100 mg diclofenac or placebo. Estimation of serum amylase level and clinical evaluation were performed in all patients. Results:, One hundred patients entered the trial, and 50 received rectal diclofenac. Fifteen patients developed pancreatitis (15%), of whom two received rectal diclofenac and 13 received placebo (P < 0.01). Conclusions:, This trial shows that rectal diclofenac given immediately after endoscopic retrograde cholangiopancreatography can reduce the incidence of acute pancreatitis. [source] Pancreatitis associated with Henoch,Schonlein purpuraJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 3 2001KM Cheung Abstract: A 7-year-old Chinese boy presented with acute pancreatitis. The characteristic rash of Henoch,Schonlein purpura (HSP) did not develop until nine days later, together with painful scalp swelling and calf pain. Acute pancreatitis has only rarely been reported in association with HSP and never before as the sole presenting feature. [source] Meta-analysis: nitroglycerin for prevention of post-ERCP pancreatitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2009U. C. BANG Summary Background, Acute pancreatitis after ERCP is a severe side effect. Aim, To evaluate the preventive effect of nitroglycerin on post-ERCP pancreatitis by a meta-analysis of randomized clinical studies. Methods, We searched on Pubmed, Embase, Cochrane Library and all abstracts presented at Digestive Disease Week and United European Gastrointestinal Week from 2004 to 2008. We used the MeSH terms ,pancreatitis' together (AND) with the terms: ,glyceryl trinitrate', ,glyceryl dinitrate', ,isosorbide dinitrate' or ,nitroglycerin'. Results, Five clinical studies evaluating the incidence of post-ERCP pancreatitis after administration of nitroglycerin were identified. Meta-analysis including all five studies showed a relative risk (RR) of 0.61 (95% CI; 0.44, 0.86) with the number needed to treat (NNT) of 26 (95% CI: 16, 82). Three studies evaluated nitroglycerin administered by a dermal patch reaching together an RR of 0.66 (95% CI; 0.43, 1.01). The use of nitroglycerin is associated with a significantly increased risk of hypotension (RR 2.25) and headache (RR 3.64). No difference in mortality was observed. Conclusions, Overall, our meta-analysis supports the use of nitroglycerin in the prevention of post-ERCP pancreatitis, but administration of nitroglycerin by the dermal route, which is the preferred route of administration, did not reach statistical significance. [source] Acute pancreatitis in dogsJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2003Jennifer L. Holm DVM Abstract Objective: To summarize current information regarding severity assessment, diagnostic imaging, and treatment of human and canine acute pancreatitis (AP). Human-based studies: In humans, scoring systems, advanced imaging methods, and serum markers are used to assess the severity of disease, which allows for optimization of patient management. The extent of pancreatic necrosis and the presence of infected pancreatic necrosis are the most important factors determining the development of multiple organ failure (MOF) and subsequent mortality. Considerable research efforts have focused on the development of inexpensive, easy, and reliable laboratory markers to assess disease severity as early as possible in the course of the disease. The use of prophylactic antibiotics, enteral nutrition, and surgery have been shown to be beneficial in certain patient populations. Veterinary-based studies: The majority of what is currently known about naturally occurring canine AP has been derived from retrospective evaluations. The identification and development of inexpensive and reliable detection kits of key laboratory markers in dogs with AP could dramatically improve our ability to prognosticate and identify patient populations likely to benefit from treatment interventions. Treatment remains largely supportive and future studies evaluating the efficacy of surgery, nutritional support and other treatment modalities are warranted. Data sources: Current human and veterinary literature. Conclusions: Pancreatitis can lead to a life-threatening severe systemic inflammatory condition, resulting in MOF and death in both humans and dogs. Given the similarities in the pathophysiology of AP in both humans and dogs, novel concepts used to assess severity and treat people with AP may be applicable to dogs. [source] Pancreatitis in adult orthotopic liver allograft recipients: Risk factors and outcomeLIVER TRANSPLANTATION, Issue 3 2000Deborah J. Verran Acute pancreatitis (AP) has been described after orthotopic liver transplantation but is uncommon in stable patients after the initial perioperative phase. The aim of this study is to review our experience with AP occurring more than 2 months after primary allografting and determine possible contributing factors plus patient outcome. A review of patient files and the unit database was performed. AP was diagnosed in 9 of 298 patients (3%) on 12 occasions. The incidence of AP was greater in men (8 of 163 men) than women (1 of 135 women; P< .04). Underlying factors to each episode of AP were biliary manipulation (4 of 12 episodes; 33%), history of recent alcohol ingestion (3 of 12 episodes; 25%), and malignancy in the region of the pancreas (2 of 12 episodes; 16%). AP was associated with a diagnosis of either hepatic artery thrombosis combined with biliary tract complications (P< .005) or malignancy (P< .004). In 7 of 12 episodes of AP (58%), conservative management alone was successful. In 3 of 9 patients (33%), subsequent surgery was required. One patient died of pancreatic malignancy. In conclusion, AP is uncommon in stable liver transplant recipients. Male sex, complications of hepatic artery thrombosis, and malignancy in the region of the pancreas are associated with AP in this study. [source] Experimental pancreatitis disturbs gastrointestinal and colonic motility in mice: effect of the prokinetic agent tegaserodNEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2007T. C. Seerden Abstract, Acute pancreatitis remains a potentially life-threatening disease associated with gastrointestinal motility disturbances. Prokinetic agents may be useful to overcome these motility disturbances. In this study, we investigated the effect of acute necrotizing pancreatitis (ANP) on gastrointestinal motility in female mice and evaluated the effect of tegaserod, a prokinetic 5-hydroxytryptamine-4 (5HT4) receptor agonist. ANP was induced by feeding mice a choline-deficient ethionine-supplemented diet during 72 h. In vivo intestinal motility was measured as the geometric centre (GC) of 25 glass beads 30-120-360 min after gavage. Colonic peristaltic activity was studied using a modified Trendelenburg set-up. ANP significantly decreased GC 30-120-360 min after bead gavage, associated with a significant increase of myeloperoxidase in the proximal small intestine and colon, but not in the stomach or distal small intestine. Tegaserod significantly ameliorated GC 360 min after bead gavage in control and pancreatitis mice. In isolated colonic segments, ANP significantly decreased the amplitude of peristaltic waves and increased the interval between peristaltic contractions. Tegaserod normalized the disturbed interval. In conclusion, ANP impairs gastric, small intestinal and colonic motility in mice. Tegaserod improves ANP-induced motility disturbances in vivo and in vitro, suggesting a therapeutic benefit of prokinetic 5HT4 receptor agonists in the treatment of pancreatitis-induced ileus. [source] Acute pancreatitis associated with systemic lupus erythematosus: Successful treatment with plasmapheresis followed by aggressive immunosuppressive therapyPEDIATRICS INTERNATIONAL, Issue 1 2008Norio Tominaga No abstract is available for this article. [source] The role of free fatty acids, pancreatic lipase and Ca2+ signalling in injury of isolated acinar cells and pancreatitis model in lipoprotein lipase-deficient miceACTA PHYSIOLOGICA, Issue 1 2009F. Yang Abstract Aim and methods:, Recurrent pancreatitis is a common complication of severe hypertriglyceridaemia (HTG) often seen in patients carrying various gene mutations in lipoprotein lipase (LPL). This study investigates a possible pathogenic mechanism of cell damage in isolated mouse pancreatic acinar cells and of pancreatitis in LPL-deficient and in wild type mice. Results:, Addition of free fatty acids (FFA) or of chylomicrons to isolated pancreatic acinar cells caused stimulation of amylase release, and at higher concentrations it also caused cell damage. This effect was decreased in the presence of the lipase inhibitor orlistat. Surprisingly, pancreatic lipase whether in its active or inactive state could act like an agonist by inducing amylase secretion, increasing cellular cGMP levels and converting cell damaging sustained elevations of [Ca2+]cyt to normal Ca2+ oscillations. Caerulein increases the levels of serum amylase and caused more severe inflammation in the pancreas of LPL-deficient mice than in wild type mice. Conclusion:, We conclude that high concentrations of FFA as present in the plasma of LPL-deficient mice and in patients with HTG lead to pancreatic cell damage and are high risk factors for the development of acute pancreatitis. In addition to its enzymatic effect which leads to the generation of cell-damaging FFA from triglycerides, pancreatic lipase also prevents Ca2+ overload in pancreatic acinar cells and, therefore, counteracts cell injury. [source] ENDOSCOPIC NECROSECTOMY UNDER DIRECT VISION AFTER ENDOSCOPIC ULTRASOUND-GUIDED CYSTGASTROSTOMY FOR ORGANIZED PANCREATIC NECROSISDIGESTIVE ENDOSCOPY, Issue 1 2008Takeshi Hisa A 56-year-old man was referred for an enlarging pancreatic pseudocyst that developed after severe acute pancreatitis with gallstones. Abdominal ultrasound showed a huge cystic lesion with a large amount of solid high echoic components. Arterial phase contrast-enhanced computed tomography scan revealed arteries across the cystic cavity. Stents were placed after endoscopic ultrasound-guided cystgastrostomy; however, the stents were obstructed by necrotic debris, and secondary infection of the pseudocyst occurred. Therefore, the cystgastrostomy was dilated by a dilation balloon, and a forward-viewing endoscope was inserted into the cystic cavity. Many vessels and a large amount of necrotic debris existed in the cavity. Under direct vision, all necrotic debris was safely removed using a retrieval net and forceps. One year after this procedure, there was no recurrence. Our case indicates that peripancreatic fat necrosis can cause exposure of vessels across/along the cystic cavity, and blind necrosectomy should be avoided. [source] OBLIQUE-VIEWING ENDOSCOPE FACILITATES ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY AND ASSOCIATED PROCEDURES IN POST-BILLROTH II GASTRECTOMY PATIENTSDIGESTIVE ENDOSCOPY, Issue 1 2005Masataka Kikuyama Background:, Endoscopic retrograde cholangiopancreatography (ERCP) and associated procedures have been reported to be difficult to perform in patients with Billroth II gastrectomy. We evaluated the feasibility of using an oblique-viewing endoscope equipped with a cannula deflector for these procedures in such patients. Patients and Methods:, Twenty-four patients with Billroth II gastrectomy were enrolled in the present study and underwent ERCP, endoscopic sphincterotomy, endoscopic nasobiliary drainage, expandable metal stent placement or tube stent placement. All procedures were performed with an oblique-viewing endoscope equipped with a cannula deflector. Results:, In all patients, afferent loops were entered. Reaching the papilla of Vater was achieved in 22 (91.7%) patients, in whom all planned procedures were accomplished. One patient experienced acute pancreatitis, hemorrhage from the papilla of Vater after sphincterotomy, and intestinal perforation. Conclusions:, We believe an oblique-viewing endoscope equipped with a cannula deflector to be useful in performing ERCP and associated procedures in many patients with Billroth II gastrectomy. However, one should be aware of major complications, such as perforation, that may occur. [source] COMPARING BALLOON DIAMETER ON PERFORMING ENDOSCOPIC PAPILLARY BALLOON DILATATION WITH ISOSORBIDE DINITRATE DRIP INFUSION FOR REMOVAL OF BILE DUCT STONESDIGESTIVE ENDOSCOPY, Issue 4 2004Hiroshi Nakagawa Background:, Endoscopic papillary balloon dilatation (EPBD) is one of the methods to remove bile duct stones. EPBD might preserve the function of the sphincter of Oddi despite the potential risk of acute pancreatitis. There are only a few reports of EPBD reducing the risk of acute pancreatitis and, at same time, preserving the function of the sphincter of Oddi. Methods:, We performed EPBD for bile duct stone removal in 60 patients using two balloons with different diameters. Patients were randomized to EPBD with a 6 mm balloon (n = 30) or an 8 mm balloon (n = 30). In both groups, isosorbide dinitrate (ISDN) was infused in a rate of 5 mg/h while low pressure EPBD were being performed. The pressure of the sphincter of Oddi was observed before and after the EPBD procedures. Also, serum amylase level after EPBD was observed for both groups. Results:, Serum amylase level of the 6 mm group was signi,cantly higher than that of the 8 mm group (P < 0.05). Acute pancreatitis occurred in two patients ( 6.7%) in the 6 mm group whereas no case was observed for the 8 mm group. The rates of duct clearance were 93% in the 6 mm group and 100% in the 8 mm group. Stone removals were dif,cult in seven cases with 6 mm balloon dilatations due to the narrow ori,ces of the papilla. In the 6 mm group, there was no signi,cant difference between the basal sphincter of Oddi pressure (BSOP) and the phasic sphincter of Oddi pressure (PSOP) before and after EPBD. However in the 8 mm group, the BSOP observed after the EPBD procedure was signi,cantly higher than BSOP before the treatments. Within this group, BSOP values after EPBD were preserved by approximately 80% of the BSOP values before the treatments. In contrast, there was no signi,cant difference in PSOP before and after the treatments. Regarding the stone numbers, no signi,cant difference was observed in BSOP before and after the treatments for the 6 mm group with less than two stones. Also, as for stone size, no signi,cant difference was observed in BSOP before and after the treatments for the 6 mm group with stones of less than 6 mm in diameter. Conclusion:, We are now conducting EPBD with ISDN infusion using a 6 mm balloon for a patient who has less than two stones with size not exceeding 6 mm in diameter. An 8 mm balloon is used for a patient with more than two stones or a stone greater than 6 mm in size. [source] Newly Developed Ultrasonic Probe With Ropeway System for Transpapillary Intraductal Ultrasonography of the Bilio,Pancreatic Ductal SystemDIGESTIVE ENDOSCOPY, Issue 3 2000Naotaka Fujita Background: Intraductal ultrasonography of the bile/pancreatic duct using a thin-caliber ultrasonic probe (IDUS) provides excellent images of these ducts and the surrounding structures. Insertion of the device through the papilla of Vater is essential to carry out this examination. We developed a new probe with a ropeway system (XUM5RG-29R; Olympus, Tokyo) for transpapillary IDUS. Its usefulness such as ease of application and safety were prospectively evaluated. Patients and methods: During the period of October 1997 to April 1998, transpapillary IDUS using the probe was performed in 194 patients at seven medical institutions. The success rates of insertion of the probe into the bile/pancreatic duct, observation of the area of interest, and the incidence of complications were evaluated. Results: Passage of the probe through the papilla was successful without difficulty in all the patients. Successful introduction of the probe into the pancreatic duct, bile duct and both of the ducts was achieved in 98.4, 100 and 85% of the patients, respectively. Once the probe was introduced into the aimed duct, it was possible to obtain IDUS images of the area of interest in all but five patients. Mild acute pancreatitis developed in eight patients (4.1%), all of whom recovered with conservative therapy only. Conclusions: It is possible to introduce the new ultrasonic probe into the desired duct once a guide wire has been inserted. This type of ultrasonic probe is quite useful when performing transpapillary IDUS of the bile and/or pancreatic duct. [source] Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreasGENES TO CELLS, Issue 7 2008Tetsu Yoshida Epiplakin1 (Eppk1) is a plakin family gene with its function remains largely unknown, although the plakin genes are known to function in interconnecting cytoskeletal filaments and anchoring them at plasma membrane-associated adhesive junction. Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice. In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium. Since Pdx1 expression overlapped with that of Sox9 at this stage, these multipotent progenitor cells are Eppk1+/Pdx1+/Sox9+ cells. Then Eppk1 expression becomes confined to Ngn3+ or Sox9+ endocrine progenitor cells, and p48+ exocrine progenitor cells, and then restricted to the duct cells and a cells at birth. In the adult pancreas, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells. Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions. In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model. Furthermore, in the partial pancreatectomy (Px) regeneration model using mice, Eppk1 is expressed in "ducts in foci", a tubular structure transiently induced. These results suggest that Eppk1 serves as a useful marker for detecting pancreatic progenitor cells in developing and regenerating pancreas. [source] Alanine transaminase rather than abdominal ultrasound alone is an important investigation to justify cholecystectomy in patients presenting with acute pancreatitisHPB, Issue 5 2010Kerry Anderson Abstract Objectives:, The aims of this study were to investigate the predictive value of an elevated level of alanine transaminase (ALT) for biliary acute pancreatitis (AP) and to reconsider the role of abdominal ultrasound (AUS). Methods:, All patients admitted to Christchurch Public Hospital with AP between July 2005 and December 2008 were identified from a prospectively collected database. Peak ALT within 48 h of presentation was recorded. Aetiology was determined on the basis of history, AUS and other relevant investigations. Results:, A total of 543 patients met the inclusion criteria. Patients with biliary AP had significantly higher median (range) ALT than those with non-biliary causes (200 units/l [63,421 units/l] vs. 33 units/l [18,84 units/l]; P < 0.001). An ALT level of >300 units/l had a sensitivity of 36%, specificity of 94%, positive predictive value of 87% and positive likelihood ratio of 5.6 for gallstones. An elevated ALT and negative AUS had a probability of 21,80% for gallstones. Conclusions:, An elevated ALT strongly supports a diagnosis of gallstones in AP. Abdominal ultrasound effectively confirms this diagnosis; however, a negative ultrasound in the presence of a raised ALT does not exclude gallstones. In some patients consideration could be given to proceeding to laparoscopic cholecystectomy based on ALT alone. [source] Haemosuccus pancreaticus: diagnostic and therapeutic challengesHPB, Issue 4 2009Velayutham Vimalraj Abstract Background:, Haemosuccus pancreaticus (HP) is a rare cause of upper gastrointestinal bleeding. The objective of our study was to highlight the challenges in the diagnosis and management of HP. Methods:, The records of 31 patients with HP diagnosed between January 1997 and June 2008 were reviewed retrospectively. Results:, Mean patient age was 34 years (11,55 years). Twelve patients had chronic alcoholic pancreatitis, 16 had tropical pancreatitis, two had acute pancreatitis and one had idiopathic pancreatitis. Selective arterial embolization was attempted in 22 of 26 (84%) patients and was successful in 11 of the 22 (50%). Twenty of 31 (64%) patients required surgery to control bleeding after the failure of arterial embolization in 11 and in an emergent setting in nine patients. Procedures included distal pancreatectomy and splenectomy, central pancreatectomy, intracystic ligation of the blood vessel, and aneurysmal ligation and bypass graft in 11, two, six and one patients, respectively. There were no deaths. Length of follow-up ranged from 6 months to 10 years. Conclusions:, Upper gastrointestinal bleeding in a patient with a history of chronic pancreatitis could be caused by HP. Diagnosis is based on investigations that should be performed in all patients, preferably during a period of active bleeding. These include upper digestive endoscopy, contrast-enhanced computed tomography (CECT) and selective arteriography of the coeliac trunk and superior mesenteric artery. Contrast-enhanced CT had a high positive yield comparable with that of selective angiography in our series. Therapeutic options consist of selective embolization and surgery. Endovascular treatment can control unstable haemodynamics and can be sufficient in some cases. However, in patients with persistent unstable haemodynamics, recurrent bleeding or failed embolization, surgery is required. [source] Use of activated protein C has no avail in the early phase of acute pancreatitisHPB, Issue 6 2008Sinan Akay Abstract Objectives. Sepsis and acute pancreatitis have similar pathogenetic mechanisms that have been implicated in the progression of multiple organ failure. Drotrecogin alfa, an analogue of endogenous protein C, reduces mortality in clinical sepsis. Our objective was to evaluate the early therapeutic effects of activated protein C (APC) in a rat model of acute necrotizing pancreatitis. Subjects and method. Acute necrotizing pancreatitis was induced by intraductal injection of 5% Na taurocholate. Hourly bolus injections of saline or recombinant human APC (drotrecogin alfa) was commenced via femoral venous catheter four hours after the induction of acute pancreatitis. The experiment was terminated nine hours after pancratitis induction. Animals in group one (n=20) had a sham operation while animals in group two (n=20) received saline and animals in group three (n=20) received drotrecogin alfa boluses after acute pancreatitis induction. Pancreatic tissue for histopathologic scores and myeloperoxidase, glutathione reductase, glutathione peroxidase, and catalase activites were collected, and blood for serum amylase, urea, creatinine, and inleukin-6 measurements was withdrawn. Results. Serum amylase activity was significantly lower in the APC treated group than the untreated group (17,435±432 U/L vs. 27,426±118 U/L, respectively). While the serum interleukin-6 concentration in the APC untreated group was significantly lower than the treated group (970±323 pg/mL vs. 330±368 pg/mL, respectively). Conclusion. In the early phase of acute pancreatitis, drotrecogin alfa treatment did not result in a significant improvement in oxidative and inflammatory parameters or renal functions. [source] Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitisHPB, Issue 5 2007ANDRE S. MATHEUS Abstract Objective. Acute pancreatitis is one the important causes of systemic inflammatory response syndrome (SIRS). SIRS results in gut barrier dysfunction that allows bacterial translocation and pancreatic infection to occur. Indomethacin has been used to reduce inflammatory process and bacterial translocation in experimental models. The purpose of this study was to determine the effect of inhibition of prostaglandin E2 (PGE2) production on pancreatic infection. Materials and methods. An experimental model of severe acute pancreatitis (AP) was utilized. The animals were divided into three groups: sham (surgical procedure without AP induction); pancreatitis (AP induction); and indomethacin (AP induction plus administration of 3 mg/kg of indomethacin). Serum levels of interleukin (IL)-6 and IL-10, PGE2, and tumor necrosis factor (TNF)-, were measured 2 h after the induction of AP. We analyzed the occurrence of pancreatic infection with bacterial cultures performed 24 h after the induction of AP. The occurrence of pancreatic infection (considered positive when the CFU/g was >105), pancreatic histologic analysis, and mortality rate were studied. Results. In spite of the reduction of IL-6, IL-10, and PGE2 levels in the indomethacin group, TNF-, level, bacterial translocation, and pancreatic infection were not influenced by administration of indomethacin. The inhibition of PGE2 production did not reduce pancreatic infection, histologic score, or mortality rate. Conclusion. The inhibition of PGE2 production was not able to reduce the occurrence of pancreatic infection and does not have any beneficial effect in this experimental model. Further investigations will be necessary to discover a specific inhibitor that would make it possible to develop an anti-inflammatory therapy. [source] Using faecal elastase-1 to screen for chronic pancreatitis in patients admitted with acute pancreatitisHPB, Issue 3 2006R.C. Turner Abstract Background: Patients presenting with acute pancreatitis may have co-existing chronic pancreatitis, the accurate diagnosis of which would potentially guide appropriate management. Gold standard tests are often invasive, costly or time-consuming, but the faecal elastase-1 assay has been shown to be comparatively accurate for moderate and severe exocrine deficiency. This study aimed to evaluate fecal elastase-1 concentration [FE-1] against clinical criteria for chronicity in an acute setting. Patients and methods: [FE-1] was performed on patients admitted with acute onset of epigastric pain and a serum lipase at least three times the upper limit of normal. Clinical diagnosis of chronic pancreatitis was defined by the presence of specific clinical, pathological or radiological criteria. A [FE-1] value of <200 µg/g was similarly considered indicative of chronic exocrine insufficiency. Thus a 2×2 table comparing [FE-1] and clinical diagnosis was constructed. Results: After exclusion of liquid stool specimens, 105 stool specimens from 87 patients were suitable for [FE-1] determination. [FE-1] was evaluated against the clinical diagnosis of chronic pancreatitis, initially for the whole sample, and then after exclusion of cases of moderate and severe acute pancreatitis (Ranson score >2). The latter analysis, based on an exocrine insufficiency threshold of 200 µg/g, yielded a sensitivity of 79.5%, specificity of 98.0%, positive predictive value of 96.9% and negative predictive value of 86.0%. Conclusion: [FE-1] is an accurate screening tool for underlying chronic exocrine insufficiency when taken in the course of a hospital admission for mild acute pancreatitis. [source] Trends in fungal colonization of pancreatic necrosis in patients undergoing necrosectomy for acute pancreatitisHPB, Issue 2 2005N. K. K. KING Abstract Background. This study examines fungal colonization of post-inflammatory pancreatic necrosis in a cohort of patients undergoing open surgical necrosectomy in a single, tertiary referral unit over a 10-year period. Methods. The charts of all patients with acute pancreatitis who underwent surgical necrosectomy during the period January 1992 to December 2001 were examined. Following exclusions a population of 30 patients were identified. There were 18 men with a median (range) age of 42 (20,69) years. Sixteen (53%) underwent surgery because of positive fine needle aspirates and the remainder underwent surgery on clinical grounds. Twenty-nine (97%) received antibiotics prior to necrosectomy. Principal outcomes were the results of microbiological culture with reference to isolation of fungi, site of isolates, trends in colonization and outcome. Results. Candida were cultured from pancreatic necrosis in 5 (17%). These 5 individuals also had positive candidal cultures from sputum or bronchial aspirates. There were no deaths in patients with fungal colonization of necrosis. There was no change in the annual incidence of fungal colonization of necrosis over the study period. Conclusion. Although this is a small study, there are two consistent observations: mortality in fungal colonization of necrosis was low and there was no change in the annual incidence of fungal colonization of necrosis over the decade. Discrepancies between these findings and those of previous reports mandate larger prospective evaluation. [source] Development of colonic stenosis following severe acute pancreatitisHPB, Issue 3 2003F Maisonnette Background Colonic necrosis after acute pancreatitis is rare. When it does occur, it is commonly due to ischaemia or inflammation and may necessitate early colonic resection. Case outline A 72-year-old man developed colonic necrosis 6 weeks after severe acute pancreatitis. CT scan revealed a bulky mass near the left colon. Barium enema and colonoscopy revealed stenosis of the left colonic flexure, and this segment of bowel was successfully resected. Discussion Severe acute pancreatitis must be recognised as a cause of colonic ischaemia and necrosis. The possible pathogenic mechanisms include severe local inflammation and an ischaemic process. This complication is associated with a very poor prognosis despite surgical intervention, but a timely resection may prevent further problems. [source] The role of the intestine in the pathophysiology and management of severe acute pancreatitisHPB, Issue 2 2003RS Flint Background The outcome of severe acute pancreatitis has scarcely improved in 10 years. Further impact will require new paradigms in pathophysiology and treatment. There is accumulating evidence to support the concept that the intestine has a key role in the pathophysiology of severe acute pancreatitis which goes beyond the notion of secondary pancreatic infection. Intestinal ischaemia and reperfusion and barrier failure are implicated in the development of multiple organ failure. Discussion Conventional management of severe acute pancreatitis has tended to ignore the intestine. More recent attempts to rectify this problem have included 1) resuscitation aimed at restoring intestinal blood flow through the use of appropriate fluids and splanchnic-sparing vasoconstrictors or inotropes; 2) enteral nutrition to help maintain the integrity of the intestinal barrier; 3) selective gut decontamination and prophylactic antibiotics to reduce bacterial translocation and secondary infection. Novel therapies are being developed to limit intestinal injury, and these include antioxidants and anti-cytokine agents. This paper focuses on the role of the intestine in the pathogenesis of severe acute pancreatitis and reviews the implications for management. [source] Abdominal compartment syndrome: a new indication for operative intervention in severe acute pancreatitisINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 12 2005K. Wong Summary The current management of severe acute pancreatitis (SAP) is maximal conservative therapy within an intensive care environment. The only commonly accepted indication for operative intervention is the presence of infected pancreatic necrosis. We present a case wherein a laparotomy performed for treatment of abdominal compartment syndrome (ACS) arising in the setting of SAP in the absence of pancreatic necrosis prevented early mortality and discuss the diagnosis and treatment of ACS as a new indication for operative intervention in SAP. [source] Calpain-mediated breakdown of cytoskeletal proteins contributes to cholecystokinin-induced damage of rat pancreatic aciniINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2009Heike Weber Summary The cytosolic cysteine protease calpain is implicated in a multitude of cellular functions but also plays a role in cell damage. Our previous results suggest that an activation of calpain accompanied by a decrease in its endogenous inhibitor calpastatin may contribute to pancreatic damage during cerulein-induced acute pancreatitis. The present study aimed at the time course of secretagogue-induced calpain activation and cellular substrates of the protease. Isolated rat pancreatic acini were incubated with a supramaximal concentration of cholecystokinin (0.1 ,M CCK) for 30 min in the presence or absence of the calpain inhibitor Z-Val-Phe methyl ester (100 ,M ZVP). The activation of calpain and the expression of calpastatin and the actin cytoskeleton-associated proteins ,II-spectrin, E-cadherin and vinculin were studied by immunoblotting. The cell damage was assessed by lactate dehydrogenase release and ultrastructural analysis including fluorescence-labelled actin filaments. Immediately after administration, CCK led to activation of both calpain isoforms, ,- and m-calpain. The protease activation was accompanied by a decrease in the E-cadherin level and formation of calpain-specific breakdown products of ,II-spectrin. A calpain-specific cleavage product of vinculin appeared concomitantly with changes in the actin filament organization. No effect of CCK on calpastatin was found. Inhibition of calpain by ZVP reduced CCK-induced damage of the actin-associated proteins and the cellular ultrastructure including the actin cytoskeleton. The results suggest that CCK-induced acinar cell damage requires activation of calpain and that the actin cytoskeleton belongs to the cellular targets of the protease. [source] Effect of mitogen-activated protein kinases on chemokine synthesis induced by substance P in mouse pancreatic acinar cellsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6 2007Raina Devi Ramnath Abstract Substance P, acting via its neurokinin 1 receptor (NK1 R), plays an important role in mediating a variety of inflammatory processes. Its interaction with chemokines is known to play a crucial role in the pathogenesis of acute pancreatitis. In pancreatic acinar cells, substance P stimulates the release of NF,B-driven chemokines. However, the signal transduction pathways by which substance P-NK1 R interaction induces chemokine production are still unclear. To that end, we went on to examine the participation of mitogen-activated protein kinases (MAPKs) in substance P-induced synthesis of pro-inflammatory chemokines, monocyte chemoanractant protein-1 (MCP-I), macrophage inflammatory protein-l, (MIP-l,) and macrophage inflammatory protein-2 (MIP-2), in pancreatic acini. In this study, we observed a time-dependent activation of ERK1/2, c-Jun N-terminal kinase (JNK), NF,B and activator protein-1 (AP-1) when pancreatic acini were stimulated with substance P. Moreover, substance P-induced ERK 1/2, JNK, NF,B and AP-1 activation as well as chemokine synthesis were blocked by pre-treatment with either extracellular signal-regulated protein kinase kinase 1 (MEK1) inhibitor or JNK inhibitor. In addition, substance P-induced activation of ERK 112, JNK, NF,B and AP-1-driven chemokine production were attenuated by CP96345, a selective NK1 R antagonist, in pancreatic acinar cells. Taken together, these results suggest that substance P-NK1 R induced chemokine production depends on the activation of MAPKs-mediated NF,B and AP-1 signalling pathways in mouse pancreatic acini. [source] Endotoxin translocation in two models of experimental acute pancreatitisJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2003C. Vasilescu Abstract To test the hypothesis that endotoxin is absorbed from the gut into the circulation in rats with experimental acute pancreatitis we studied two different animal models. In the first model necrotizing pancreatitis was induced by the ligation of the disatl bilio-pancreatic duct while in the second, experimental oedematous acute pancreatitis was induced by subcutaneous injections of caerulein. In both experiments, in the colon of rats with acute pancreatitis endotoxin from Salmonella abortus equi was injected. Endotoxin was detected by immunohistochemistry in peripheral organs with specific antibodies. The endotoxin was found only in rats with both acute pancreatitis and endotoxin injected into the colon and not in the control groups. The distribution of endotoxin in liver at 3 and 5 days was predominantly at hepatocytes level around terminal hepatic venules, while in lung a scattered diffuse pattern at the level of alveolar macrophages was identified. A positive staining was observed after 12 hours in the liver, lung, colon and mesenteric lymph nodes of rats with both caerulein pancreatitis and endotoxin injected into the colon. We conclude that the experimental acute pancreatitis leads to early endotoxin translocation from the gut lumen in the intestinal wall and consequent access of gut-derived endotoxin to the mesenteric lymph nodes, liver and lung. [source] | |||||||||||||||||||||||||||||||||||||