Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our purpose was to determine if cytokines are produced systemically during acute pancreatitis. Proinflammatory cytokines are elevated during acute pancreatitis and have been implicated in the progression of pancreatitis-associated multiple organ dysfunction. Whether these mediators are produced within all tissues or very few specific organs is not known. Edematous pancreatitis was induced in adult male mice by IP injection of cerulein. Necrotizing pancreatitis was induced in young female mice by feeding a choline-deficient, ethionine supplemented diet. Animals were sacrificed as pancreatitis worsened, with multiple organs prepared for tissue mRNA and protein analysis by RT-PCR and immunoblotting. Pancreatitis severity was established by histologic grading and serum amylase and lipase. There was no cytokine mRNA or protein detectable prior to the induction of pancreatitis. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta) mRNA and protein were detected within the pancreas early in the course of pancreatitis in both models, coinciding with the development of hyperamylasemia (both P < 0.001). Interleukin-6 was produced in the pancreas after pancreatitis was more fully developed (P < 0.001). IL-1 beta and TNF-alpha were subsequently produced in large amounts in lung, liver, and spleen but never within kidney, cardiac muscle, or skeletal muscle. A significant delay between pancreatic and distant organ cytokine production was always observed. It is concluded that proinflammatory cytokines are produced within the pancreas and within organs known to develop dysfunction during severe pancreatitis. Cytokine production is tissue specific, correlates with disease severity, and occurs within the pancreas first and subsequently within distant organs.
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PMID:Tissue-specific cytokine production during experimental acute pancreatitis. A probable mechanism for distant organ dysfunction. 928 48

Acute necrotizing pancreatitis (ANP) is an uncommon but serious complication of endoscopic retrograde cholangiopancreatography (ERCP). This study compares the severity, clinical course, and long-term outcome of ERCP-induced ANP with ANP induced by other causes. A review of 72 consecutive patients with ANP treated surgically at the Mayo Clinic identified ERCP as the cause in 6 patients (8%). Compared to the remaining 66 patients, the post-ERCP group had higher APACHE II scores on admission (mean, 13 vs. 10) and more extensive pancreatic necrosis (mean, 55 vs. 47%). The post-ERCP group had a higher rate of infected necrosis (100 vs. 75%) and required earlier necrosectomy after the onset of pancreatitis (9 vs. 13 days). The rate of postoperative pancreatic and enteric fistulae was also higher (50 vs. 33%). Although the mortality rate in the post-ERCP group was lower (17 vs. 29%), they were significantly younger (50 vs. 62 years; p = 0.02) and all the survivors had residual long-term morbidity. ANP is more severe when ERCP-induced; infection introduced during the ERCP may, in part, account for this severity.
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PMID:ERCP-induced acute necrotizing pancreatitis: is it a more severe disease? 933 83

Acute necrotizing pancreatitis is a highly morbid and lethal condition. We performed a retrospective study of all patients admitted to Louisiana State University Medical Center between 1980 and 1995 with a diagnosis of pancreatitis (N = 617) and specifically examined those (N = 26) who developed acute necrotizing pancreatitis. During the period 1980 to 1989, there were 7 patients who progressed to acute necrotizing pancreatitis. Six of these seven patients died (mortality, 86%). These patients were managed with multiple operations for debridement and necrosectomy. The age ranged from 31 to 86 years in this group, with a mean of 58.5. The patients' total hospital days ranged from 2 to 125 days with a mean of 63.5 days. In 1989, we adopted an initial nonoperative approach to necrotizing pancreatitis and began using CT-guided catheter drainage for this condition. During this time period, 19 patients have progressed to necrotizing pancreatitis. The range of hospital days was from 13 to 90 days, with a mean of 43.8 days. There were 2 deaths in this last group, resulting in a mortality rate of 10.5 per cent. All of these patients were treated nonoperatively in the acute phase of their illness. Two patients (15.8%) subsequently underwent laparotomy and drainage when the collections were not amenable to CT-guided drainage. Morbidity in this population approached 70 per cent; however, the mortality was only 10 per cent compared to 86 per cent in the previous group. Although nonoperative therapy has its associated morbidity, and although we understand the controversy surrounding the management of this condition, it appears at least in this population to have much less mortality than those who were treated operatively in the acute phase.
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PMID:Nonoperative therapy for acute necrotizing pancreatitis. 939 62

Activation of cytokine cascade is a decisive factor in determining the pathobiology of different inflammatory processes including acute pancreatitis. The purposes of this study were to determine the TNF and IL-6 levels after the induction of acute necrotizing pancreatitis, and to establish the effects of pentoxifylline on the cytokine production and the severity of pancreatitis. Acute necrotizing pancreatitis was induced by the retrograde injection of 200 microliters taurocholic acid into the pancreatic duct in male Wistar rats. TNF was titrated in a bioassay on cell line WEHI clone 164. IL-6 was measured via its proliferative action on the IL-6 dependent mouse hybridoma cell line B-9. Seven mg/kg pentoxifylline was administered intraperitoneally at the time of operation and/or 24 hours later. Rats were sacrificed, 48 or 72 hours after the operation. The TNF bioassay revealed high levels of TNF (36.6 +/- 6.0 U/ml) in the control group whereas levels decreased to zero in the pentoxifylline-treated group. The IL-6 bioassay likewise demonstrated high levels of IL-6 in the control group and markedly decreased levels in the pentoxifylline treated group (7083 +/- 2844 pg/ml, 6463 +/- 1307 pg/ml vs. 137.5 +/- 85.5 pg/ml, respectively, p < 0.05). The high mortality observed in the control group (43%) was sharply decreased by pentoxifylline administration to 11%. The data suggest that pentoxifylline is capable of modifying the cytokine production after 48 hours of induction of acute pancreatitis.
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PMID:Plasma levels of TNF and IL-6 following induction of acute pancreatitis and pentoxifylline treatment in rats. 940 54

Pancreatitis may be acute or chronic, mild or severe. Acute necrotizing pancreatitis remains the most serious form of acute pancreatitis and accounts for the majority of complications. Although there is an established nomenclature for pancreatitis and pancreatic fluid collections, such as pancreatic pseudocysts, it is not widely understood or recognized by gastroenterologists. Because the management options for the treatment of pancreatic fluid collections continues to evolve with an increased use of endoscopic therapy, gastroenterologists will be increasingly called on to treat patients with pancreatitis and its complications. This article addresses and summarizes pancreatic fluid collections and their management, with an emphasis on endoscopic drainage.
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PMID:Pancreatic fluid collections: diagnosis and endoscopic management. 956 12

Intestinal barrier failure and subsequent translocation of bacteria from the gut play a decisive role in the development of systemic infections in severe acute pancreatitis. Glutamine (GLN) has been shown to stabilize gut barrier function and to reduce bacterial translocation in various experimental settings. The aim of this study was to evaluate whether GLN reduces gut permeability and bacterial infection in a model of acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 50 rats under sterile conditions by intraductal infusion of glycodeoxycholic acid and intravenous infusion of cerulein. Six hours after the induction of pancreatitis, animals were randomly assigned to one of two groups: standard total parental nutrition (TPN) or TPN combined with GLN (0.5 g/kg(-1)/day(-1)). After 96 hours, the animals were killed. The pancreas was prepared for bacteriologic examination, and the ascending colon was mounted in a Ussing chamber for determination of transmucosal resistance and mannitol flux as indicators of intestinal permeability. Transmucosal resistance was 31% higher in the animals treated with GLN- supplemented TPN compared to the animals given standard TPN. Mannitol flux through the epithelium was decreased by 40%. The prevalence of pancreatic infections was 33% in animals given GLN-enriched TPN as compared to 86% in animals receiving standard TPN (P < 0.05). Adding GLN to standard TPN not only reduces the permeability of the colon but decreases pancreatic infections in acute necrotizing pancreatitis in the rat. This confirms previous reports that GLN decreases bacterial translocation by stabilizing the intestinal mucosal barrier. The present findings provide the first evidence suggesting that stabilizing the intestinal barrier can reduce the prevalence of pancreatic infection in acute pancreatitis and that GLN may be useful in preventing septic complications in clinical pancreatitis.
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PMID:Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis. 983 29

Necrotizing pancreatitis is still associated with considerable morbidity and mortality. Formerly, surgical treatment with early and extensive pancreatic resection has been the standard. Improvements in our understanding of the pathogenesis of the disease and progress in the field of intensive care therapy have made conservative therapy the initial standard in the treatment of necrotizing pancreatitis. A considerable percentage of patients with sterile necrosis can be managed with low morbidity and mortality by conservative treatment without operation. Nevertheless, surgical treatment is indicated in patients with infected necrosis and in sterile necrosis if multiorgan failure persists over a limited period of time despite maximum intensive care therapy. Pancreatic resection should be abandoned for surgical treatment of pancreatic necrosis, as results with regard to morbidity, mortality and long-term outcome are unsatisfactory. Today the surgical standard is careful digital necrosectomy, which must be followed by either postoperatve drainage, repeated open lavage or continuous closed lavage. In experienced hands, all three procedures provide similar results with regard to morbidity and mortality.
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PMID:[Necrosectomy or anatomically guided resection in acute pancreatitis]. 1078 44

Heat-shock proteins (HSPs) function in the cellular response to injury. Increased expression of these proteins was first described in response to hyperthermia, although their production may be prompted by a variety of metabolic insults. HSPs protect cellular proteins from degradation. The self-limited pancreatitis induced by hyperstimulation with supramaximal doses of cerulein is accompanied by increased HSP expression. It may be that HSPs serve a protective function in pancreatitis. We hypothesized that hyperthermia-induced production of HSP-70 would improve survival in a lethal murine model of necrotizing pancreatitis. Necrotizing pancreatitis was induced in two groups of 30 female Swiss Webster mice by feeding them a choline-deficient diet supplemented with 0.5 g% ethionine (CDE) for 72 hours. Immediately before initiation of the CDE diet, the core body temperatures of the mice in the experimental group were elevated to 42 degrees C for 12.5 minutes. Twenty mice from each group were killed after 24 hours. Pancreata were harvested, and pancreatic proteins were extracted from half of the pancreata. HSP-70 was assessed according to a standard Western blotting protocol. The remaining pancreata were used to make histologic comparisons. Serum interleukin 6 and tumor necrosis factor-alpha were determined by enzyme-linked immunosorbent assay (ELISA). Survival was determined by observation of the remaining mice. HSP-70 was expressed in pancreatic protein from all mice exposed to hypothermia but in none of the mice subjected to the CDE diet alone. Mortality was significantly reduced in mice pretreated with hyperthermia compared with control mice (p < 0.05). Survival in the hyperthermia group was 80%, whereas in the control group it was 30%. Hyperthermia resulted in expression of pancreatic HSP-70 in mice. Hyperthermia also reduced mortality in this lethal murine model of necrotizing pancreatitis. It is plausible that a causal relationship exists between HSP-70 production and improved survival in this model.
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PMID:Hyperthermia induces heat-shock protein expression, reduces pancreatic injury, and improves survival in necrotizing pancreatitis. 1097 4

Acute necrotising pancreatitis is the most serious form of acute pancreatitis and accounts for the majority of complications. Treatment of patients with pancreatic necrosis is still controversial. There is a well-established definition for acute pancreatitis and consequent pancreatic fluid collections. However, it has been identified a group of patients who represent a separate entity and whose collections may prompt additional change from the definition of acute pancreatitis. Imaging investigations in these patients have well defined subacute collections that evolve from severe acute necrotising pancreatitis involving greater than 30% of the gland. Although these collections are not completely liquefied, they do not meet criteria for pseudocysts, however, at the same time, they are morphologically different from acute pancreatic necrosis seen during initial presentation of acute pancreatitis. It has been used to call "subacute" these collections of necrotic pancreatic tissue or "subacute pancreatic necrosis". The purpose of this review is to summarise the subacute collections of necrotic pancreatic tissue and its complications, discussing treatment options of the complex pancreatic and peripancreatic collections found in these patients, focusing on the management of subacute pancreatic necrosis.
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PMID:Subacute pancreatic necrosis. 1129 92

Necrotizing pancreatitis still remains a life-threatening disease despite several improvements in diagnosis, prevention and treatment. In recent years, some important questions have been answered such as the need for early intensive medical treatment rather than early surgery, but others are still strongly debated. The aim of this paper is to present an up-to-date assessment of current challenges in the management of necrotizing pancreatitis in order to prevent infection.
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PMID:Infection prevention in necrotizing pancreatitis: an old challenge with new perspectives. 1151 78


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