Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are a few prospective studies assessing the severity of acute pancreatitis with exclusive criteria for biliary etiology. In a cohort prospective study, Ranson (biliary etiology), Glasgow-modified, APACHE-II, and APACHE-O prognostic criteria were assessed in 65 patients with acute biliary pancreatitis (ABP). Local complications such as necrosis with fluid peripancreatic collection (3 patients), fluid collection with pancreas enlargement (3 patients), pancreatic fistula (1 patients), and pancreatic pseudocyst (1 patients); and organic failure such as renal (5 patients), hemodynamic (3 patients), and respiratory (3 patients) were found. The prognostic criteria performance, according to parameter number or positive variables evidenced that relative risk (RR) varied from 4.7 to 11.2, sensibility from 33.3% to 83.3%, specificity from 79.2% to 98.1%, positive predictive value from 45.0% to 83.3%, negative predictive value from 86.4% to 95.5%, and accuracy from 78.5% to 89.6%. In isolation, most important parameters correlated to severity included white blood cell count >18,000/mm3, lactate dehydrogenase (LDH) >400 UI/l, 10% drop of the hematocrit, serum calcium <8 mg/dl, increase of urea nitrogen >2 mg/dl, aspartate aminotransferase (AST) >200 mg/dl, LDH >600 UI/l, white blood cell count >15,000/mm3, urea >45 mg/dl, arterial pH < or = 7.33 or > or = 7.49, creatinin < or = 0.6 or > or = 1.4, hematocrit < or = 30 or > or = 45.9, white blood cell count < or = 3,000/mm3 or > or = 14,900/mm3. Ranson, Glasgow-modified, APACHE-II, and APACHE-O acute biliary pancreatitis severity criteria all present good sensibility and excellent specificity.
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PMID:Evaluation of Ranson, Glasgow, APACHE-II, and APACHE-O criteria to predict severity in acute biliary pancreatitis. 1199 72

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

Interleukin-6 (IL-6) exerts a wide spectrum of regulatory activities during immune and inflammatory responses. The aim of this study was to investigate the role of endogenous IL-6 in the inflammatory response associated with acute pancreatitis. Acute pancreatitis was induced by hourly (x5) i.p. injections of cerulein (50 microg/kg, suspended in saline solution) in IL-6 deficient mice (IL-6-KO) and wild-type (IL-6WT) littermates. IL-6KO mice exhibited a more severe tissue injury and a higher rate of mortality and when compared to IL-6WT mice. Acute pancreatitis was characterized by edema, neutrophil infiltration, tissue hemorrhage and cell necrosis, upregulation of P-selectin and intercellular adhesion molecule-1 (ICAM-1), as well as increases in the serum levels of amylase and lipase. The degree of oxidative and nitrosative tissue damage was significantly greater in IL-6KO mice than in wild-type littermates, as indicated by higher tissue levels of malondialdehyde and nitrosylated proteins. Plasma levels of the inflammatory cytokines tumour necrosis factor-alpha and interleukin-1beta were also greatly enhanced in IL-6KO mice when compared to wild-type mice. These events were correlated with an increase in the staining (immunoreactivity) for poly (ADP-ribose) polymerase (PARP) in the pancreas of cerulein-treated IL-6WT. The staining for PARP was more pronounced in IL-6KO mice subjected to acute pancreatitis than in the corresponding WT mice. These data demonstrate that endogenous IL-6 exerts an anti-inflammatory role during acute pancreatitis, possibly by regulating the expression of adhesion molecules, the subsequent adhesion and activation of neutrophils and finally the generation of cytokine and reactive oxygen or nitrogen species.
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PMID:Absence of endogenous interleukin-6 enhances the inflammatory response during acute pancreatitis induced by cerulein in mice. 1216 Nov 3

Studies have shown that protein catabolism increases by 80% and energy expenditure by 20% in acute pancreatitis, indicating that nutritional requirements are elevated. Other studies have associated the resolution of negative nitrogen balance by nutrition support with improved outcome. Consequently, the need for effective nutrition is one cornerstone of management of acute pancreatitis. Concerns that feeding may exacerbate the disease process by stimulating the synthesis of proteolytic enzymes in the acinar cell and perpetuating autolysis has led to the widespread use of total parenteral nutrition (TPN) and bowel rest. Unfortunately, the use of TPN in clinical practice has been associated with major metabolic and infective complications, possibly because 1). patients with acute pancreatitis are intolerant of glucose due to coexistent pancreatic endocrine dysfunction and 2). the disease causes immune suppression. This has led to the search for alternatives. Based on physiologic studies, infusion of nutrients into the distal jejunum bypasses the stimulatory effect of feeding on pancreatic secretion. Many controlled trials have compared TPN with jejunal feeding. No study has shown that jejunal feeding exacerbates the disease. Further, jejunal feeding is associated with fewer infectious and metabolic complications. These observations and the fact that enteral feeding is one-tenth the cost of TPN has resulted in the general acceptance of jejunal feeding as the preferred mode for maintaining nutrition in patients with acute pancreatitis.
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PMID:Nutrition support during acute pancreatitis. 1243 14

In this work, a simple isocratic reversed-phase HPLC method for determination of alpha-tocopherol in human erythrocytes has been developed and validated. After separation of plasma the erythrocytes were washed three times with 0.9% sodium chloride containing 0.01% butylated hydroxytoluene (BHT) as antioxidant and then were diluted 1:1 (v/v) with the same solution. In the liquid-liquid extraction (LLE) procedure, 2500 microL of n-hexane was added to 500 microL of erythrocytes. After 2 min this mixture was deproteinized by addition of cool ethanol (500 microL, 5 min) denatured with 5% methanol containing alpha-tocopherol acetate (20 micromol L(-1)), as internal standard, and then extracted for 5 min by vortex mixing. After centrifugation (10 min, 1600xg) an aliquot (2000 microL) of the clean extract was separated and evaporated under nitrogen. The residue was dissolved in 400 microL methanol and analysed by reversed-phase HPLC on a 4.6 mmx150 mm, 5 microm Pecosphere C18 column; the mobile phase was 100% methanol, flow rate 1.2 mL min(-1). The volume injected was 100 microL and detection was by diode-array detector at a wavelength of 295 nm. The extraction recovery of alpha-tocopherol from human erythrocytes was 100.0+/-2.0%. The detection limit was 0.1 micromol L(-1) and a linear calibration plot was obtained in the concentration range 0.5-20.0 micromol L(-1). Within determination precision was 5.2% RSD (n=10), between determination precision was 6.1% RSD (n=10). The method was applied successfully in a clinical study of patients with acute pancreatitis and for determination of the reference values in the healthy Czech population.
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PMID:Development and validation of HPLC method for the determination of alpha-tocopherol in human erythrocytes for clinical applications. 1271 55

Inflammatory response leading to organ dysfunction and failure continues to be the major problem after injury in many clinical conditions such as sepsis, severe burns, acute pancreatitis, haemorrhagic shock, and trauma. In general terms, systemic inflammatory response syndrome (SIRS) is an entirely normal response to injury. Systemic leukocyte activation, however, is a direct consequence of a SIRS and if excessive, can lead to distant organ damage and multiple organ dysfunction syndrome (MODS). When SIRS leads to MODS and organ failure, the mortality becomes high and can be more than 50%. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is a major component of MODS of various aetiologies. Inflammatory mediators play a key role in the pathogenesis of ARDS, which is the primary cause of death in these conditions. This review summarizes recent studies that demonstrate the critical role played by inflammatory mediators such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, platelet activating factor (PAF), IL-10, granulocyte macrophage-colony stimulating factor (GM-CSF), C5a, intercellular adhesion molecule (ICAM)-1, substance P, chemokines, VEGF, IGF-I, KGF, reactive oxygen species (ROS), and reactive nitrogen species (RNS) in the pathogenesis of ARDS. It is reasonable to speculate that elucidation of the key mediators in ARDS coupled with the discovery of specific inhibitors would make it possible to develop clinically effective anti-inflammatory therapy.
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PMID:Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. 1474 96

Leptospirosis, the most common vasculitic zoonosis in the world, is characterized with jaundice and acute renal failure. However, pancreatitis is an uncommon complication of leptospirosis. In this report, an acute pancreatitis case due to Weil's disease has been presented. A 31-year-old female patient with high levels of glucose, blood urea nitrogen, creatinine, creatine kinase, bilirubin, amylase and lipase, has been diagnosed to have leptospirosis by the high positive result (1/800) of microscopic agglutination test against Leptospira interrogans serogroup icterohemorrhagiae. The patient has been treated with supportive and symptomatic therapy, and with penicillin G for leptospirosis. Following triple hemodialysis, all the blood biochemistry tests returned to normal on the tenth day of therapy. This case was reported to draw attention to Leptospira infections which should be considered in the differential diagnosis of patients with jaundice and pancreatitis.
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PMID:[A case of acute pancreatitis due to Weil's disease]. 1474 67

We investigated the effect of alpha-melanocyte stimulating hormone (alpha-MSH) on cerulein induced acute pancreatitis in rats. alpha-MSH treatment (50 microg per rat, intraperitoneally) prior to cerulein reduced the plasma amylase level, pancreatic weight, pancreatic myeloperoxidase activity and the severity of the lesions microscopically. These data suggest that alpha-MSH has a protective effect on cerulein-induced acute pancreatitis and this effect could be attributed, at least in part, to decreased tissue leukocyte infiltration and thus, to decreased pro-inflammatory cytokine production and/or oxygen- and nitrogen-derived reactive metabolite release.
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PMID:Alpha-melanocyte stimulating hormone has beneficial effects on cerulein-induced acute pancreatitis. 1500 65

During the early stages of acute pancreatitis, acute respiratory distress syndrome often occurs. This is associated with the release of proinflammatory mediators into the blood, but it remains unclear why these mediators induce inflammation especially in the lung. One of the first events occurring during the progression of acute pancreatitis is the induction of P-selectin expression in the endothelial cells of the lung. This expression has been associated with the generation of superoxide radicals by circulating xanthine oxidase. Because this enzyme needs molecular oxygen to perform the reaction, we have hypothesized that oxygen present in the alveolar space favors the generation of free radicals by xanthine oxidase and explains why P-selectin is expressed only in the lung. For this purpose, we evaluated the progression of the inflammatory process in rats with induced acute pancreatitis and one lung breathing nitrogen while the other lung continued breathing air. Acute pancreatitis was induced by intraductal administration of taurocholate and myeloperoxidase; P-selectin expression was measured 3 h after induction. Results indicated that, in the absence of oxygen in the alveolar space, the xanthine oxidase-dependent P-selectin expression did not occur and lung inflammation was significantly reduced.
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PMID:Oxygen in the alveolar air space mediates lung inflammation in acute pancreatitis. 1547 15

Reactive oxygen and nitrogen species (ROS and RNS) play an important role in signal transduction and cell injury processes. Nitric oxide synthase (NOS)-the key enzyme producing nitric oxide (NO)-is found in neuronal structures, vascular endothelium and, possibly, in acinar and ductal epithelial cells in the pancreas. NO is known to regulate cell homeostasis, and its effects on the acinar cells are reviewed here. ROS are implicated in the early events within the acinar cells, leading to the development of acute pancreatitis. The available data on ROS/RNS involvement in the apoptotic and necrotic death of pancreatic acinar cells will be discussed.
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PMID:Free radicals and the pancreatic acinar cells: role in physiology and pathology. 1632 97


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