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

Two cases of pancreatitis induced by autoimmunity with PET images using F-18 fluoro-2-deoxy-D-glucose (FDG) are reported. The patients had abdominal pain and were thought to have possible pancreatic neoplasms. In one patient, PET showed intense uptake of the entire pancreas, but a Ga-67 scan yielded a negative result. Because the serum immunoglobulin G level was high, autoimmune pancreatitis was diagnosed in this patient. He underwent steroid therapy and fully recovered. In another patient with positive antinuclear antibodies and hyperglobulinemia, focal intense uptake was found in the head of the pancreas on the FDG PET. She also recovered with steroid therapy. Autoimmune pancreatitis is a relatively new form of chronic pancreatitis and should be kept in mind when making a differential diagnosis of pancreatic cancer with the assistance of FDG PET.
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PMID:Autoimmune pancreatitis with F-18 fluoro-2-deoxy-D-glucose PET findings 1051 4

The alterations that progressively appear in plasma membrane glycoconjugates of rat pancreatic cells at different stages of acute pancreatitis induced by duct obstruction have been analyzed on individual cells by flow cytometry using the fluoresceinated lectins, wheat germ agglutinin (WGA), Tetragonolobus purpureus agglutinin (TP) and Concanavalin A (Con A), which specifically bind to N-acetyl D-glucosamine, L-fucose and D-mannose, respectively. Two populations of pancreatic cells were differentiated according to the forward scatter (size), which showed different density of saccharidic terminals located at external positions in the glycoconjugates of the plasma membrane. A significant increase in WGA and TP binding was found 1.5 h after pancreatic obstruction, which could be due to the fusion of zymogen granules with the plasma membrane as suggested by the basolateral exocytosis observed by electron microscopy at this stage. The most external sugar residues of membrane glycoconjugates are removed 12 h after pancreatic duct obstruction as a consequence of an advanced state of pancreatitis. The hydrolytic process reaches greater depths in the membrane 48 h after obstruction. At this stage a significant decrease in WGA, TP and ConA binding was found in all pancreatic cells, indicating the loss of N-acetyl D-glucosamine and/or sialic acid, L-fucose and even D-mannose which is located in the core of the glycan. The results provide information about the progressive degradation induced by acute pancreatitis in pancreatic cell membrane glycoconjugates.
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PMID:Alterations in the glycoconjugates of pancreatic cell membrane induced by acute pancreatitis. 1071 27

Chronic alcohol ingestion appears to increase susceptibility of the pancreas to pancreatitis through multiple mechanisms. The aim of the current study was to determine the effect of chronic low- and high-dose alcohol consumption on the neurohormonal control of the exocrine pancreas in rats. Male Wistar rats were fed Lieber DeCarli liquid control-, low-, and high-dose alcohol diets for 3 months. Pancreatic exocrine secretion was measured under basal and 2-deoxy-D-glucose (2-DG)-, CCK-, bethanechol-, or meal-stimulated conditions while on chronic alcohol diets and after 2-DG or CCK stimulation during alcohol withdrawal in awake rats. Chronic alcohol ingestion was associated with a dose-related inhibition of basal pancreatic protein secretion, which was reversed upon alcohol withdrawal. Low-dose alcohol feeding had no effect on bethanechol-stimulated pancreatic secretion but altered 2-DG-stimulated pancreatic secretion. In chronic high-dose alcohol rats, meal- and bethanechol-stimulated protein secretion was significantly potentiated during early and late phases. The response to CCK appeared to be disinhibited, whereas the response to 2-DG was uniformly blunted. Upon withdrawal of low-dose alcohol, the response to 2-DG was potentiated, whereas with the withdrawal of high-dose alcohol, the response to CCK was potentiated. Adaptation to chronic alcohol consumption differs depending on the alcohol dose. The most significant effects were seen after high-dose alcohol withdrawal, with apparent loss of central inhibitory regulation combined with exaggerated response at the acinar cell level. This combination of factors could increase susceptibility to acute alcoholic pancreatitis through a hyperstimulation mechanism.
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PMID:Chronic alcohol-induced alterations in the pancreatic secretory control mechanisms. 1525 3

The literature considers hyperthermic intraoperative intraperitoneal chemotherapy a safe and effective procedure for peritoneal carcinomatosis, but a technical improvement is necessary. Regional chemotherapy anticipates the "downfall" of tumoral cells in the peritoneum. The Authors considered 5 patients--female, age 27-45 years, ASA 2--operated of peritonectomy in ovaric neoplasia with peritoneal metastasis. The hyperthermic intraoperative intraperitoneal chemotherapy has been made at the end of the surgery with a hot solution (43 degrees C): 3000 ml of dextrose 1.5% with mytomicina C 25 mg e cysplatino 75 mg/m2. We considered variation of emodinamic parametres (blood pressure, central venous pressure, stroke volume, etc.) and biochemical parametres (Na, K, CI-, CO2, etc.). These parametres have been correlated with some complications: fistula, anastomotic leakage, pancreatitis and postoperative bleeding.
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PMID:[Anaesthesiologic problems about hyperthermic intraoperative intraperitoneal chemotherapy]. 1575 60

Acute inflammatory response is a complex process associated with the production of both pro- and anti-inflammatory mediators. Although it is generally considered to be a single homeostatic mechanism, there are differences associated with the nature and the site of inflammation. We examined the changes of N-linked glycans released from the serum of a patient with sepsis and a patient with acute pancreatitis during the first eight days of the disease. Sera were taken from patients at the time of reporting to hospital and then three more times. The blood from a healthy individual was drawn on one occasion only. Glycans were released using N-glycosidase F and were subjected to normal phase and weak anion exchange high-performance liquid chromatography, exoglycosidase digestions, and mass spectrometry. The levels of identified structures have been followed through the course of disease and compared to the control levels. Changes in serum glycans were found to occur very early in acute inflammation. The most prominent differences include the increase in ratio of outer arm to core fucose, increase in the amount of tetrasialylated structures, changes in the levels of mannose structures, and in the degree of branching. The relative proportions of different glycans changed daily and some differences were also observed between sepsis and pancreatitis, probably reflecting that in these two conditions, the acute phase response is triggered by a different stimulus that is associated with different patterns of production of cytokines.
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PMID:Changes of serum glycans during sepsis and acute pancreatitis. 1794 56

Previously we showed that oxidative stress induces apoptosis of pancreatic acinar cells with nuclear loss of DNA repair proteins. Oxidative stress has an important role in the pathogenesis of pancreatitis. Pancreatitis-associated protein 1 (PAP-1) is a protein secreted upon induction of acute pancreatitis. In this study, we investigated the role of PAP-1 on oxidative stress-induced cell death of pancreatic acinar AR42J cells. AR42J cells were transfected with or without full-length sense cDNA of PAP-1 (PAP-1 S cDNA) or antisense cDNA of PAP-1 (PAP-1 AS cDNA) and received oxidative stress caused by glucose oxidase acting on beta-D-glucose, glucose/glucose oxidase. PAP-1 mRNA expression and cell viability were determined. As a result, oxidative stress induced PAP-1 mRNA expression in AR42J cells in a time-dependent manner. Cell viability decreased with the concentration of glucose oxides delivered to the cells that had received glucose. Oxidative stress-induced PAP-1 expression was augmented in the cells transfected with PAP-1 S cDNA compared with wild-type cells or cells transfected with control vector pcDNA. PAP-1 induction by oxidative stress decreased in the cells transfected with PAP-1 AS cDNA. Cell death caused by oxidative stress was inhibited in the cells transfected with PAP-1 S cDNA, but it increased in the cells transfected with PAP-1 AS cDNA. These results indicate that PAP-1 may be a defensive gene for oxidative stress-induced cell death of pancreatic acinar cells.
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PMID:Role of pancreatitis-associated protein 1 on oxidative stress-induced cell death of pancreatic acinar cells. 1972 2

Heparin and/or insulin stimulate lipoprotein lipase and are known to decrease serum triglyceride level. However, their efficacy in hypertriglyceridemia-induced acute pancreatitis in nondiabetic patients is not well documented. We report a case of hypertriglyceridemia-induced pancreatitis in 43-year-old nondiabetic woman in whom treatment with insulin was accompanied by reduction in serum triglyceride level and the resolution of pancreatitis. She presented to the emergency department with abdominal pain and biochemical evidence of acute pancreatitis. Her medical history was unremarkable. There was no history of alcohol consumption, and biliary imaging was not remarkable. Subsequent laboratory investigation revealed marked hypertriglyceridemia (1,951 mg/dL), impaired fasting glucose, and normal HbAlc level. The Ransons score and APATCH II score were 1 and 4. Abdominal CT showed diffuse enlargement of pancreas, peripancreatic fat infiltration, and multiple fluid collections around the pancreas. We treated the patient with the infusion of 5% dextrose and 1.5 unit/hr regular insulin to reduce serum triglyceride level. The level of serum triglyceride was decreased to 305 mg/dL on day 5. During the remainder of hospitalization, her clinical symptoms and laboratory values gradually improved.
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PMID:[Hypertriglyceridemia-induced pancreatitis treated with insulin in a nondiabetic patient]. 2057 9

The lysosomal protease cathepsin B is thought to play a crucial role in the intracellular activation cascade of digestive proteases and in the initiation of acute pancreatitis. Although cathepsin B has been shown to be physiologically present in the secretory pathway of pancreatic acinar cells it has been suggested that premature activation of zymogens requires an additional redistribution of cathepsin B into the secretory compartment. Here, we studied the role of cathepsin B targeting during caerulein-induced pancreatitis in mouse mutants lacking the cation-independent mannose 6-phosphate/insulin-like growth factor II receptor (CI-MPR) which normally mediates the trafficking of cathepsin B to lysosomes. Absence of the CI-MPR led to redistribution of cathepsin B to the zymogen granule enriched subcellular fraction and to a substantial formation of large cytoplasmic vacuoles that contained both, trypsinogen and cathepsin B. However, this did not cause premature intracellular trypsin activation in saline-treated control animals lacking the CI-MPR. During caerulein-induced pancreatitis, trypsinogen activation in the pancreas of CI-MPR-deficient animals was about 40% higher than in wild-type animals but serum amylase levels were reduced and lung damage was unchanged. These data suggest that subcellular redistribution of cathepsin B, in itself, induces neither spontaneous trypsinogen activation nor pancreatitis. Furthermore, we clearly show that a marked increase in intracellular trypsinogen activation is not necessarily associated with greater disease severity.
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PMID:Missorting of cathepsin B into the secretory compartment of CI-MPR/IGFII-deficient mice does not induce spontaneous trypsinogen activation but leads to enhanced trypsin activity during experimental pancreatitis--without affecting disease severity. 2108

This review considers drug combinations and newer treatment strategies for patients with severe hypertriglyceridemia. Hypertriglyceridemia is associated with an atherogenic metabolic profile and in most studies with increased cardiovascular disease risk. Patients with severe hypertriglyceridemia also have increased incidence of pancreatitis. All types of severe hypertriglyceridemia are associated with a reduction in lipoprotein lipase activity. Patients with severe hypertriglyceridemia and abdominal pain or pancreatitis should be hospitalized and treated with hypolipidemic drugs and, if needed, with insulin/dextrose infusion or therapeutic apheresis. Fibrates are the first-line treatment in patients with severe hypertriglyceridemia. Omega-3 fatty acids and niacin are very useful drugs for patients with hypertriglyceridemia. Statins in high doses exhibit a significant hypotriglyceridemic activity. Drugs that interfere with chylomicron production such as orlistat are also useful for hypertriglyceridemic patients. In most patients with severe hypertriglyceridemia drug combinations are needed to maintain an acceptable triglyceride concentration. Gene therapy is under development for patients with known genetic abnormalities of triglyceride metabolism. Clinicians should be vigilant for the recognition and prompt treatment of patients with severe hypertriglyceridemia aimed to avoid the serious complication of pancreatitis and to reduce their cardiovascular risk.
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PMID:Recommendations for severe hypertriglyceridemia treatment, are there new strategies? 2362 80

Lipoprotein apheresis is applied to deplete low density lipoprotein and other apolipoprotein B containing lipoproteins in patients with severe familial hypercholesterolemia, hypertriglyceridemia associated pancreatitis, or lipoprotein (a)-hyperlipoproteinemia. Anticoagulation of the extracorporeal circuit may influence cellular activation, as evidenced by a reduction of inflammatory parameters during regional citrate anticoagulation with acid citrate dextrose A (ACD-A) commonly used in whole blood lipid apheresis. While the citrate concentration in the extracorporeal circuit has to ensure efficient anticoagulation, citrate infusion into the patient should be limited to avoid citrate overload. We assessed the influence of citrate concentration on cellular activation during in vitro circulation of whole blood containing 2.8 mM citrate (ACD-A 1:40), 5.6 mM citrate (ACD-A 1:20), or 13 mM citrate over polyacrylate-based adsorbents for lipoprotein apheresis. We found increased platelet adhesion for anticoagulation with 2.8 mM citrate as compared to 5.6 or 13 mM citrate, as shown by cell counting and confirmed by scanning electron microscopy of adsorbent beads as well as by elevated levels of platelet activation markers and of platelet-derived microvesicles. Leukocytes showed an equivalent adhesion pattern, while red blood cells remained unaffected at all citrate concentrations. Passage of blood over two consecutive columns resulted in enhanced platelet adhesion to the second column, presumably due to upstream preactivation. In conclusion, citrate influences activation and adhesion of platelets and leukocytes in a concentration-dependent manner, and ACD-A 1:20, equivalent to a citrate concentration of 5.6 mM in whole blood, ensures minimal cellular activation during passage of whole blood over polyacrylate-based adsorbents.
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PMID:The impact of citrate concentration on adhesion of platelets and leukocytes to adsorbents in whole blood lipoprotein apheresis. 2785 40


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