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

The glycogen storage disorders (GSD)-I, -III, -VI and -VIII are associated with hypertriglyceridaemia or mixed hyperlipidaemia which poses the question whether these patients have an increased risk for atherosclerosis. The atherogenicity of triglycerides has remained controversial, while increased plasma cholesterol levels are generally accepted as a significant risk factor for coronary heart disease. However, clinical data show that one has to differentiate between metabolic conditions where triglycerides are atherogenic and those which are not significantly related to early onset of atherosclerosis but may cause other disorders such as pancreatitis. Among the disorders of carbohydrate metabolism patients with diabetes mellitus frequently have enhanced plasma triglycerides associated with a higher risk for coronary heart disease, while patients with certain types of glycogen storage disease have high triglyceride levels but do not seem to have an enhanced risk for atherosclerosis. Here we have compared the biochemical abnormalities and the atherogenic risk of three different disorders of glucose metabolism including GSD-I (glucose-6-phosphatase deficiency), favism (glucose-6-phosphate dehydrogenase deficiency), and diabetes mellitus which are related to either hyper- or hypolipidaemia. The available data indicate that glucose-6-phosphate (Glc-6-P) is a central molecule in cellular glucose metabolism which critically influences pentose phosphate cycle activity and, via NADPH2-generation, regulates glutathione peroxidase activity for radical detoxification and also cholesterol and triglyceride synthesis. Radical detoxification is a major protective factor for cell membrane integrity and together with an appropriate renewal of membrane lipids may protect against the development of atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose-6-phosphate: a key compound in glycogenosis I and favism leading to hyper- or hypolipidaemia. 831 30

Bradykinin mediates the inflammatory process of acute pancreatitis characterized by an increase of microvascular permeability, vasodilation and leukocyte activation. These phenomena are characteristic also for the ischemia/reperfusion injury of the pancreas, which in time is considered a causative factor in the pathogenesis of acute pancreatitis. The aim of this study was to investigate the influence of the bradykinin B2 receptor antagonist CP-0597. After complete ischemia/reperfusion of the pancreas in rats there is progression from postischemic acute edema to necrotizing pancreatitis over a reperfusion period of 5 days. In 8 Sprague-Dawley rats (treatment group) 18 micrograms/kg/h CP-0597 was administered intraperitoneally over 5 days with an osmotic minipump starting 15 min before release of 2 h ischemia. Animals of the placebo group (n = 8) were identically treated, but received the solvent, phosphate buffer. Animals of a control group (n = 7) underwent sham operation without ischemia. After 5 days the animals were sacrificed for histology. No morphological changes of the pancreatic gland were observed in the control group. Ischemia for 2 h resulted in necrotizing pancreatitis with high mortality (4/8 animals) during the reperfusion period of 5 days. In contrast, all animals in the treatment group survived without clinical or histological signs of necrotizing pancreatitis.
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PMID:The bradykinin antagonist CP-0597 can limit the progression of postischemic pancreatitis. 885 57

Despite being a common disease in humans, little is known about the etiopathogenesis of and effective therapeutic approaches to chronic pancreatitis, due mainly to the fact that few simple animal models suitable to study inflammatory and fibrogenetic processes have been described in the pancreas. Trinitrobenzene sulfonic acid (TNBS) induces chronic colitis and cholangitis in the rat. We hypothesized that TNBS instillation into the pancreatic ducts could also result in the development of a chronic pancreatic disease. The biliopancreatic duct of rats was cannulated and tied close to the liver. TNBS [0.4 ml of 2% TNBS in phosphate-buffered saline (PBS)-10% ethanol, pH 8] was infused into the pancreas under a continuous controlled-pressure system. Control rats underwent the same procedure using vehicle only. Pathology assessment of TNBS-treated rats examined at 48 h was consistent with severe acute necrotizing pancreatitis, having a morality rate of 31% and serum amylase activity of 37.4 +/- 8.8 U/ml at 24 h and 13.3 +/- 1.7 U/ml at 48 h (p < 0.01 for both time points compared to PBS/ethanol-treated rats). Groups of 10 rats each were killed at 3, 4, and 6 week after the surgical procedure. Morphological examination revealed changes mimicking features of chronic pancreatitis in humans in 80% (32 of 40) of TNBS-treated rats, consisting in various degrees of periductal and lobular fibrosis, duct stenosis, patchy acute and chronic inflammatory cell infiltrates, and signs of gland atrophy. Animals developing chronic disease had a weight gain rate significantly lower than that of control rats. Serum amylase, fasting glucose, and a glucose tolerance test were not different in diseased or control rats. In conclusion, we were able to induce chronic fibrogenetic inflammatory disease in the pancreas after a single pulse instillation of TNBS into the pancreatic ducts. This might be a useful animal model to study the pathophysiology of inflammatory, fibrogenetic, and reparative processes in pancreatic tissue.
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PMID:Induction of chronic pancreatic disease by trinitrobenzene sulfonic acid infusion into rat pancreatic ducts. 933 99

We studied the pancreatic high-energy phosphates in two models of acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo. Alcoholic pancreatitis was induced by acute ethanol intoxication and an obstruction-hyperstimulation mechanism. Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10% taurocholate-Na+. In addition to the obligate control groups, a simple ischemia experiment was performed. The high-energy phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of taurocholate showed an increase in inorganic phosphate with a concomitant decrease in ATP levels, similar to pancreatic ischemia. This irreversible decrease was accompanied histologically by severe pancreatic hemorrhage. After induction of alcoholic acute pancreatitis a reversible decrease in ATP was occasionally seen. Even when alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy phosphates seems to occur as a result of pancreatic cell death rather than being a cause of pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in acute pancreatitis.
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PMID:Different changes in high-energy phosphates in alcoholic acute pancreatitis and taurocholate acute pancreatitis in rats using NMR spectroscopy at 2.0 T. 936 Oct 88

Intra-acinar cell activation of digestive enzyme zymogens including trypsinogen is generally believed to be an early and critical event in acute pancreatitis. We have found that the phosphatidylinositol 3-kinase inhibitor wortmannin can reduce the intrapancreatic activation of trypsinogen that occurs during two dissimilar experimental models of rodent acute pancreatitis, secretagogue- and duct injection-induced pancreatitis. The severity of both models was also reduced by wortmannin administration. In contrast, the NF-kappa B activation that occurs during the early stages of secretagogue-induced pancreatitis is not altered by administration of wortmannin. Ex vivo, caerulein-induced trypsinogen activation is inhibited by wortmannin and LY294002. However, the cytoskeletal changes induced by caerulein were not affected by wortmannin. Concentrations of caerulein that induced ex vivo trypsinogen activation do not significantly increase phosphatidylinositol-3,4-bisphosphate or phosphatidylinositol 3,4,5-trisphosphate levels or induce phosphorylation of Akt/PKB, suggesting that class I phosphatidylinositol 3-kinases are not involved. The concentration of wortmannin that inhibits trypsinogen activation causes a 75% decrease in phosphatidylinositol 3-phosphate, which is implicated in vesicle trafficking and fusion. We conclude that a wortmannin-inhibitable phosphatidylinositol 3-kinase is necessary for intrapancreatic activation of trypsinogen and regulating the severity of acute pancreatitis. Our observations suggest that phosphatidylinositol 3-kinase inhibition might be of benefit in preventing acute pancreatitis.
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PMID:Phosphatidylinositol 3-kinase-dependent activation of trypsinogen modulates the severity of acute pancreatitis. 1169 67

Estramustine phosphate is associated with estrogenic complications. However, hypertriglyceridemia has not yet been associated with estramustine phosphate. We describe a patient in whom severe hypertriglyceridemia and pancreatitis developed after treatment with estramustine phosphate. A 59-year-old man with hormone-refractory prostate cancer was treated with estramustine phosphate, docetaxel, and carboplatin. After three cycles, the patient was admitted with triglyceride levels of 12,210 mg/dl and pancreatitis. After resolution of hypertriglyceridemia and pancreatitis, chemotherapy with docetaxel and carboplatin was continued without recurrence of hypertriglyceridemia. We conclude that estramustine phosphate has the potential to cause hypertriglyceridemia in susceptible individuals.
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PMID:Hypertriglyceridemia and pancreatitis associated with estramustine phosphate. 1215 61

The objective of this study was to determine whether laboratory testing currently available is able to provide prognostic information in canine pancreatitis. A prospective study of dogs with naturally occurring pancreatitis was undertaken. Twenty-two cases with histologically confirmed pancreatic inflammation were included in the study. Each dog had routine haematology parameters, serum biochemistry (including lipase and amylase), serum trypsin-like immunoreactivity and trypsinogen activation peptides (TAP) in urine and plasma measured. Twelve of the dogs were classified as having severe disease. These dogs had statistically significant increases in urinary TAP-creatinine ratio (UTCR) measurement, serum lipase, serum phosphate and serum creatinine concentrations. Additionally dogs with severe pancreatitis had significantly decreased urine specific gravity levels. The most sensitive and specific test to assess the severity of pancreatitis was the measurement of UTCR.
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PMID:Assessing the severity of canine pancreatitis. 1258 38

The hallmark of acute hypocalcemia (ionized calcium <0.75 mmol/l) is tetany, which is characterized by neuromuscular irritability. The symptoms may be mild with circumoral numbness, paresthesias of hands and feet, and muscular cramps or severe with laryngospasm, focal or generalized tonic muscle cramps, or seizures. Myocardial dysfunction and prolongation of QT interval also may occur. Most often, acute hypocalcemia occurs after thyroid or parathyroid surgery. Rarer cases are intravascular binding of ionized calcium by phosphate, citrate, or drugs such as foscarnet or bisphosphonates. The most appropriate treatment is intravenous calcium, in the form of 100-200 mg of elemental calcium. Thereafter, the therapy depends on the underlying disease. In most cases vitamin D has to be added to calcium substitution. In cases of hypomagnesemia, magnesium and not calcium has to be substituted. It has not yet been proven in clinical trials whether substitution of magnesium and/or calcium influences the clinical outcome in patients with severe sepsis or pancreatitis who show both hypomagnesemia and hypocalcemia.
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PMID:[Tetany]. 1468 85

The release of the immunomodulator, interleukin 18 (IL-18) into sera early in acute pancreatitis (AP) corresponds to disease severity. IL-18 induces nitric oxide (NO), which is involved in the pathophysiology of pancreatitis. The objective of this study was to clarify the role of IL-18 in pathogenesis and NO production during early AP using recombinant mouse (rm) IL-18 protein and IL-18 gene knockout (KO) mice. After pretreatment with phosphate-buffered saline or rmIL-18, wild-type (WT) or KO mice were injected intraperitoneally with phosphate-buffered saline (sham) or cerulein (AP) hourly for 3 h. Blood, pancreas, spleen, and liver were collected until 24 h after the first dose. Main outcome measures were serum IL-18, amylase and lipase levels, histological evaluation of the pancreas with parenchyma vacuolization of acinar cells, mRNA expression of inducible NO synthase (iNOS) in the pancreas, and spleen, liver, and plasma NO metabolite level. Serum IL-18 was significantly increased immediately after induction of AP in WT mice. Serum amylase, lipase, and the numbers of acinar cells with parenchyma vacuolization were significantly higher in the group AP/KO than in the group AP/WT, but these parameters were improved by dose-dependent pretreatment with rmIL-18 administration in both groups. Pancreatic iNOS gene expression and plasma NO metabolites were significantly increased by 6 h after the initiation of AP, but were significantly lower in the group AP/KO than in the AP/WT mice. Pretreatment with rmIL-18 also significantly increased these levels in both groups. Splenic and hepatic iNOS expression was not changed after the initiation of AP in WT mice, whereas pretreatment with rmIL-18 also increased these levels. Administration of aminoguanidine, a selective iNOS inhibitor, before AP induction abolished the protective effect of pretreatment with rmIL-18 on pancreatic injury. IL-18 appears to protect the pancreas during early induced-induced AP in mice, probably through induction of NO release from an iNOS source. IL-18 may be a target for new AP therapeutics.
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PMID:Role of interleukin 18 in nitric oxide production and pancreatic damage during acute pancreatitis. 1631 88

Severe hypophosphatemia (<1.0 mg/dl) is a rarely reported complication of acute pancreatitis; when it does occur, it is typically attributed to alcohol abuse rather than the pancreatitis itself (1-5). In the literature, pancreatitis is not cited as a cause of hypophosphatemia (5, 6-16). Both pancreatitis and hypophosphatemia have widespread ramifications on human physiology, affecting hematologic, neural, hepatic, endocrine, respiratory, and renal systems. Given the possible synergistic consequences of pancreatitis and low serum phosphate, we emphasize the importance of recognizing hypophosphatemia as a complication of pancreatic inflammation.Herein, we report a case of acute pancreatitis unrelated to alcohol abuse associated with severe hypophosphatemia and review the pathophysiology.
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PMID:Severe hypophosphatemia associated with gallstone pancreatitis: a case report and review of the literature. 1664 27


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