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Query: UMLS:C0001339 (acute pancreatitis)
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This paper reviews the current practice of nutritional support in acute pancreatitis. Appropriate interventions depend on the severity and duration of the pancreatitis and its complications. Current trends are away from restriction of oral or enteral intake, instead preferring this route to parenteral administration if possible. The role of the gut mucosal barrier in the pathogensis of the systemic response in pancreatitis has led to attempts to use enteral nutritional support to prevent complications, in addition to meeting nutritional needs in patients with long-term severe illness. Many clinicians believe that the management of acute pancreatitis should start from the concept of "pancreatic rest." Based on a simple understanding of pancreatic physiology and a belief that further stimulation of the pancreas during an attack of pancreatitis would exacerbate the inflammatory process by releasing more enzymes, traditional teaching has been that it is necessary to avoid all oral intake to prevent any inappropriate stimulation of pancreatic enzyme production. Accordingly, patients with acute pancreatitis are often deprived of enteral nutrition, and may be given intravenous parenteral nutritional support. Such an approach to nutritional support needs to be revised, since evidence emerging from many recent studies consistently indicates that an enteral route of nutrition is far superior.
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PMID:Nutritional support in acute pancreatitis. 1562 41

In severe acute pancreatitis, multiple organ failure in the early stage after onset, and sepsis in the late stage, due to infection of pancreatic or peripancreatic devitalized tissue, contribute to its high mortality. In analogy with sepsis, evidence has accumulated of the significance of apoptotic cell death in the systemic manifestations associated with acute pancreatitis. Since we identified apoptosis-inducing activity in pancreatitis-associated ascitic fluid in 1995, a number of investigators, including our group, have reported, through animal experiments, that apoptosis occurred in the parenchymal cells constituting organs, such as alveolar epithelial cells in the lung, renal tubular cells in the kidney, and hepatocytes in the liver, and this apoptosis was involved in organ dysfunction with severe acute pancreatitis. Moreover, through clinical and experimental investigations, apoptosis has been revealed to be involved in the mechanism of infectious complications in acute pancreatitis. Namely, apoptosis in lymphatic tissues and peripherally circulating lymphocytes is involved in the impairment of cellular immunity, and apoptosis in gut epithelial cells is implicated in bacterial translocation. These results suggest that apoptotic cell death may play a considerable role in affecting mortality and morbidity in severe acute pancreatitis. Control of apoptosis could be a potent strategy for improvement of the clinical outcome in severe acute pancreatitis.
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PMID:Significance of apoptotic cell death in systemic complications with severe acute pancreatitis. 1569 83

Polyarteritis nodosa (PAN) is a term that includes patients with necrotizing inflammation of medium sized arteries, and excludes those with microscopic vessel involvement. Its manifestations are protean and include constitutional symptoms such as fever, malaise, weight loss, myalgia, peripheral neuropathy, rash, and gut and renal involvement. Although gastrointestinal manifestations have been noted in up to a third of patients with PAN, clinical presentation with pancreatic involvement has been reported only rarely. We describe a patient with PAN who developed acute pancreatitis with pseudocyst formation as well as infarcts in the spleen and liver.
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PMID:Acute pancreatitis with pseudocyst formation in a patient with polyarteritis nodosa. 1569 6

Nutritional management during acute pancreatitis has the purpose to avoid a negative influence on the outcome and to preserve the morphofunctional integrity of the gut, preventing bacterial translocation. When the patient would start again normal nutrition after a period shorter than a week, thanks to the resolution of the clinical picture, and when the initial nutritional state of the patient is satisfactory, a particular nutritional support is not necessary. When the course of the disease is longer and the severity is higher, an early artificial nutritional support is advisable. Caloric needs thought to be useful are 25-30 kcal/kg/die; 40-60% of nutrient mixture should consist of carbohydrates and 20-30% of lipids. Proteins should be approximately 1.0-1.5 g/kg/die. On the basis of recent randomised, prospective clinical trials, enteral jejunal feeding is indicated as a first choice nutritional way, because of its ability to maintain the integrity of the intestinal barrier and its minimal effect on pancreatic secretion, acting significantly on inflammatory parameters and on prognostic markers. This procedure is not indicated when ileum is present and when it causes nausea, vomiting, abdominal pain and an increase of hepatic enzymes. In this case, parenteral feeding is an alternative. Hydroly-sated formulas, containing short peptides and a low percentage of long chain fat acids, are recommended.
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PMID:[Nutrition in acute pancreatitis]. 1578 88

Although acute pancreatitis runs a benign self limiting course in 80% of cases, acute necrotizing form of it still remained a severe disease associated with significant morbidity and mortality. Severity assessment thus plays an important role in identifying patients with high risk of local and/or systemic complications. Locally, development of necrosis especially if it becomes infected accounts for high mortality, but systemic inflammatory response syndrome (SIRS) and multiple organ failure (MOF) following necrosis further increases the risk of fatal outcome. Several scoring systems, contrast-enhanced CT scan can help to recognize patients requiring early intensive management. Prophylactic systemic antibiotic treatment and nasojejunal feeding improves prognosis by decreasing the gut derived infection of necrosis. CT guided fine needle aspiration sample must be cultured to detect infection. Conservative therapy should be continued while necrosis remains sterile, but surgical and/or CT guided percutaneous catheter drainage is mandatory when infected necrosis developed. Results of therapeutic influence on the proinflammatory cytokine cascade in acute pancreatitis are still controversial. Enteral feeding seems to be the only proven tool in attenuating acute phase response and improving disease severity.
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PMID:[Changes in the management of acute pancreatitis as related to its pathogenesis]. 1581 88

Maintenance of the gut environment is a key factor in determining outcome in the care of critically ill and postoperative patients. It is especially important to maintain both gastrointestinal secretions, full o anti-infectious and anti-inflammatory compounds, and the gut flora. Prebiotics, usually polysaccharides, exhibit strong bio-activity and the ingestion of prebiotics has been shown to reduce the rate of infection and restore health in sick and postoperative patients. Probiotics may have at least five functions, all of great importance to the sick patients: the reduction or elimination of potentially pathogenic micro-organism of various kinds; the reduction or elimination of various toxins, mutagens, carcinogens, etc.; modulation of the innate and adaptive immune defence mechanisms; the promotion of apoptosis; and the release of numerous nutrient, antioxidant, growth, coagulation and other factors necessary for recovery. A combination of pre and probiotics is referred to as "synbiotics". Our experience of synbotic treatment in critically ill patients is limited, but cutting-edge results from studies of severe acute pancreatitis, chronic hepatitis and liver transplantation offer great hope for the future. This is especially importante as pharmaceutical treatment, including the use of antibiotics, has largely failed, and the medical world is in much need of new treatment paradigms.
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PMID:[Symbiotics: a new strategy in critically ill patients treatment]. 1581 99

The aim of the present study was to investigate the potential effect of treatment with a platelet-activating factor (PAF) antagonist, lexipafant (BB-882), on gut endothelial and epithelial barrier dysfunction and leukocyte recruitment in rats with acute pancreatitis. Severe acute pancreatitis was induced by the intraductal administration of 5% sodium taurodeoxycholate and pancreatitis-associated gut barrier dysfunction was characterized by increased exudation of radiolabelled albumin into the interstitium and alterations in bidirectional (over both the endothelial and epithelial barrier components) permeability of the intestine at the early stage of bile salt-induced acute pancreatitis. Levels of interleukin 1beta and 6, ileal and colonic myeloperoxidase (MPO) content, clearance of radiolabelled albumin from blood to the gut lumen or gut lumen to blood, and leakage of radiolabelled albumin to the ileum or colon were measured 3 and 12h after induction of acute pancreatitis. Treatment with lexipafant 30 min and 6h after pancreatitis reduced severity of pancreatitis-associated intestinal dysfunction, associated with a diminish in systemic concentrations of IL-1 and local leukocyte recruitment. The findings imply that PAF plays a critical role in the development of pancreatitis-associated gut barrier dysfunction and that PAF antagonist in some forms may represent potential candidates for future therapeutic intervention.
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PMID:Severity of pancreatitis-associated gut barrier dysfunction is reduced following treatment with the PAF inhibitor lexipafant. 1582 3

Rifaximin (4-deoxy-4'-methylpyrido[1',2'-1,2]imidazo- [5,4-c]-rifamycin SV) is a synthetic antibiotic designed to modify the parent compound, rifamycin, in order to achieve low gastrointestinal (GI) absorption while retaining good antibacterial activity. Both experimental and clinical pharmacology clearly show that this compound is a nonsystemic antibiotic with a broad spectrum of antibacterial action covering Gram-positive and Gram-negative organisms, both aerobes and anaerobes. Being virtually nonabsorbed, its bioavailability within the GI tract is rather high with intraluminal and fecal drug concentrations that largely exceed the minimal inhibitory concentration values observed in vitro against a wide range of pathogenic organisms. The GI tract represents, therefore, the primary therapeutic target and GI infections the main indication. The appreciation of the pathogenic role of gut bacteria in several organic and functional GI diseases has increasingly broadened its clinical use, which is now extended to hepatic encephalopathy, small intestine bacterial overgrowth, inflammatory bowel disease and colonic diverticular disease. Potential indications include the irritable bowel syndrome and chronic constipation, Clostridium difficile infection and bowel preparation before colorectal surgery. Because of its antibacterial activity against the microorganism and the lack of strains with primary resistance, some preliminary studies have explored the rifaximin potential for Helicobacter pylori eradication. Oral administration of this drug, by getting rid of enteric bacteria, could also be employed to achieve selective bowel decontamination in acute pancreatitis, liver cirrhosis (thus preventing spontaneous bacterial peritonitis) and nonsteroidal anti-inflammatory drug (NSAID) use (lessening in that way NSAID enteropathy). This antibiotic has, therefore, little value outside the enteric area and this will minimize both antimicrobial resistance and systemic adverse events. Indeed, the drug proved to be safe in all patient populations, including young children. Although rifaximin has stood the test of time, it still attracts the attention of both basic scientists and clinicians. As a matter of fact, with the advancement of the knowledge on microbial-gut interactions in health and disease novel indications and new drug regimens are being explored. Besides widening the clinical use, the research on rifaximin is also focused on the synthesis of new derivatives and on the development of original formulations designed to expand the spectrum of its clinical use.
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PMID:Rifaximin, a poorly absorbed antibiotic: pharmacology and clinical potential. 1585 48

Patients with acute pancreatitis have elevated nutritional needs due to increased energy expenditure and catabolism. It is a clinical challenge to provide adequate nutrition to these patients while maintaining gut function, preventing pancreatic stimulation, and minimizing the risk of septic and metabolic complications associated with nutritional support. We present the case of a patient who had severe acute pancreatitis and was initially given total parenteral nutrition. After a period of initial improvement, he developed hyperglycemia, bacteremia, and sepsis. Parenteral nutrition was discontinued and infection was treated with antibiotics. Subsequent nutritional support consisted of enteral feeding with an elemental diet infused via a nasojejunal feeding tube. His condition improved gradually and he made a full recovery. This case illustrates the difficulties encountered while managing a case of severe acute pancreatitis and provides an evidence based approach to the nutritional management of severe acute pancreatitis in the intensive care unit setting.
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PMID:Severe acute pancreatitis: nutritional management in the ICU. 1621 93

Kallikreins are serine proteases, which are divided into plasma kallikrein and tissue kallikrein. Kallikreins cleave kininogen, theirs main substrate to release bradykinin, a potent inflammatory mediator. Kinins act directly by B2 and B1 receptors, or indirectly stimulating synthesis of nitric oxide, prostanoids and cytokinines by epithelial cells, smooth muscle cells, endothelial cells and fibroblasts. Recent experimental studies and clinical data indicate a pathogenic role of the kallikrein-kinin system in gastrointestinal disorders including inflammatory bowel disease, acute pancreatitis, colorectal and gastric cancer and pathogenesis of ascites. New molecular biology techniques and development of specific antibodies permit to evaluate the expression of genes and localization of proteins of the kallikrein-kinin components. Experimental studies indicate a modulatory effect of a specific kallikrein inhibition and kinin receptor antagonist suggesting its therapeutic potential in human gut diseases.
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PMID:[A role of kallikrein-kinin system in gut diseases]. 1623 27


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