The complications associated with PN have led us and others to explore the use of specialized forms of enteral feeding (EN). In the five major randomized comparative studies published thus far, enteral feeding has been shown consistently to be superior to PN with regard to cost, complications and outcome [34-38]. A recent metanalysis concluded that enteral nutrition should be the preferred route of nutritional support in acute pancreatitis . While most of us have used jejunal feeding with semi-elemental formulae to minimize pancreatic stimulation, one study just reported from Glasgow, Scotland, found that patients could simply be fed by nasogastric tube without obvious exacerbation of the pancreatitis . How can we explain the better results seen utilizing these forms of EN compared to TPN considering the pathophysiology of acute pancreatitis? It is not because any of the specialized forms of feeding used in these studies avoided pancreatic stimulation, as studies of ours in healthy volunteers have shown that even the avoidance of the cephalic and gastric phases of pancreatic stimulation by post-pyloric infusion failed to reduce food-induced pancreatic secretion  (Fig. 5.4). Furthermore, even the use of an intestinal elemental formula diet only reduced the stimulatory effect by 50%, a rate considerably higher than that measured during fasting or IV feeding . Another suggestion, based on experimental studies, was that the pancreas becomes unresponsive in acute pancreatitis. Investigating this possibility, we indeed found that the duodenal secretory response to feeding was reduced roughly 90% . However, when we measured the de novo rate of synthesis of secreted trypsin by isotope-labeling techniques, we found that even in patients with necrotizing disease affecting over 50% of the gland trypsin continued to be synthesized and that a good proportion of the reduction in luminal secretion could be attributed to leakage of enzymes into the inflammatory mass and the bloodstream . Further studies showed that the low rate of
secretion in acute pancreatitis could be increased by conversion from PN to enteral feeding [40, 41]. These findings led us to the conclusion that the superiority of proximal enteral feeding over PN could not be accounted for by its beneficial effects on the pancreas, but by the greater efficiency of enteral feeding in preserving intestinal function and splanchnic metabolism, and by the avoidance of PN-associated complications. Support for this conclusion was gained by our further observation that in acute pancreatitis, splanchnic amino acid flux and mucosal turnover were increased three-fold and that compartmentation between the splanchnic and systemic amino acid circulations was increased, thus preventing thorough mixing of IV and splanchnic amino acids . Consequently, enteral feeding would be better positioned than PN to target the region of increased metabolic demand for tissue repair. Furthermore, if we refer back to our illustration in Fig. 5.2, one of the chief effects of acute pancreatitis is to provoke intestinal ischemia, which in turn leads to mucosal leakage and the risk of bacterial organism and endotoxin translocation. For example, Rahman et al. demonstrated in patients with severe acute pancreatitis that the urinary excretion of intestinal fatty acid-binding protein, an accepted measure of intestinal ischemia, positively correlated with severity of disease, mucosal permeability (urinary PEG 400:3,500), CRP and with endotoxin levels . Enteral nutrition undoubtedly plays a key role in preventing this cycle of events as it is the most potent stimulator of blood flow, through its stimulation of intestinal growth factors [44, 45] because of its content of arginine, which is the natural precursor for nitric oxide . Experimental studies in the rat acute pancreatitis model have shown that nitric oxide antagonizes endothelin-A and that endothelin-A receptor blockade abolished the acute pancreatitis-associated capilliary constriction and attenuated the inflammation-associated leukocytic response and pancreatic injury .
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WHAT IT IS A three-phase plan that has been likened to the low-carbohydrate Atkins program because during the first two weeks, South Beach eliminates most carbs, including bread, pasta, potatoes, fruit and most dairy products. In PHASE 2, healthy carbs, including most fruits, whole grains and dairy products are gradually reintroduced, but processed carbs such as bagels, cookies, cornflakes, regular pasta and rice cakes remain on the list of foods to avoid or eat rarely.