dc.description.abstract |
The nutritional management of acute pancreatitis has evolved dramatically over the past few decades from the early regimen of ‘pancreatic rest’ to the modern paradigm of early enteral nutrition, or ‘gut rousing’. This modern regimen has significantly improved clinical outcomes such as reducing infectious complications, multi-organ failure, and mortality for patients with acute pancreatitis; however the mechanisms behind these benefits remain largely unknown. In addition, despite these improvements, this has not eradicated the presence of a common nutrition-related complication; oral feeding intolerance (OFI). Characterised by pain relapse, nausea and/or vomiting, OFI has been associated with greater length of hospital stays and costs. As substantiated by literature there is a need for accurate, readily-available predictive markers that are capable of predicting OFI. Recently it was discovered that adipokines, mediators involved in inflammation and metabolism, have an early role in predicting the clinical severity of acute pancreatitis, thus it was hypothesised that adipokines may also provide insight into the mechanisms behind the benefits of early enteral nutrition, and may be predictors of other clinical outcomes. The aims of the study were to first investigate the effect of enteral nutrition on adipokine levels early in the course of acute pancreatitis, by comparing levels between patients receiving nasogastric tube feeding (a promising nutritional support therapy avenue) and those receiving nil-by-mouth (the conventional regime). The second aim was to investigate if adipokines could predict the primary outcome, OFI, and two secondary outcomes, systemic inflammatory response syndrome and prolonged hospitalisation, which often occur in acute pancreatitis. The five adipokines measured were adiponectin, leptin, omentin, resistin, and visfatin. Results obtained showed that two adipokines, omentin and leptin, were significantly higher in patients who received enteral nutrition compared to those who were nil-by-mouth. Literature shows that this may mediate the beneficial effects of early EN by having an anti-inflammatory effect, and may be protective against the development of insulin resistance and diabetes due to the role of these adipokines in insulin signalling pathways. Second, while none of the adipokines were significant predictors of OFI, resistin, a pro-inflammatory adipokine, was predictive of a prolonged hospitalisation; which could serve as a useful clinical indictor for patients who require more intensive monitoring. Future research should be directed towards understanding what role the increased levels play and whether they are responsible for the therapeutic benefits of enteral nutrition. Additionally, research should be directed towards determining the levels of omentin during AP and comparing them in differing levels of severity, to understand the role of this relatively new adipokine in AP. There is also great demand for research to investigate the mechanisms that cause and perpetuate OFI, to refine optimal refeeding practice and to ultimately understand how to prevent OFI. |
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