Clinical nutrition : official journal of the European Society of Parenteral and Enteral Nutrition
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Review Meta Analysis
The use of pre- pro- and synbiotics in adult intensive care unit patients: systematic review.
This review investigated whether the administration of enteral pre-, pro- and synbiotics compared with controls in adult intensive care unit (ICU) patients reduced the incidence of nosocomial infections, length of ICU stay, hospital mortality and specifically pneumonia. ⋯ The use of pre- pro- or synbiotics in adult critically ill patients confers no statistically significant benefit in the outcome criteria studied. There is currently a lack of evidence to support the use of pre- pro- or synbiotics in patients admitted to adult ICUs, and a large well-designed trial is needed in this area.
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The "gut origin of sepsis" hypothesis proposes that enteric bacteria may cause sepsis at distant extra-intestinal sites. Whilst there is much circumstantial evidence to support this hypothesis, there is no conclusive proof in humans. The nature of translocating bacteria remains unclear. The aim of this study was to establish the origin of Escherichia coli (E. coli) cultured from mesenteric lymph nodes (MLN) and determine if they belonged to any recognized pathotypes known to cause infections in humans. ⋯ This study confirms the gut origin of translocating bacteria. Most translocating E. coli do not belong to any recognised pathotype and are therefore normal commensal microflora. Our results suggest that bacterial translocation is more dependent upon the gut epithelium rather than the virulence properties of resident enteric bacteria.
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Acute and chronic kidney failure lead to catabolism with loss of lean body mass. Up-regulation of hepatic urea synthesis may play a role for the loss of body nitrogen and for the level of uraemia. The aims were to investigate the effects of early and late experimental renal failure on the regulation of hepatic urea synthesis and the expression of urea cycle enzyme genes in the liver. ⋯ Early uraemia down-regulated urea synthesis, so hepatic ureagenesis was not in itself involved in the negative N-balance. In contrast, late uraemia up-regulated urea synthesis, which probably contributed towards the reduced N-balance of this condition. These time-dependent, opposite effects on the uraemia-induced regulation of urea synthesis in vivo were not related to food restriction and probably mostly reflected regulation on gene level.