BACKGROUND: A body of evidence exists for the occurrence of bacterial translocation and its relationship to multiple organ failure (MOF). METHODS: Relevant articles on bacterial translocation (the phenomenon defined as the passage of microbes and endotoxin across the intestinal barrier) in patients prone to develop MOF and in representative animal studies were selected. To interpret and evaluate the evidence for bacterial translocation in current literature, the endpoints generally used are discussed. RESULTS: Fractional data from individual manuscripts were tabulated and assessed for statistical significance with chi 2 analysis. Various clinically relevant stimuli, postulated as important causative factors for the development of MOF, appeared to be interrelated and related to bacterial translocation itself. CONCLUSIONS: Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.
BACKGROUND: A body of evidence exists for the occurrence of bacterial translocation and its relationship to multiple organ failure (MOF). METHODS: Relevant articles on bacterial translocation (the phenomenon defined as the passage of microbes and endotoxin across the intestinal barrier) in patients prone to develop MOF and in representative animal studies were selected. To interpret and evaluate the evidence for bacterial translocation in current literature, the endpoints generally used are discussed. RESULTS: Fractional data from individual manuscripts were tabulated and assessed for statistical significance with chi 2 analysis. Various clinically relevant stimuli, postulated as important causative factors for the development of MOF, appeared to be interrelated and related to bacterial translocation itself. CONCLUSIONS: Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.
Authors: Vassilios G Margaritis; Kriton S Filos; Marina A Michalaki; Chrisoula D Scopa; Iris Spiliopoulou; Vassiliki N Nikolopoulou; Constantine E Vagianos Journal: World J Surg Date: 2005-10 Impact factor: 3.352
Authors: Inaki Eizaguirre; Pablo Aldazabal; Nerea Garcia Urkia; Anabel Asensio; Jose María García Arenzxana Journal: Pediatr Surg Int Date: 2011-07-12 Impact factor: 1.827