We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Bacterial translocation in multiple organ failure: Cause or epiphenomenon still unproven.
- Authors
Lemaire, L. C. J. M.; van Lanschot, J. J. B.; Stoutenbeek, C. P.; van Deventer, S. J. H.; Wells, C. L.; Gouma, D. J.
- Abstract
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 χ2 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.
- Publication
British Journal of Surgery, 1997, Vol 84, Issue 10, p1340
- ISSN
0007-1323
- Publication type
Article
- DOI
10.1111/j.1365-2168.1997.00520.x