PURPOSE OF REVIEW: In clinical research, increased permeability has been scrutinized as a potential indicator of the severity of gastrointestinal disease and as a potential cause of the perpetuation of severe inflammatory activity in infectious states. This review discusses old and recent epidemiological and clinical evidence to establish whether increased permeability in sepsis is a sequel or a cause of multiple organ failure. In addition, old and new evidence linking inflammation and permeability in abnormal gastrointestinal anatomy and function to liver abnormalities in susceptible patients will be reviewed. RECENT FINDINGS: Intestinal permeability has been found to be increased in several gastrointestinal diseases but not to be a very good marker of the severity of disease. Evidence is put forward supporting the claim that increased intestinal permeability is part of generalized leakiness of tight junctions in multiple organ failure and to play a less strong role as a primary event in its pathogenesis. Endemic malnutrition has been shown to be caused by interplay between malnutrition and intestinal inflammation. Recently experimental evidence has been put forward suggesting that enteral fat has anti-inflammatory effects on the intestine via the autonomic nervous system. Old clinical and new epidemiological evidence links intestinal inflammation, disruption of the enterohepatic cycle of bile acids, and liver disease. SUMMARY: The implications of the described findings are that inflammatory activity, locally induced by abnormal intestinal anatomy and disruption of the bile acid pool, or systemically by severe and uncontrolled inflammation/infection, should be the focus of treatment or research. In addition, the connection between intestinal inflammation and liver disease should be investigated.
|Journal||Current Opinion in Clinical Nutrition and Metabolic Care|
|Publication status||Published - 1 Jan 2007|