title: Role of intestinal function in cachexia.
abstract: OBJECTIVE
  Cachexia is a prominent feature in many chronic diseases, but its pathogenesis is still not fully understood. This article reviews recent research into the role of the gut barrier in the pathogenesis of inflammation and cachexia with special emphasis on two potentially catabolic diseases: liver cirrhosis and chronic heart failure.
  
  
  RESULTS
  There is increasing evidence that catabolic diseases such as liver cirrhosis and chronic heart failure are associated with increased gut permeability, endotoxemia and enhanced expression of proinflammatory cytokines. In liver cirrhosis normalization of portal hypertension by insertion of a transjugular intrahepatic portosystemic stent shunt obviously causes improvement not only of gut barrier function, but also of nutritional status.
  
  
  CONCLUSIONS
  Although its pathogenesis is not yet completely understood, proinflammatory cytokines have been implicated in the onset and progression of cachexia. Recent data support the hypothesis that impaired gut barrier function and increased permeability further translocation of endotoxins. Increased endotoxemia might be a potent trigger of systemic inflammatory response which is involved in the pathogenesis of the cachexia syndrome. Thus, it is tempting to speculate that therapeutic strategies for the improvement of gut barrier function will concomitantly improve nutritional status.
authors.affiliation: Medizinische Klinik, Gastroenterologie, Hepatologie und Endokrinologie, Charité - Universitätsmedizin Berlin, Berlin, Germany. matthias.pirlich@charite.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Pirlich
authors.forename: Kristina
authors.initials: K
authors.lastname: Norman
authors.forename: Herbert
authors.initials: H
authors.lastname: Lochs
authors.forename: Jürgen
authors.initials: J
authors.lastname: Bauditz
mesh_terms: D018988:Bacterial Translocation; D002100:Cachexia / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis / Q000378:metabolism*; D004731:Endotoxins / Q000502:physiology; D006333:Heart Failure / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007421:Intestine, Small / Q000502:physiology*; D008103:Liver Cirrhosis / Q000378:metabolism
chemical_list: D016207:Cytokines; D004731:Endotoxins