title: Studies on bacterial endotoxin and intestinal absorption function in patients with chronic heart failure.
abstract: BACKGROUND
  Small intestinal function may be altered in decompensated chronic heart failure (CHF) and translocating LPS may contribute to systemic inflammation observed in CHF.
  
  
  METHODS
  We measured intestinal permeability (melibiose and rhamnose), active (3-O-methyl-d-glucose (3-OMG)) and passive (d-xylose) carrier-mediated absorption in 20 CHF patients (12 edematous and 8 non-edematous) and 8 controls by saccharide absorption technique assessing urinary recovery of orally administered sugars. We additionally measured LPS concentrations in 42 patients with decompensated heart failure and after recompensation.
  
  
  RESULTS
  CHF patients had a 54% reduction of active carrier-mediated intestinal transport compared to controls (p<0.0001). This reduction was strongest in edematous compared to non-edematous patients and controls (recovery in urine: 13.2±2.0% vs. 20.8±2.4% vs. 36.0 ± 3.7%, all p ≤ 0.05). Patients showed a 34% reduction of passive carrier-mediated transport, strongest in edematous patients (p=0.006). A greater impairment of active carrier-mediated transport remained significant after adjustment for non-mucosal factors in CHF (p=0.0004). Non carrier-mediated intestinal permeability was not altered. Data from 42 decompensated patients showed a decrease in LPS after recompensation (p=0.004). Edematous patients had highest blood concentrations of LPS, TNF and sTNF-R1 (p<0.04). CHF patients with abnormal LPS concentrations >0.50EU/mL (n=7) had the highest concentrations of TNF (7.0 ± 1.6 vs. 3.1 ± 0.3pg/mL, p<0.02), and sTNF-R1 (3499 ± 52 vs. 1599±219 pg/mL, p=0.02).
  
  
  CONCLUSIONS
  Active carrier-mediated intestinal transport is reduced in decompensated CHF indicating epithelial dysfunction possibly as a consequence of intestinal ischemia. Higher LPS concentrations in edematous CHF relate to inflammation. LPS decreased after recompensation. This suggests a cause/effect relationship between edematous gut wall, epithelial dysfunction and translocating LPS.
authors.affiliation: Dept. of Cardiology, Charité-Universitätsmedizin, Berlin, Germany. s.anker@cachexia.de
authors.forename: Anja
authors.initials: A
authors.lastname: Sandek
authors.forename: Ingvar
authors.initials: I
authors.lastname: Bjarnason
authors.forename: Hans-Dieter
authors.initials: HD
authors.lastname: Volk
authors.forename: Roger
authors.initials: R
authors.lastname: Crane
authors.forename: Jonathan B
authors.initials: JB
authors.lastname: Meddings
authors.forename: Josef
authors.initials: J
authors.lastname: Niebauer
authors.forename: Paul R
authors.initials: PR
authors.lastname: Kalra
authors.forename: Sabine
authors.initials: S
authors.lastname: Buhner
authors.forename: Ralph
authors.initials: R
authors.lastname: Herrmann
authors.forename: Jochen
authors.initials: J
authors.lastname: Springer
authors.forename: Wolfram
authors.initials: W
authors.lastname: Doehner
authors.forename: Stephan
authors.initials: S
authors.lastname: von Haehling
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
authors.forename: Mathias
authors.initials: M
authors.lastname: Rauchhaus
mesh_terms: D000368:Aged; D002908:Chronic Disease; D004731:Endotoxins / Q000378:metabolism; D005260:Female; D006333:Heart Failure / Q000378:metabolism* / Q000382:microbiology; D006801:Humans; D007408:Intestinal Absorption / Q000502:physiology*; D007413:Intestinal Mucosa / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
chemical_list: D004731:Endotoxins; D008070:Lipopolysaccharides