TY - JOUR
T1 - Studies on bacterial endotoxin and intestinal absorption function in patients with chronic heart failure
AU - Sandek, Anja
AU - Bjarnason, Ingvar
AU - Volk, Hans Dieter
AU - Crane, Roger
AU - Meddings, Jonathan B.
AU - Niebauer, Josef
AU - Kalra, Paul R.
AU - Buhner, Sabine
AU - Herrmann, Ralph
AU - Springer, Jochen
AU - Doehner, Wolfram
AU - Von Haehling, Stephan
AU - Anker, Stefan D.
AU - Rauchhaus, Mathias
PY - 2012/5/17
Y1 - 2012/5/17
N2 - 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 > 0.50 EU/mL (n = 7) had the highest concentrations of TNF (7.0 ± 1.6 vs. 3.1 ± 0.3 pg/mL, p <0.02), and sTNF-R1 (3499 ± 52 vs. 1599 ± 219 pg/mL, p = 0.02). Conclusion: 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.
AB - 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 > 0.50 EU/mL (n = 7) had the highest concentrations of TNF (7.0 ± 1.6 vs. 3.1 ± 0.3 pg/mL, p <0.02), and sTNF-R1 (3499 ± 52 vs. 1599 ± 219 pg/mL, p = 0.02). Conclusion: 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.
KW - Heart failure
KW - Immune activation
KW - Intestinal permeability
KW - Small intestinal function
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U2 - 10.1016/j.ijcard.2010.12.016
DO - 10.1016/j.ijcard.2010.12.016
M3 - Article
C2 - 21190739
AN - SCOPUS:84860233765
VL - 157
SP - 80
EP - 85
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
IS - 1
ER -