Studies on bacterial endotoxin and intestinal absorption function in patients with chronic heart failure

Anja Sandek, Ingvar Bjarnason, Hans Dieter Volk, Roger Crane, Jonathan B. Meddings, Josef Niebauer, Paul R. Kalra, Sabine Buhner, Ralph Herrmann, Jochen Springer, Wolfram Doehner, Stephan Von Haehling, Stefan D. Anker, Mathias Rauchhaus

Research output: Contribution to journalArticlepeer-review

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 > 0.50 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.

Original languageEnglish
Pages (from-to)80-85
Number of pages6
JournalInternational Journal of Cardiology
Volume157
Issue number1
DOIs
Publication statusPublished - May 17 2012

Keywords

  • Heart failure
  • Immune activation
  • Intestinal permeability
  • Small intestinal function

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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