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

摘要

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.