PMID- 10359409
OWN - NLM
STAT- MEDLINE
DCOM- 19990624
LR  - 20220318
IS  - 0140-6736 (Print)
IS  - 0140-6736 (Linking)
VI  - 353
IP  - 9167
DP  - 1999 May 29
TI  - Endotoxin and immune activation in chronic heart failure: a prospective cohort 
      study.
PG  - 1838-42
AB  - BACKGROUND: Immune activation in patients with chronic heart failure may be 
      secondary to endotoxin (lipopolysaccharide) action. We investigated the 
      hypothesis that altered gut permeability with bacterial translocation and 
      endotoxaemia would be increased in patients with oedema secondary to congestive 
      heart failure. METHODS: We compared 20 patients who had chronic heart failure 
      with recent-onset peripheral oedema (mean age 64 years [SD 10], New York Heart 
      Association [NYHA] class 3.3 [0.7]), 20 stable non-oedematous patients with 
      chronic heart failure (mean age 63 years [19], NYHA class 2.6 [0.7]), and 14 
      healthy volunteers (mean age 55 years [16]). Biochemical markers of endotoxaemia, 
      inflammation, and immune activation were measured. Ten patients were studied 
      within 1 week of complete resolution of oedema. Five patients survived longer 
      than 6 months and were restudied again after remaining free of oedema for more 
      than 3 months. FINDINGS: Mean endotoxin concentrations were higher in oedematous 
      patients with chronic heart failure than in stable patients with chronic heart 
      failure (0.74 [SD 0.45] vs 0.37 EU/mL [0.23], p=0.0009) and controls (0.46 EU/mL 
      [0.21], p=0.02). Oedematous patients had the highest concentrations of several 
      cytokines. After short-term diuretic treatment, endotoxin concentrations 
      decreased from 0.84 EU/mL [0.49] to 0.45 EU/mL [0.21], p<0.05) but cytokines 
      remained raised. After freedom of oedema for more than 3 months after oedema 
      resolved, endotoxin concentrations remained unchanged from the previous visit 
      (0.49 EU/mL [0.06], p=0.45). INTERPRETATION: Raised concentrations of endotoxin 
      and cytokines are found in patients with chronic heart failure during acute 
      oedematous exacerbation. Intensified diuretic treatment can normalise endotoxin 
      concentrations. Our preliminary findings suggest that endotoxin may trigger 
      immune activation in patients with chronic heart failure during oedematous 
      episodes.
FAU - Niebauer, J
AU  - Niebauer J
AD  - Cardiac Medicine, National Heart and Lung Institute, Imperial College School of 
      Medicine, London, UK.
FAU - Volk, H D
AU  - Volk HD
FAU - Kemp, M
AU  - Kemp M
FAU - Dominguez, M
AU  - Dominguez M
FAU - Schumann, R R
AU  - Schumann RR
FAU - Rauchhaus, M
AU  - Rauchhaus M
FAU - Poole-Wilson, P A
AU  - Poole-Wilson PA
FAU - Coats, A J
AU  - Coats AJ
FAU - Anker, S D
AU  - Anker SD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Lancet
JT  - Lancet (London, England)
JID - 2985213R
RN  - 0 (Acute-Phase Proteins)
RN  - 0 (Carrier Proteins)
RN  - 0 (Cytokines)
RN  - 0 (Diuretics)
RN  - 0 (Endotoxins)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (lipopolysaccharide-binding protein)
SB  - IM
CIN - Lancet. 1999 May 29;353(9167):1812-3. PMID: 10359399
CIN - Lancet. 1999 Aug 14;354(9178):599-600. PMID: 10470730
MH  - Acute-Phase Proteins/analysis
MH  - Bacterial Translocation
MH  - Carrier Proteins/blood
MH  - Cohort Studies
MH  - Cytokines/blood/*immunology
MH  - Diuretics/therapeutic use
MH  - Edema, Cardiac/drug therapy/etiology/*immunology
MH  - Endotoxemia/*complications/immunology
MH  - Endotoxins/*adverse effects
MH  - Heart Failure/drug therapy/etiology/*immunology
MH  - Humans
MH  - *Membrane Glycoproteins
MH  - Middle Aged
MH  - Prospective Studies
MH  - Time Factors
EDAT- 1999/06/08 00:00
MHDA- 1999/06/08 00:01
CRDT- 1999/06/08 00:00
PHST- 1999/06/08 00:00 [pubmed]
PHST- 1999/06/08 00:01 [medline]
PHST- 1999/06/08 00:00 [entrez]
AID - S0140-6736(98)09286-1 [pii]
AID - 10.1016/S0140-6736(98)09286-1 [doi]
PST - ppublish
SO  - Lancet. 1999 May 29;353(9167):1838-42. doi: 10.1016/S0140-6736(98)09286-1.