title: Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation.
abstract: OBJECTIVE
  Exposure to bacterial endotoxin, perhaps due to bowel congestion or ischaemia and altered gut permeability, may result in immune activation that is characteristic for patients with severe heart failure. It is known that blood procalcitonin rises in response to bacterial endotoxin exposure.
  
  
  METHODS
  We measured procalcitonin in a group of 29 patients with acute cardiogenic shock and no sign of infection (all without bacteraemia) and 26 with septic shock. Blood was analysed for procalcitonin, interleukin-6, tumour necrosis factor-alpha (TNF-alpha), c-reactive protein (CRP) and neopterin. Patients were managed conventionally in an intensive care unit with no further experimental procedures.
  
  
  RESULTS
  Three cardiogenic (10%) and seven septic shock patients (27%) survived. Most patients with acute heart failure surviving 12 h or more (18 of 20) developed a pyrexia (738.0 degrees C) of unknown origin in the absence of positive cultures, with a rise in procalcitonin (1.4+/-0.8 to 48.0+/-16.2 ng/ml, P<0.001), CRP (76.5+/-16.4 to 154.7+/-22.9 mg/l, P<0.001) and neopterin (20.7+/-3.5 to 41.2+/-6.7 nmol/l, P<0.001). Patients with septic shock had higher initial levels of cytokines, and higher peak levels. Those with heart failure surviving (n=3) and those dying in the first 12 h (n=9) had no rise in cytokine levels. The patients with high procalcitonin had a higher temperature (38.9+/-0.3 vs. 37.3+/-0.23 degrees C, P<0.05), TNF-alpha (43.95+/-9.64 vs. 16.43+/-4.33 pg/ml; P<0.005) and CRP (146.1+/-18.4 vs. 68.2+/-39.6 mg/ml, P<0.005). Peak procalcitonin levels correlated with peak temperature (r=0.74, P<0.001).
  
  
  CONCLUSIONS
  Cardiogenic shock causes a pyrexia of unknown origin in patients surviving for 12 h and that is associated with a rise in procalcitonin levels. This lends support to the hypothesis that patients with cardiogenic shock may be being exposed to bacterial endotoxin at a time when bowel wall congestion and or ischaemia is likely to be present.
authors.affiliation: Krankenhaus Zehlendorf, Department of Internal Medicine, Berlin, Germany. station01@gmx.de
authors.forename: F M
authors.initials: FM
authors.lastname: Brunkhorst
authors.forename: A L
authors.initials: AL
authors.lastname: Clark
authors.forename: Z F
authors.initials: ZF
authors.lastname: Forycki
authors.forename: S D
authors.initials: SD
authors.lastname: Anker
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018988:Bacterial Translocation; D002116:Calcitonin / Q000097:blood*; D015740:Calcitonin Gene-Related Peptide; D016207:Cytokines / Q000097:blood; D004731:Endotoxins / Q000378:metabolism; D005260:Female; D005335:Fever of Unknown Origin / Q000209:etiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011498:Protein Precursors / Q000097:blood*; D012770:Shock, Cardiogenic / Q000097:blood / Q000150:complications / Q000276:immunology* / Q000401:mortality; D012772:Shock, Septic / Q000097:blood / Q000276:immunology / Q000382:microbiology / Q000401:mortality; D016019:Survival Analysis
chemical_list: C000606589:CALCA protein, human; D016207:Cytokines; D004731:Endotoxins; D011498:Protein Precursors; D002116:Calcitonin; D015740:Calcitonin Gene-Related Peptide