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Endotheliopathy is associated with higher levels of cell-free DNA following major trauma: A prospective observational study.

Abstract Cell free deoxyribonucleic acid (cfDNA) has been proposed as a biomarker of secondary complications following trauma. Raised thrombomodulin and syndecan-1 levels have been used to indicate endotheliopathy, and are associated with inflammation, coagulopathy, and mortality. The current study aimed to analyse the association between cfDNA and biomarkers of endotheliopathy in a cohort of trauma patients, and whether raised levels of cfDNA were associated with poorer clinical outcomes.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 29261771
OWN - NLM
STAT- In-Process
LR  - 20171224
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - Endotheliopathy is associated with higher levels of cell-free DNA following major
      trauma: A prospective observational study.
PG  - e0189870
LID - 10.1371/journal.pone.0189870 [doi]
AB  - BACKGROUND: Cell free deoxyribonucleic acid (cfDNA) has been proposed as a
      biomarker of secondary complications following trauma. Raised thrombomodulin and 
      syndecan-1 levels have been used to indicate endotheliopathy, and are associated 
      with inflammation, coagulopathy, and mortality. The current study aimed to
      analyse the association between cfDNA and biomarkers of endotheliopathy in a
      cohort of trauma patients, and whether raised levels of cfDNA were associated
      with poorer clinical outcomes. METHODS: Serum thrombomodulin and syndecan-1 were 
      used as biomarkers of endotheliopathy and compared to plasma cfDNA in trauma
      patients from two prospective longitudinal observational studies. Cohort A (n =
      105) had a predicted injury severity score (ISS) >8, and had blood sampled within
      1h of injury and at 4-12h. Cohort B (n = 17) had evidence of haemorrhagic shock, 
      and had blood sampled at a median time of 3.5h after injury. Relationships
      between biomarkers were tested using multivariable linear regression models that 
      included the covariates of gender, age, ISS, Glasgow Coma Scale, lactate,
      systolic blood pressure, and heart rate. A model was fitted to investigate
      whether changes in cfDNA were associated with similar changes in endothelial
      biomarkers. RESULTS: The mean age was 41 (SD 19), and the median ISS was 25 (IQR 
      12-34). There was a significant association between cfDNA levels and both
      syndecan-1 and thrombomodulin levels (both p<0.001). This was independent of all 
      covariates except for ISS, which significantly correlated with cfDNA levels. 50
      ng/ml change in syndecan-1 and 1 ng/ml change in thrombomodulin corresponded to
      15% and 20% increases in cfDNA levels respectively (both p<0.001). Patients who
      died had significantly higher prehospital and in-hospital cfDNA levels (both
      p<0.05). CONCLUSIONS: Raised cfDNA levels are associated with markers of
      endotheliopathy following trauma, and are associated with mortality. This
      relationship is present within the first hour of injury, and a change in one
      biomarker level is reflected by similar changes in the others. These findings are
      in keeping with the hypothesis that circulating DNA and endothelial injury share 
      a common pathway following trauma.
FAU - Naumann, David N
AU  - Naumann DN
AUID- ORCID: http://orcid.org/0000-0003-2243-2325
AD  - Academic Department of Military Surgery and Trauma, Royal Centre for Defence
      Medicine, Queen Elizabeth Hospital, Birmingham, United Kingdom.
AD  - NIHR Surgical Reconstruction and Microbiology Research Centre, Queen Elizabeth
      Hospital, Birmingham, United Kingdom.
FAU - Hazeldine, Jon
AU  - Hazeldine J
AD  - NIHR Surgical Reconstruction and Microbiology Research Centre, Queen Elizabeth
      Hospital, Birmingham, United Kingdom.
AD  - Institute of Inflammation and Ageing, University of Birmingham, Birmingham,
      United Kingdom.
FAU - Dinsdale, Robert J
AU  - Dinsdale RJ
AD  - Institute of Inflammation and Ageing, University of Birmingham, Birmingham,
      United Kingdom.
FAU - Bishop, Jon R
AU  - Bishop JR
AD  - NIHR Surgical Reconstruction and Microbiology Research Centre, Queen Elizabeth
      Hospital, Birmingham, United Kingdom.
FAU - Midwinter, Mark J
AU  - Midwinter MJ
AD  - Department of Surgery, University of Queensland, Rural Clinical School,
      Bundaberg, Queensland, Australia.
FAU - Harrison, Paul
AU  - Harrison P
AD  - Institute of Inflammation and Ageing, University of Birmingham, Birmingham,
      United Kingdom.
FAU - Hutchings, Sam D
AU  - Hutchings SD
AD  - Department of Intensive Care Medicine, Kings College Hospital, Denmark Hill,
      London, United Kingdom.
FAU - Lord, Janet M
AU  - Lord JM
AD  - Institute of Inflammation and Ageing, University of Birmingham, Birmingham,
      United Kingdom.
LA  - eng
PT  - Journal Article
DEP - 20171219
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5736230
EDAT- 2017/12/21 06:00
MHDA- 2017/12/21 06:00
CRDT- 2017/12/21 06:00
PHST- 2017/06/13 00:00 [received]
PHST- 2017/12/04 00:00 [accepted]
PHST- 2017/12/21 06:00 [entrez]
PHST- 2017/12/21 06:00 [pubmed]
PHST- 2017/12/21 06:00 [medline]
AID - 10.1371/journal.pone.0189870 [doi]
AID - PONE-D-17-22563 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 19;12(12):e0189870. doi: 10.1371/journal.pone.0189870.
      eCollection 2017.