In the
September 13th issue of PLoS One (link),
John D. Storey and colleagues report on inflammation-related gene expression signatures
associated with differential clinical outcome in acute trauma patients. Specifically, the authors analyzed the
expression of inflammation-related genes in 168 blunt-force trauma patients over
a 28-day period. The genes and gene
pathways that clustered differently between patients’ clinical outcome subgroups
(based on Marshall multiple
organ failure clinical score) were assembled into predictive modules of
clinical outcomes. Of particularly
interest, the down-regulation of MHC II expression within 48 hours of trauma and
up-regulation of p38-MAPK within 100 hours of trauma were particularly robust independent
predictors of negative clinical outcome in this patient sample.
Considering
that up to 60% of late trauma mortality is caused by infections, sepsis, and
multiple organ failure multiple organ, the management of these
inflammation-related complications remains a major unmet medical need. In particular, the ability to predict the
individual patient clinical trajectory early during trauma treatment remains a
significant challenge for the medical community. Therefore, the prospect of using gene
expression as a prognostic biomarker to manage the care of trauma patients is
of particular significance.
Thierry
Sornasse for Integrated Biomarker Strategy
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