FM AUGUST 2018 ISSUE1 - digital edition

diagnostics
Taming sepsis
Molecular diagnostics, genetic tools offer new hope for sepsis management by
pinning down causes behind the irrepressible host response
S
epsis is among the most
common causes of death in
hospitals the world over.
Diagnosis of this condition, which arises
from the host’s response to an
infection, so far relied purely on
nonspecific physiological criteria and
culture-based pathogen detection.
Obviously, this has often led to
diagnostic uncertainty and therapeutic
delays, which have been a key
challenge for physicians
across specialities.
However, recent breakthroughs in finding
new biomarkers for pathogen detection
and their genetic analysis have resulted in
not only better therapeutic decisions, but
also hope for developing new drugs for
targeted therapy.
In sepsis, the host response involves
hundreds of mediators and single
molecules. These mediators and single
molecules have now been proposed
as biomarkers, though it is unlikely that
one single biomarker will be able to
satisfy all the needs of sepsis screening
and management.
According to earlier studies, procalcitonin
(PCT) had shown some usefulness as an
infection marker among the biomarkers
that are measurable by assays approved
for clinical use. But several recent studies
have found possible new approaches,
including molecular strategies, to
improve pathogen detection and
molecular diagnostics, and prognostics
based on transcriptomic, proteomic, or
metabolic profiling.
These novel approaches to diagnosing
sepsis promise to transform sepsis from
a physiologic syndrome into a group of
distinct biochemical disorders and help in
the development of better diagnostic tools
and effective adjunctive sepsis therapies.
Since sepsis arises from the host response
to infection, which is directed to kill the
invading pathogens, patient outcomes
are determined not only by the viability
of the invading pathogen but also by the
exuberance of host response. While the
growth of the pathogen can be directly toxic
and destructive to tissues, the intensity of
host response results in collateral organ and
tissue damage due as the highly potent
effectors do not discriminate between
microbial and host targets.
34 / FUTURE MEDICINE / AUGUST 2018