Clinical and Molecular Hepatology,
Journal Year:
2021,
Volume and Issue:
27(3), P. 437 - 445
Published: Jan. 28, 2021
Patients
with
cirrhosis
are
susceptible
to
develop
infections
because
of
immune
dysfunction,
changes
in
microbiome
and
increase
bacterial
translocation
from
the
gut
systemic
circulation.
Bacterial
can
worse
clinical
course
disease,
triggering
development
complications
such
as
acute
kidney
injury,
hepatic
encephalopathy,
organ
failures
on
chronic
liver
failure.
In
recent
years,
spread
multi
drug
resistant
bacteria
made
more
challenging
management
patients
cirrhosis.
Hence,
mortality
rate
associated
sepsis
is
increasing
these
patients.
Therefore,
optimization
has
a
high
priority
Herein
we
reviewed
epidemiology
The Lancet Regional Health - Europe,
Journal Year:
2021,
Volume and Issue:
12, P. 100240 - 100240
Published: Nov. 4, 2021
Cirrhosis
is
known
to
have
a
high
prevalence
and
mortality
worldwide.
However,
in
Europe,
the
epidemiology
of
cirrhosis
possibly
undergoing
demographic
changes,
etiologies
may
changed
due
improvements
standard
care.
The
aim
this
population-based
study
was
analyze
trends
course
liver
its
complications
recent
years
Germany.
Hepatology International,
Journal Year:
2025,
Volume and Issue:
19(1), P. 1 - 69
Published: Feb. 1, 2025
Acute-on-chronic
liver
failure
(ACLF)
is
a
condition
associated
with
high
mortality
in
the
absence
of
transplantation.
There
have
been
various
definitions
proposed
worldwide.
The
first
consensus
report
working
party
Asian
Pacific
Association
for
Study
Liver
(APASL)
set
2004
on
ACLF
was
published
2009,
and
"APASL
Research
Consortium
(AARC)"
formed
2012.
AARC
database
has
prospectively
collected
nearly
10,500
cases
from
countries
Asia-Pacific
region.
This
instrumental
developing
score
grade
ACLF,
concept
'Golden
Therapeutic
Window',
'transplant
window',
plasmapheresis
as
treatment
modality.
Also,
data
key
to
identifying
pediatric
ACLF.
European
Liver-Chronic
Failure
(EASL
CLIF)
North
American
End
Stage
Disease
(NACSELD)
West
added
concepts
organ
infection
precipitants
development
CLIF-Sequential
Organ
Assessment
(SOFA)
NACSELD
scores
prognostication.
Chinese
Group
Severe
Hepatitis
B
(COSSH)
COSSH-ACLF
criteria
manage
hepatitis
b
virus-ACLF
without
cirrhosis.
literature
supports
these
be
equally
effective
their
respective
cohorts
patients
mortality.
To
overcome
differences
develop
global
consensus,
APASL
took
initiative
invited
stakeholders,
including
opinion
leaders
Asia,
EASL
AASLD,
other
researchers
field
identify
issues
an
evidence-based
document.
document
presented
hybrid
format
at
annual
meeting
Kyoto
March
2024.
'Kyoto
Consensus'
below
carries
final
recommendations
along
relevant
background
information
areas
requiring
future
studies.
Critical Care,
Journal Year:
2022,
Volume and Issue:
26(1)
Published: Sept. 26, 2022
Abstract
Organ
dysfunction
or
overt
failure
is
a
commonplace
event
in
the
critically
ill
affecting
up
to
70%
of
patients
during
their
stay
ICU.
The
outcome
depends
on
resolution
impaired
organ
function,
while
domino-like
deterioration
organs
other
than
primarily
affected
ones
paves
way
for
increased
mortality.
“Acute
Liver
Failure”
was
defined
1970s
as
rare
and
potentially
reversible
severe
liver
injury
absence
prior
disease
with
hepatic
encephalopathy
occurring
within
8
weeks.
Dysfunction
general
reflects
critical
“Multiple
Syndrome”
due
immunologic,
regulatory
metabolic
functions
parenchymal
non-parenchymal
cells.
Dysregulation
inflammatory
response,
persistent
microcirculatory
(hypoxic)
impairment
drug-induced
are
leading
problems
that
result
“secondary
failure,”
i.e.,
acquired
without
underlying
preexisting
(chronic)
(“Acute-on-Chronic
Failure”).
Conventional
laboratory
markers,
such
transaminases
bilirubin,
limited
provide
insight
into
complex
facets
immunologic
dysfunction.
Furthermore,
inhomogeneous
definitions
these
entities
lead
widely
ranging
estimates
incidence.
In
present
work,
we
review
different
improve
understanding
perpetrator
(and
therapeutic
target)
multiple
syndrome
care.
Graphic
JHEP Reports,
Journal Year:
2022,
Volume and Issue:
4(7), P. 100493 - 100493
Published: April 20, 2022
Bacterial
infections
in
cirrhosis
are
associated
with
increased
bleeding
risk.
To
assess
the
factors
responsible
for
tendency
patients
bacterial
infections,
we
conducted
a
prospective
study
comparing
all
3
aspects
of
hemostasis
(platelets,
coagulation,
and
fibrinolysis)
hospitalized
decompensated
vs.
without
infections.Primary
assessment
included
whole
blood
platelet
aggregation
von
Willebrand
factor
(VWF).
Coagulation
procoagulant
(fibrinogen,
II,
V,
VII,
VIII,
IX,
X,
XI,
XII,
XIII),
natural
anticoagulants
(protein
C,
protein
S,
antithrombin)
thrombomodulin-modified
thrombin
generation
test.
Fibrinolysis
fibrinolytic
(plasminogen,
t-PA,
PAI-1,
α2-AP,
TAFIa/ai)
plasmin-antiplasmin
complex
(PAP).Eighty
were
(40
40
infections).
Severity
count
comparable
between
groups.
At
baseline,
had
significantly
lower
aggregation,
significant
differences
VWF.
Regarding
reduced
VII
reduction
anticoagulants.
However,
was
Finally,
although
mixed
potentially
hypo-fibrinolytic
(lower
plasminogen)
hyper-fibrinolytic
(higher
t-PA)
changes
present
level
PAP
detected
both
Upon
resolution
infection
(n
=
29/40),
further
deteriorated
whereas
coagulation
fibrinolysis
returned
to
levels
observed
infections.In
cirrhosis,
decrease
anticoagulants,
which
may
unbalance
increase
risk
thrombosis.Bacterial
common
issue
(i.e.
due
severe
complications
advanced
chronic
liver
disease).
Patients
who
acquire
be
at
following
invasive
procedures
(that
is
procedure
body
penetrated
or
entered,
instance
by
needle
tube).
As
high
decompensation
death,
there
an
urgent
need
understand
such
tendency.
Herein,
investigated
alterations
physiological
process
clot
formation
stability)
infections.
We
found
that
development
these
(particularly
platelets
clotting
cascade)
thrombotic
complications.
Gut,
Journal Year:
2023,
Volume and Issue:
72(8), P. 1581 - 1591
Published: Feb. 14, 2023
Background
and
aims
Current
prognostic
scores
of
patients
with
acutely
decompensated
cirrhosis
(AD),
particularly
those
acute-on-chronic
liver
failure
(ACLF),
underestimate
the
risk
mortality.
This
is
probably
because
systemic
inflammation
(SI),
major
driver
AD/ACLF,
not
reflected
in
scores.
SI
induces
metabolic
changes,
which
impair
delivery
necessary
energy
for
immune
reaction.
investigation
aimed
to
identify
metabolites
associated
short-term
(28-day)
death
design
metabolomic
models.
Methods
Two
prospective
multicentre
large
cohorts
from
Europe
investigating
ACLF
development
ACLF,
CANONIC
(discovery,
n=831)
PREDICT
(validation,
n=851),
were
explored
by
untargeted
serum
metabolomics
validate
could
allow
improved
modelling.
Results
Three
strongly
selected
build
4-Hydroxy-3-methoxyphenylglycol
sulfate
a
norepinephrine
derivative,
may
be
derived
brainstem
response
SI.
Additionally,
galacturonic
acid
hexanoylcarnitine
are
mitochondrial
dysfunction.
Model
1
included
only
these
three
age.
2
was
built
around
4-hydroxy-3-methoxyphenylglycol
sulfate,
hexanoylcarnitine,
bilirubin,
international
normalised
ratio
(INR)
In
discovery
cohort,
both
models
more
accurate
predicting
within
7,
14
28
days
after
admission
compared
MELDNa
score
(C-index:
0.9267,
0.9002
0.8424,
0.9369,
0.9206
0.8529,
model
2,
respectively).
Similar
results
found
validation
cohort
0.940,
0.834
0.791,
0.947,
0.857
0.810,
Also,
outperformed
prediction
Conclusions
Models
including
(CLIF-C
MET)
reflecting
SI,
dysfunction
sympathetic
system
activation
better
predictors
mortality
than
based
on
organ
(eg,
MELDNa),
especially
ACLF.
JHEP Reports,
Journal Year:
2023,
Volume and Issue:
5(9), P. 100807 - 100807
Published: June 8, 2023
Acute-on-chronic
liver
failure
(ACLF)
is
the
most
severe
form
of
acutely
decompensated
cirrhosis
and
characterised
by
presence
one
or
more
organ
failures,
intense
systemic
inflammation,
peripheral
blood
lymphopenia,
a
high
risk
death
without
transplantation
within
28
days.
Herein,
we
propose
hypothesis
that
inflammation
may
lead
to
failures
through
five
different
non-mutually
exclusive
mechanisms.
First,
pathogen-associated
molecular
patterns
inflammatory
mediators
(i.e.
cytokines
lipid
mediators)
stimulate
production
vasorelaxant
nitric
oxide
in
walls
splanchnic
arterioles,
leading
enhanced
vasodilation
which,
turn,
induces
activity
endogenous
vasoconstrictor
systems
causing
renal
vasoconstriction
acute
kidney
injury.
Second,
neutrophils
reach
circulation
are
prone
adhere
vascular
endothelium.
Cytokines
act
on
endothelium
microvessels
vital
organs,
an
effect
favours
migration
(and
probably
other
leukocytes)
surrounding
tissues
where
can
cause
tissue
damage
thereby
contribute
failure.
Third,
promote
formation
microthrombi
impair
microcirculation
oxygenation.
Fourth,
stimulates
catabolism
amino
acids
whose
products
be
metabotoxins
hepatic
encephalopathy.
Fifth,
responses,
which
include
broad
variety
biomolecules
(proteins
lipids),
increase
biomass
(i.e.,
granulopoiesis
requiring
de
novo
nucleotide
synthesis),
among
others,
energetically
expensive
processes
require
large
amounts
nutrients.
Therefore,
immunity
competes
with
maintenance
programmes
for
energy.
The
brain
stem
integrates
energy
demand
each
system,
considered
top
priority.
"decide"
make
trade-off
involves
induction
dormancy
programme
permits
shutdown
mitochondrial
respiration
oxidative
phosphorylation
organs.
In
context
cirrhosis,
consequence
ATP
would
dramatic
decrease
function.
Gut,
Journal Year:
2024,
Volume and Issue:
73(6), P. 1015 - 1024
Published: March 25, 2024
The
progression
of
cirrhosis
with
clinically
significant
portal
hypertension
towards
decompensated
remains
challenging
and
the
evolution
acute-on-chronic
liver
failure
(ACLF),
one
or
more
extrahepatic
organ
failures,
is
associated
very
high
mortality.
In
last
decade,
progress
has
been
made
in
understanding
mechanisms
leading
to
decompensation
ACLF.
As
advances,
bacterial
translocation
across
an
impaired
gut
barrier
culminates
endotoxaemia,
systemic
inflammation
cirrhosis-associated
immune
dysfunction
(CAID).
Gut-derived
CAID
have
become
logical
targets
for
innovative
therapies
that
prevent
hepatic
episodes
Furthermore,
classification
disease
biomarker
discovery
personalise
care
advanced
field.
This
review
discusses
personalisation
treatment