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
Journal of Hepatology,
Journal Year:
2023,
Volume and Issue:
79(2), P. 516 - 537
Published: March 27, 2023
Liver
disease
accounts
for
two
million
deaths
annually
and
is
responsible
4%
of
all
(1
out
every
25
worldwide);
approximately
two-thirds
liver-related
occur
in
men.
Deaths
are
largely
attributable
to
complications
cirrhosis
hepatocellular
carcinoma,
with
acute
hepatitis
accounting
a
smaller
proportion
deaths.
The
most
common
causes
worldwide
related
viral
hepatitis,
alcohol,
non-alcoholic
fatty
liver
disease.
Hepatotropic
viruses
the
aetiological
factor
cases
but
drug-induced
injury
increasingly
significant
cases.
This
iteration
global
burden
an
update
2019
version
focuses
mainly
on
areas
where
new
information
available
like
alcohol-associated
disease,
carcinoma.
We
also
devote
separate
section
Africa,
area
world
typically
neglected
such
documents.
Journal of Hepatology,
Journal Year:
2020,
Volume and Issue:
74(3), P. 670 - 685
Published: Dec. 7, 2020
Acute
decompensation
(AD)
of
cirrhosis
is
defined
by
the
development
ascites,
hepatic
encephalopathy
and/or
variceal
bleeding.
Ascites
traditionally
attributed
to
splanchnic
arterial
vasodilation
and
left
ventricular
dysfunction,
hyperammonaemia,
haemorrhage
portal
hypertension.
Recent
large-scale
European
observational
studies
have
shown
that
systemic
inflammation
a
hallmark
AD.
Here
we
present
working
hypothesis,
suggesting
through
an
impairment
functions
one
or
more
major
organ
systems
may
be
common
theme
act
synergistically
with
traditional
mechanisms
involved
in
Systemic
impair
system
function
which
are
not
mutually
exclusive.
The
first
mechanism
nitric
oxide-mediated
accentuation
preexisting
vasodilation,
resulting
overactivation
endogenous
vasoconstrictor
elicit
intense
vasoconstriction
hypoperfusion
certain
vascular
beds,
particular
renal
circulation.
Second,
cause
immune-mediated
tissue
damage,
process
called
immunopathology.
Finally,
induce
important
metabolic
changes.
Indeed,
inflammatory
responses
energetically
expensive
processes,
requiring
reallocation
nutrients
(glucose,
amino
acids
lipids)
fuel
immune
activation.
also
inhibits
nutrient
consumption
peripheral
(non-immune)
organs,
effect
provide
prioritisation
fuels
for
responses.
However,
decrease
organs
result
decreased
mitochondrial
production
ATP
(energy)
subsequently
impaired
function.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(9), P. 4496 - 4496
Published: April 26, 2021
Hypoalbuminemia
is
associated
with
the
acquisition
and
severity
of
infectious
diseases,
intact
innate
adaptive
immune
responses
depend
on
albumin.
Albumin
oxidation
breakdown
affect
interactions
bioactive
lipid
mediators
that
play
important
roles
in
antimicrobial
defense
repair.
There
bio-mechanistic
plausibility
for
a
causal
link
between
hypoalbuminemia
increased
risks
primary
secondary
infections.
Serum
albumin
levels
have
prognostic
value
complications
viral,
bacterial
fungal
infections,
non-infective
chronic
conditions.
predicts
development
healthcare-associated
particularly
Clostridium
difficile.
In
coronavirus
disease
2019,
correlates
viral
load
degree
acute
lung
injury
organ
dysfunction.
Non-oncotic
properties
pharmacokinetics
pharmacodynamics
antimicrobials.
Low
serum
inadequate
treatment.
Infusion
human
solution
(HAS)
supplements
endogenous
patients
cirrhosis
liver
effectively
supported
therapy
randomized
controlled
trials
(RCTs).
Evidence
beneficial
effects
HAS
infections
hypoalbuminemic
without
largely
observational.
Prospective
RCTs
are
underway
and,
if
hypotheses
confirmed,
could
lead
to
changes
clinical
practice
management
or
at
risk
complications.
Journal of Hepatology,
Journal Year:
2021,
Volume and Issue:
75, P. S67 - S81
Published: May 23, 2021
Cirrhosis
-
the
common
end-stage
of
chronic
liver
disease
is
associated
with
a
cascade
events,
which
intestinal
bacterial
overgrowth
and
dysbiosis
are
central.
Bacterial
toxins
entering
portal
or
systemic
circulation
can
directly
cause
hepatocyte
death,
while
also
affects
gut
barrier
function
increases
translocation,
leading
to
infections,
inflammation
vasodilation,
contribute
acute
decompensation
organ
failure.
Acute
its
severe
forms,
pre-acute-on-chronic
failure
(ACLF)
ACLF,
characterised
by
sudden
dysfunction
(and
failure)
high
short-term
mortality.
Patients
pre-ACLF
ACLF
present
high-grade
inflammation,
usually
precipitated
proven
infection
and/or
alcoholic
hepatitis.
However,
no
precipitant
identified
in
30%
these
patients,
whom
translocation
from
microbiota
assumed
be
responsible
for
decompensation.
Different
profiles
may
influence
rate
thereby
outcome
patients.
Thus,
targeting
promising
strategy
prevention
treatment
decompensation,
ACLF.
Approaches
include
use
antibiotics
such
as
rifaximin,
faecal
microbial
transplantation
enterosorbents
(e.g.
Yaq-001),
bind
factors
without
exerting
direct
effect
on
growth
kinetics.
This
review
focuses
role
strategies
prevent
The American Journal of Gastroenterology,
Journal Year:
2022,
Volume and Issue:
unknown
Published: Jan. 10, 2022
In
patients
with
cirrhosis
and
chronic
liver
disease,
acute-on-chronic
failure
is
emerging
as
a
major
cause
of
mortality.
These
guidelines
indicate
the
preferred
approach
to
management
represent
official
practice
recommendations
American
College
Gastroenterology.
The
scientific
evidence
for
these
was
evaluated
using
Grading
Recommendations,
Assessment,
Development,
Evaluation
process.
instances
where
not
appropriate
Evaluation,
but
there
consensus
significant
clinical
merit,
key
concept
statements
were
developed
expert
consensus.
are
meant
be
broadly
applicable
should
viewed
preferred,
only,
scenarios.
JHEP Reports,
Journal Year:
2021,
Volume and Issue:
3(4), P. 100316 - 100316
Published: June 5, 2021
Portal
hypertension,
defined
as
increased
pressure
in
the
portal
vein,
develops
a
consequence
of
intrahepatic
vascular
resistance
due
to
dysregulation
liver
sinusoidal
endothelial
cells
(LSECs)
and
hepatic
stellate
(HSCs),
frequently
arising
from
chronic
diseases.
Extrahepatic
haemodynamic
changes
contribute
aggravation
hypertension.
The
pathogenic
complexity
hypertension
unsuccessful
translation
preclinical
studies
have
impeded
development
effective
therapeutics
for
patients
with
cirrhosis,
while
counteracting
extrahepatic
mechanisms
also
pose
major
obstacle
treatment.
In
this
review
article,
we
will
discuss
following
topics:
i)
cellular
molecular
focusing
on
LSECs,
HSCs
microvascular
thrombosis,
well
vasculature,
since
these
are
contributors
hypertension;
ii)
translational/clinical
advances
our
knowledge
iii)
future
directions.
