Frontiers in Medicine,
Journal Year:
2024,
Volume and Issue:
11
Published: July 17, 2024
After
the
introduction
of
antiretroviral
therapy,
care
given
to
people
living
with
HIV
has
become
complicated
by
appearance
comorbidities
as
a
result
and
HAART
toxicities,
in
which
cardiovascular
disease
got
most
attention.
So,
this
study
aimed
assess
serum
uric
acid
high-sensitivity
C-reactive
protein
levels
among
on
dolutegravir
(DTG)
ritonavir-boosted
atazanavir
(ATV/r)-based
therapy.
Kidney International Reports,
Journal Year:
2022,
Volume and Issue:
8(2), P. 229 - 239
Published: Dec. 6, 2022
Gout
and
hyperuricemia
are
present
in
25%
60%
of
patients
with
chronic
kidney
disease
(CKD),
respectively.
Despite
the
common
association,
role
uric
acid
progression
metabolic
complications
remains
contested.
Some
authorities
argue
that
treatment
asymptomatic
CKD
is
not
indicated,
some
have
even
suggested
may
be
beneficial.
Here,
we
review
various
arguments
both
for
against
treatment.
The
weight
evidence
suggests
likely
injurious,
but
it
primarily
relate
to
subgroups,
those
who
systemic
crystal
deposits,
frequent
urinary
crystalluria
or
stones,
high
intracellular
levels.
We
recommend
carefully
designed
clinical
trials
test
if
lowering
hyperuricemic
subjects
cardiometabolic
protective.
Cell Communication and Signaling,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 3, 2025
Oxidative
stress
and
neuroinflammation
are
recognized
as
key
factors
in
the
development
of
neurodegenerative
diseases,
yet
effective
interventions
biomarkers
to
address
oxidative
these
conditions
limited.
Uric
acid
(UA),
traditionally
associated
with
gout,
is
now
gaining
prominence
a
potential
target
diseases.
Soluble
UA
stands
out
one
most
vital
antioxidant
compounds
produced
by
human
body,
accounting
for
up
55%
extracellular
capacity
neutralize
free
radicals.
While
there
increasing
evidence
supporting
neuroprotective
properties
Parkinson's
disease
Alzheimer's
disease,
gaps
knowledge
still
exist
regarding
underlying
mechanisms
how
effectively
translate
benefits
into
clinical
practice.
Moreover,
current
elevation
therapy
exhibits
unstable
properties,
individual
variability,
even
adverse
effects,
limiting
its
applications.
This
review
consolidates
recent
advancements
understanding
exerts
effects
on
diseases
emphasizes
dual
roles
managing
neuroinflammation.
Additionally,
elucidates
through
which
confers
neuroprotection.
Based
this,
underscores
significance
biomarker
aims
provide
comprehensive
therapeutic
target,
while
also
addressing
possible
challenges
implementation.
Philosophical Transactions of the Royal Society B Biological Sciences,
Journal Year:
2023,
Volume and Issue:
378(1885)
Published: July 24, 2023
The
fructose
survival
hypothesis
proposes
that
obesity
and
metabolic
disorders
may
have
developed
from
over-stimulation
of
an
evolutionary-based
biologic
response
(survival
switch)
aims
to
protect
animals
in
advance
crisis.
is
characterized
by
hunger,
thirst,
foraging,
weight
gain,
fat
accumulation,
insulin
resistance,
systemic
inflammation
increased
blood
pressure.
process
initiated
the
ingestion
or
stimulating
endogenous
production
via
polyol
pathway.
Unlike
other
nutrients,
reduces
active
energy
(adenosine
triphosphate)
cell,
while
blocking
its
regeneration
stores.
This
mediated
intracellular
uric
acid,
mitochondrial
oxidative
stress,
inhibition
AMP
kinase
stimulation
vasopressin.
Mitochondrial
phosphorylation
suppressed,
glycolysis
stimulated.
While
this
aimed
be
modest
short-lived,
humans
exaggerated
due
gain
‘thrifty
genes’
coupled
with
a
western
diet
rich
foods
contain
generate
fructose.
We
propose
excessive
metabolism
not
only
explains
but
epidemics
diabetes,
hypertension,
non-alcoholic
fatty
liver
disease,
obesity-associated
cancers,
vascular
Alzheimer's
dementia,
even
ageing.
Moreover,
unites
current
hypotheses
on
obesity.
Reducing
activation
and/or
pathway
benefit
health-span.
article
part
discussion
meeting
issue
‘Causes
obesity:
theories,
conjectures
evidence
(Part
I)’.
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(2), P. 518 - 518
Published: Jan. 15, 2025
Background/Objectives:
The
accumulation
of
uric
acid
in
arteriosclerotic
plaques
has
recently
attracted
attention.
Because
the
interaction
between
hyperuricemia
and
atherosclerosis
is
complex,
details
remain
obscure.
We
aimed
to
elucidate
clinical
effect
monosodium
urate
monohydrate
(MSU)
deposition
on
carotid
plaques.
Methods:
This
study
enrolled
89
patients
with
MSU
deposits
were
confirmed
using
Gomori’s
methenamine
silver
staining
endarterectomy
(CEA)
specimens.
To
evaluate
macrophage
microvessel
marker
counts,
we
used
CD68
CD31.
Plaque
composition
was
investigated
inflammation.
also
examined
use
dual-energy
computed
tomography
(DECT)
compensated
for
pathological
findings
detect
crystal
Results:
Of
who
underwent
CEA,
31
(34.8%)
had
hyperuricemia.
Overall,
22
(24.7%)
participants
67
(75.3%)
did
not.
deposits,
CD31-positive
microvessels,
CD68-positive
cells
observed
shoulder
lesions.
number
microvessels
higher
than
those
without
deposits.
Most
expressing
intraplaque
hemorrhage.
consistency
deposit
identification
histopathology
DECT
poor
(kappa
=
0.34).
Conclusions:
may
be
related
inflammation
Postgraduate Medicine,
Journal Year:
2024,
Volume and Issue:
136(6), P. 615 - 623
Published: July 8, 2024
Serum
uric
acid
(SUA)
has
garnered
an
increased
interest
in
recent
years
as
important
determinant
of
cardiovascular
disease.
Uric
acid,
a
degradation
product
purine
metabolism,
is
affected
by
several
inheritable
and
acquired
factors,
such
genetic
mutation,
metabolic
syndrome,
chronic
kidney
disease,
medication
interactions.
Even
though
elevated
SUA
have
been
commonly
associated
with
the
development
gout,
it
significant
impact
hypertension,
both
crystalline
soluble
forms,
plays
key
role
induction
inflammatory
cascade
atherosclerotic
diseases.
This
concise
reappraisal
emphasizes
features
about
complex
challenging
progression
atherosclerosis
It
explores
pathogenesis
historical
significance
highlights
interplay
between
components
focuses
on
pro-inflammatory
pro-atherogenic
effects
well
discusses
urate
lowering
therapies
mitigating
risk
disease
while
providing
latest
evidence
to
healthcare
professionals
focusing
clinical
importance
levels
regards
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(12), P. 3169 - 3169
Published: Nov. 28, 2023
Gout
results
from
elevated
serum
urate
(SU)
levels,
or
hyperuricemia,
and
is
a
globally
widespread
increasingly
burdensome
disease.
Recent
studies
have
illuminated
the
pathophysiology
of
gout/hyperuricemia
its
epidemiology,
diagnosis,
treatment,
complications.
The
genetic
involvement
transporters
enzymes
also
proven.
URAT1,
molecular
therapeutic
target
for
gout/hyperuricemia,
was
initially
derived
research
into
hereditary
renal
hypouricemia
(RHUC).
RHUC
often
accompanied
by
complications
such
as
exercise-induced
acute
kidney
injury,
which
indicates
key
physiological
role
uric
acid.
Several
revealed
both
an
anti-oxidant
pro-oxidant,
acting
scavenger
generator
reactive
oxygen
species
(ROSs).
These
discoveries
prompted
interest
in
SU
xanthine
oxidoreductase
(XOR),
enzyme
that
produces
ROSs,
status
progression
biomarkers
chronic
disease
cardiovascular
notion
"the
lower,
better"
therefore
incorrect;
better
understanding
acid
handling
metabolism/transport
comes
awareness
excessively
high
low
levels
cause
problems.
We
summarize
here
current
body
evidence,
demonstrate
much
more
than
metabolic
waste
product,
finally
propose
novel
concept
"dysuricemia"
on
path
toward
"normouricemia",
optimal
level,
to
take
advantage
dual
roles
Our
proposal
should
help
interpret
spectrum
hyperuricemia/gout
single
category.
