Frontiers in Cardiovascular Medicine,
Год журнала:
2021,
Номер
8
Опубликована: Ноя. 19, 2021
Background:
Thrombosis
is
a
characteristic
complication
in
coronavirus
disease
2019
(COVID-19).
Since
coagulopathy
has
been
observed
over
the
entire
clinical
course,
thrombosis
might
be
clue
to
understanding
specific
pathology
COVID-19.
Currently,
there
limited
epidemiological
data
of
COVID-19-associated
Japanese
population
and
none
regarding
variant
strains
SARS-CoV-2.
Here,
we
elucidate
risk
factors
pattern
COVID-19
patients.
Methods:
The
patients
consecutively
admitted
Tokyo
Medical
Dental
University
Hospital
with
were
retrospectively
analyzed.
SARS-CoV-2
variants
concern/interest
(VOC/VOI)
carrying
spike
protein
mutants
E484K,
N501Y,
or
L452R
identified
by
PCR-based
analysis.
All
thrombotic
events
diagnosed
symptoms,
ultrasonography,
and/or
radiological
tests.
Results:
Among
516
patients,
32
experienced
42
thromboembolic
events.
Advanced
age,
severe
respiratory
conditions,
several
abnormal
laboratory
markers
associated
development
thrombosis.
While
occurred
13%
condition,
those
still
2.5%
who
did
not
require
oxygen
therapy.
Elevated
D-dimer
ferritin
levels
on
admission
independent
(adjusted
odds
ratio
9.39
3.11,
95%
confidence
interval
2.08-42.3,
1.06-9.17,
respectively).
Of
events,
22
venous,
whereas
20
arterial.
received
anticoagulation
antiinflammatory
therapies
higher
proportion,
mortality
rate,
organ
dysfunctions,
bleeding
complications
these
than
without
incidence
became
less
frequent
time,
such
as
during
replacement
earlier
VOC/VOI
increased
use
anticoagulatory
therapeutics.
Conclusion:
This
study
elucidated
that
elevated
are
useful
biomarkers
comparable
arterial
venous
required
further
considerations
for
management
Further
studies
would
identify
high-risk
populations
establish
appropriate
interventions
Virchows Archiv,
Год журнала:
2021,
Номер
478(1), С. 137 - 150
Опубликована: Янв. 1, 2021
The
lung
is
the
main
affected
organ
in
severe
coronavirus
disease
2019
(COVID-19)
caused
by
novel
SARS-CoV-2,
and
damage
leading
cause
of
death
vast
majority
patients.
Mainly
based
on
results
obtained
autopsies,
seminal
features
fatal
COVID-19
have
been
described
many
groups
worldwide.
Early
changes
encompass
edema,
epithelial
damage,
capillaritis/endothelialitis,
frequently
combined
with
microthrombosis.
Subsequently,
patients
manifest
respiratory
insufficiency
exhibit
exudative
diffuse
alveolar
(DAD)
hyaline
membrane
formation
pneumocyte
type
2
hyperplasia,
variably
complicated
superinfection,
which
may
progress
to
organizing/fibrotic
stage
DAD.
These
features,
however,
are
not
specific
for
can
be
found
other
disorders
including
viral
infections.
Clinically,
early
characterized
high
load,
lymphopenia,
massive
secretion
pro-inflammatory
cytokines
hypercoagulability,
documented
elevated
D-dimers
an
increased
frequency
thrombotic
thromboembolic
events,
whereas
virus
loads
cytokine
levels
tend
decrease
late
stages,
when
tissue
repair
angiogenesis
prevails.
present
review
describes
spectrum
pathology
current
literature
authors'
personal
experience
derived
from
clinical
tries
summarize
our
understanding
open
questions
pathophysiology
pulmonary
COVID-19.
Cells,
Год журнала:
2023,
Номер
12(5), С. 688 - 688
Опубликована: Фев. 22, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
causes
disease
2019
(COVID-19).
About
45%
of
COVID-19
patients
experience
several
symptoms
a
few
months
after
the
initial
infection
and
develop
post-acute
sequelae
SARS-CoV-2
(PASC),
referred
to
as
“Long-COVID,”
characterized
by
persistent
physical
mental
fatigue.
However,
exact
pathogenetic
mechanisms
affecting
brain
are
still
not
well-understood.
There
is
increasing
evidence
neurovascular
inflammation
in
brain.
precise
role
neuroinflammatory
response
that
contributes
severity
long
COVID
pathogenesis
clearly
understood.
Here,
we
review
reports
spike
protein
can
cause
blood–brain
barrier
(BBB)
dysfunction
damage
neurons
either
directly,
or
via
activation
mast
cells
microglia
release
various
molecules.
Moreover,
provide
recent
novel
flavanol
eriodictyol
particularly
suited
for
development
an
effective
treatment
alone
together
with
oleuropein
sulforaphane
(ViralProtek®),
all
which
have
potent
anti-viral
anti-inflammatory
actions.
International Journal of Immunopathology and Pharmacology,
Год журнала:
2021,
Номер
35
Опубликована: Янв. 1, 2021
COVID-19
is
a
highly
heterogeneous
and
complex
medical
disorder;
indeed,
severe
probably
amongst
the
most
of
conditions
known
to
science.
While
enormous
strides
have
been
made
in
understanding
molecular
pathways
involved
patients
infected
with
coronaviruses
an
overarching
comprehensive
pathogenesis
lacking.
Such
essential
formulation
effective
prophylactic
treatment
strategies.
Based
on
clinical,
proteomic,
genomic
studies
as
well
autopsy
data
disease
can
be
considered
connection
three
basic
pathologic
processes,
namely
pulmonary
macrophage
activation
syndrome
uncontrolled
inflammation,
complement-mediated
endothelialitis
together
procoagulant
state
thrombotic
microangiopathy.
In
addition,
platelet
release
serotonin
degranulation
mast
cells
contributes
hyper-inflammatory
state.
Auto-antibodies
demonstrated
large
number
hospitalized
which
adds
end-organ
damage
pro-thrombotic
This
paper
provides
clinical
overview
major
pathogenetic
mechanism
leading
disease.
Clinics in Dermatology,
Год журнала:
2021,
Номер
39(6), С. 966 - 984
Опубликована: Июль 25, 2021
A
total
of
22
patients
who
had
developed
an
adverse
cutaneous
reaction
to
the
Moderna
or
Pfizer
vaccine
underwent
biopsies.
Each
patient
was
assessed
light
microscopically,
and,
in
select
biopsies,
spike
glycoprotein
and
cytokine
assessment
were
also
conducted.
The
self-limited
reactions
often
described
clinically
as
urticarial
eczematous
within
1
day
4
weeks
after
receiving
first
second
dose
vaccine.
Classic
clinical
morphologic
depictions
type
IV
hypersensitivity
with
features
dermatitis,
interface
granulomatous
inflammation,
and/or
lymphocytic
vasculitic
component
observed.
Clinical
histologic
perniosis,
pityriasis
rosea,
rubra
pilaris,
guttate
psoriasis
seen
cases.
In
2
cases
dominant
picture
vasculitis,
possibly
reflective
Arthus
III
immune
complex
action.
biopsy
specimens
normal
skin
post
affected
by
post-vaccine
eruption
showed
rare
deep
microvessels
positive
for
no
complement
deposition
contrasting
greater
vascular
protein
biopsies
from
experiencing
severe
coronavirus
disease
2019
(COVID-19).
It
is
concluded
that
occur
owing
a
substance
found
vehicle
(eg,
polyethylene
glycol).
An
response
directed
against
human-manufactured
has
be
considered
because
some
histologically
closely
resemble
mild
COVID-19.
Finally,
vaccine-associated
enhancement
largely
attributable
adjuvant
properties
may
unmask
certain
inflammatory
milieus
operational
psoriasis,
atopic
subclinical
hypersensitivity.
Journal of Biomedical Science,
Год журнала:
2022,
Номер
29(1)
Опубликована: Окт. 26, 2022
Abstract
Severe
acute
respiratory
syndrome-associated
coronavirus-2
(SARS-CoV-2)
is
the
causal
agent
of
coronavirus
disease-2019
(COVID-19),
a
systemic
illness
characterized
by
variably
severe
pulmonary
symptoms,
cardiac
conduction
abnormalities,
diarrhea,
and
gastrointestinal
bleeding,
as
well
neurologic
deficits,
renal
insufficiency,
myalgias,
endocrine
other
perturbations
that
reflect
widespread
microvascular
injury
pro-inflammatory
state.
The
mechanisms
underlying
various
manifestations
viral
infection
are
incompletely
understood
but
most
data
suggest
COVID-19
results
from
virus-driven
in
immune
system
resultant
tissue
injury.
Aberrant
interferon-related
responses
lead
to
alterations
cytokine
elaboration
deplete
resident
cells
while
simultaneously
recruiting
hyperactive
macrophages
functionally
altered
neutrophils,
thereby
tipping
balance
adaptive
immunity
innate
immunity.
Disproportionate
activation
these
neutrophils
further
depletes
normal
activity
B-cells,
T-cells,
natural
killer
(NK)
cells.
In
addition,
this
state
stimulates
uncontrolled
complement
development
neutrophil
extracellular
traps
(NETS),
both
which
promote
coagulation
cascade
induce
“thrombo-inflammation”.
These
have
similar
multiple
organ
systems,
frequently
show
pathologic
findings
related
thrombosis
large
small
vessels.
However,
patients
with
generally
more
pronounced
than
those
organs.
Not
only
do
they
feature
inflammatory
thromboses
endothelial
injury,
much
parenchymal
damage
stems
failed
maturation
alveolar
pneumocytes,
interactions
between
type
2
pneumocytes
non-resident
macrophages,
greater
degree
NET
formation.
purpose
review
discuss
pathogenesis
can
occur
SARS-CoV-2
infection.
Understanding
important
future
therapies
for
COVID-19,
many
will
likely
target
specific
components
system,
particularly
induction,
cytokines,
subpopulations
Acta Haematologica,
Год журнала:
2021,
Номер
144(5), С. 476 - 483
Опубликована: Янв. 1, 2021
Background:
Histopathological
analysis
can
provide
additional
clues
in
COVID-19
understanding.
During
the
last
year,
autopsy
reports
have
revealed
that
diffuse
alveolar
damage
(DAD)
is
most
significant
observed
finding.
The
aim
of
this
study
to
review
cases
literature
about
autopsies
reported
microthrombi
different
organs.
Methods:
We
performed
a
systematic
PubMed,
Virtual
Health
Library
(VHL),
and
Google
Scholar.
Results:
In
total,
151
were
included,
91
presented
lung
(73%),
heart
(11.2%),
kidney
(24%),
liver
(16.3%).
age
range
was
between
27
96
years.
Males
64.8%.
patients
with
had
more
comorbidities
such
as
arterial
hypertension
(62%),
obesity
or
overweight
(64%),
diabetes
mellitus
type
2
(51%),
disease
(53%).
common
histopathological
changes
found
microthrombosis
DAD
exudative
phase
(78%),
pulmonary
embolism
(59%),
infarct
(81%).
Presence
associated
(p
<
0.0001)
proliferative
phases
=
0.02).
Discussion:
these
results
shows
may
be
organs
are
frequent
comorbidities,
embolism,
infarct.