COVID-19
is
the
important
global
problem.
This
new
coronavirus
can
cause
several
hematological
changes.
Thrombosis
a
problem
might
occur
in
COVID-19.
In
COVID-19,
thrombosis
be
result
of
endothelial
dysfunction,
platelet
activation,
increasd
blood
viscosity,
and
flow
disturbance.
The
change
viscosity
patients
with
possible
but
little
mentioned.
Here,
authors
report
on
preliminary
data
assessment
among
41
patients.
According
to
estimation,
estimated
values
are
72.4
±
18.6
18.2
2.2
for
high
low
shear
rates.
Based
this
report,
increased
detected
patient
it
associated
thrombohemostatic
Immunology,
Год журнала:
2021,
Номер
165(4), С. 386 - 401
Опубликована: Дек. 27, 2021
Abstract
Coronavirus
disease
2019
(COVID‐19)
pandemic
caused
by
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
has
led
to
an
unprecedented
setback
for
global
economy
and
health.
Vaccination
is
one
of
the
most
effective
interventions
substantially
reduce
death
due
SARS‐CoV‐2
infection.
programmes
are
being
rolled
out
globally,
but
these
vaccines
have
been
approved
without
extensive
studies
on
their
side‐effects
efficacy.
Recently,
new‐onset
autoimmune
phenomena
after
COVID‐19
vaccination
reported
increasingly
(e.g.
immune
thrombotic
thrombocytopenia,
liver
diseases,
Guillain–Barré
syndrome,
IgA
nephropathy,
rheumatoid
arthritis
systemic
lupus
erythematosus).
Molecular
mimicry,
production
particular
autoantibodies
role
certain
vaccine
adjuvants
seem
be
substantial
contributors
phenomena.
However,
whether
association
between
manifestations
coincidental
or
causal
remains
elucidated.
Here,
we
summarize
emerging
evidence
about
occurring
in
response
vaccines.
Although
information
pertaining
risk
as
a
consequence
controversial,
merely
propose
our
current
understanding
associated
with
vaccine.
In
fact,
do
not
aim
disavow
overwhelming
benefits
mass
preventing
morbidity
mortality.
These
reports
could
help
guide
clinical
assessment
management
vaccination.
Over
the
past
16
years,
three
coronaviruses
(CoVs),
severe
acute
respiratory
syndrome
CoV
(SARS-CoV)
in
2002,
Middle
East
(MERS-CoV)
2012
and
2015,
SARS-CoV-2
2020,
have
been
causing
fatal
human
epidemics.
The
unpredictability
of
coronavirus
disease-19
(COVID-19)
poses
a
major
burden
on
health
care
economic
systems
across
world.
This
is
caused
by
paucity
in-depth
knowledge
risk
factors
for
COVID-19,
insufficient
diagnostic
tools
detection
SARS-CoV-2,
as
well
absence
specific
effective
drug
treatments.
While
protective
humoral
cellular
immune
responses
are
usually
mounted
against
these
betacoronaviruses,
to
SARS-CoV2
sometimes
derail
towards
inflammatory
tissue
damage,
leading
rapid
admissions
intensive
units.
lack
mechanisms
that
tilt
balance
between
two
opposite
outcomes
threats
many
ongoing
clinical
trials
dealing
with
immunostimulatory
or
immunoregulatory
therapeutics.
review
will
discuss
innate
cognate
underlying
deleterious
reactions
pathogenic
coronaviruses.
Abstract
The
angiotensin-converting
enzyme
2
(ACE2)
is
the
host
functional
receptor
for
new
virus
SARS-CoV-2
causing
Coronavirus
Disease
2019.
ACE2
expressed
in
72
different
cell
types.
Some
factors
that
can
affect
expression
of
are:
sex,
environment,
comorbidities,
medications
(e.g.
anti-hypertensives)
and
its
interaction
with
other
genes
renin-angiotensin
system
pathways.
Different
risk
infection
determine
severity
symptoms.
a
negative
regulator
RAS
various
organ
systems.
It
immunity,
inflammation,
increased
coagulopathy,
cardiovascular
disease.
In
this
review,
we
describe
genetic
molecular
functions
relation
physiological
pathological
conditions
to
better
understand
how
involved
pathogenesis
COVID-19.
addition,
it
reviews
comorbidities
interact
which
also
plays
an
important
role.
describes
have
influence
activities
receptor.
goal
provide
reader
understanding
complexity
importance
Thrombosis Research,
Год журнала:
2021,
Номер
202, С. 191 - 198
Опубликована: Апрель 20, 2021
Severe
COVID-19
can
manifest
as
multiorgan
dysfunction
with
pulmonary
involvement
being
the
most
common
and
prominent.
As
more
reports
emerge
in
literature,
it
appears
that
an
exaggerated
immune
response
form
of
unfettered
complement
activation
a
cytokine
storm
may
be
key
driver
widespread
organ
injury
seen
this
disease.
In
addition,
these
patients
are
also
known
to
hypercoagulable
high
rate
thrombosis
higher-than-expected
failure
anticoagulation.
While
macrovascular
is
individuals,
frequent
finding
extensive
microvascular
thromboses
several
series
case
reports,
raises
possibility
thrombotic
microangiopathy
(TMA)
contributing
factor
multi-organ
complications
If
correct,
rapidly
identifying
TMA
treating
underlying
pathophysiology
allow
for
better
outcomes
critically
ill
patients.
To
further
explore
this,
we
reviewed
published
literature
on
COVID-19,
looking
describing
TMA-like
presentations.
We
summarize
our
findings
here
along
discussion
about
presentation,
pathophysiology,
suggested
treatment
algorithm.
Journal of Molecular Medicine,
Год журнала:
2021,
Номер
99(7), С. 899 - 915
Опубликована: Апрель 6, 2021
Abstract
The
severe
acute
respiratory
syndrome-coronavirus-2
(SARS-CoV-2)
pandemic
has
proven
a
challenge
to
healthcare
systems
since
its
first
appearance
in
late
2019.
global
spread
and
devastating
effects
of
coronavirus
disease
2019
(COVID-19)
on
patients
have
resulted
countless
studies
risk
factors
progression.
Overweight
obesity
emerged
as
one
the
major
for
developing
COVID-19.
Here
we
review
biology
infections
relation
obesity.
In
particular,
literature
about
impact
adiposity-related
systemic
inflammation
COVID-19
severity,
involving
cytokine,
chemokine,
leptin,
growth
hormone
signaling,
discuss
involvement
hyperactivation
renin-angiotensin-aldosterone
system
(RAAS).
Due
sheer
number
publications
COVID-19,
cannot
be
completed,
therefore,
apologize
all
that
do
not
cite.
Postgraduate Medical Journal,
Год журнала:
2021,
Номер
98(1159), С. 395 - 402
Опубликована: Апрель 13, 2021
Rising
incidence
of
thromboembolism
secondary
to
COVID-19
has
become
a
global
concern,
with
several
surveys
reporting
increased
mortality
rates.
Thrombogenic
potential
the
SARS-CoV-2
virus
been
hypothesised
originate
from
its
ability
produce
an
exaggerated
inflammatory
response
leading
endothelial
dysfunction.
Anticoagulants
have
remained
primary
modality
treatment
for
decades.
However,
there
is
no
universal
consensus
regarding
timing,
dosage
and
duration
anticoagulation
in
as
well
need
postdischarge
prophylaxis.
This
article
seeks
review
present
guidelines
recommendations
ongoing
trials
on
use
anticoagulants
COVID-19,
identify
discrepancies
between
all
these,
provide
comprehensive
strategy
usage
these
drugs
current
pandemic.
