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Advances in the pathophysiology and treatment of heparin-induced thrombocytopenia.
[heparin-induced thrombocytopenia]
To
review
the
recent
developments
in
understanding
the
pathophysiology
of
heparin-induced
thrombocytopenia
(
HIT
)
and
in
applying
this
knowledge
to
the
treatment
of
patients
with
suspected
and
proven
HIT
.
HIT
pathophysiology
is
dynamic
and
complex
.
HIT
pathophysiology
is
initiated
by
four
essential
components--heparin
(
Hep
)
,
platelet
factor
4
(
PF
4
)
,
IgG
antibodies
against
the
Hep-
PF
4
complex
,
and
platelet
FcγRIIa
.
HIT
is
propagated
by
activated
platelets
,
monocytes
,
endothelial
cells
,
and
coagulation
proteins
.
Insights
into
the
unique
HIT
antibody
response
continue
to
emerge
,
but
without
consensus
as
to
the
relative
roles
of
B
cells
,
T
cells
,
and
antigen-presenting
cells
.
Platelet
activation
via
FcγRIIa
,
the
sine
qua
non
of
HIT
,
has
become
much
better
appreciated
.
Therapy
remains
challenging
for
several
reasons
.
Suspected
HIT
is
more
frequent
than
proven
HIT
,
because
of
the
widespread
use
of
Hep
and
the
inadequacies
of
current
diagnostic
tests
and
scoring
systems
.
In
proven
HIT
,
approved
treatments
reduce
but
do
not
eliminate
thrombosis
,
and
have
substantial
bleeding
risk
.
Rational
novel
therapeutic
strategies
,
directed
at
the
initiating
steps
in
HIT
pathophysiology
and
with
potential
combinations
staged
over
time
,
are
in
various
phases
of
development
.
Progress
continues
in
understanding
the
breadth
of
molecular
and
cellular
players
in
HIT
.
Translation
to
improved
diagnosis
and
treatment
is
needed
.
Diseases
Validation
Diseases presenting
"the widespread use of hep"
symptom
heparin-induced thrombocytopenia
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