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Heparin-independent, PF4-dependent binding of HIT antibodies to platelets: implications for HIT pathogenesis.
[heparin-induced thrombocytopenia]
Antibodies
specific
for
platelet
factor
4
(
PF
4
)
/
heparin
complexes
are
the
hallmark
of
heparin-induced
thrombocytopenia
/
thrombosis
(
HIT
)
but
many
antibody-
positive
patients
have
normal
platelet
counts
.
The
basis
for
this
is
not
fully
understood
,
but
it
is
believed
that
antibodies
testing
positive
in
the
serotonin
release
assay
(
SRA
)
are
most
likely
to
cause
disease
.
We
addressed
this
issue
by
characterizing
PF
4
-
dependent
binding
of
HIT
antibodies
to
intact
platelets
and
found
that
most
antibodies
testing
positive
in
the
SRA
,
but
none
of
those
testing
negative
,
bind
to
and
activate
platelets
when
PF
4
is
present
without
any
requirement
for
heparin
(
p
<
0
.
0001
)
.
Binding
of
SRA-
positive
antibodies
to
platelets
was
inhibited
by
chondroitinase
ABC
digestion
(
p
<
0
.
05
)
and
by
addition
of
chondroitin-
4
-
sulfate
(
CS
)
or
heparin
in
excess
quantities
.
The
findings
suggest
that
,
although
all
HIT
antibodies
recognize
PF
4
in
a
complex
with
heparin
,
only
a
subset
recognize
more
subtle
epitopes
induced
in
PF
4
when
it
binds
to
CS
,
the
major
platelet
glycosaminoglycan
.
Antibodies
having
this
property
could
explain
"
delayed
HIT
"
seen
in
some
individuals
after
discontinuation
of
heparin
and
the
high
risk
of
thrombosis
that
persists
for
weeks
in
patients
recovered
from
HIT
.
Diseases
Validation
Diseases presenting
"many antibody-positive patients"
symptom
heparin-induced thrombocytopenia
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