TROMBOSITOPENIA PADA PENGOBATAN DENGAN HEPARIN

Abstract

Heparin induced thrombocytopenia (HIT), a well known side effect of heparin therapy, occurs in 1–5% of adults exposed to heparin.
Unlike other drug induced thrombocytopenia, HIT does not usually cause bleeding, but instead cause thrombosis about 50% of HIT.
The thrombosis in HIT can lead to limb gangrene or even death. The Importance to know the HIT is the wide use of heparin led to
the increasing recognition of untoward complications including HIT, relatively uncommon but severe side effect of heparin therapy,
unpredictable, and difficulty in diagnosing and treating HIT. HIT is mediated by an antibody that recognizes an epitope on the platelet
factor (PF4)-heparin complex. The platelet factor (PF4)-heparin complex binds to FcgRII receptor on the platelet surface and crosslinks
the
receptors.
This
induces
intense
platelet
activation
and
aggregation
and
simultaneously
activates
blood
coagulation
pathways,

these
changes
are
probably
the
basis
of
the
thrombosis
events
in
HIT.
HIT
was
classified
into
type
1
and
2
base
on
the
pathogenesis
and

the
severity
of
HIT.
Regular
platelet
count
monitoring
is
best
suited
for
early
diagnosis
of
HIT.
Functional
(serotonin
release,
platelet

aggregation
test)
and
antigen
assays
(solid
phase
enzyme
immunoassay,
fluid
phase,
and
particle
gel
immunoassay)
are
available
to

confirm
HIT.
HIT
was
made
base
on
the
clinical
finding
and
laboratory
examination.
Once
HIT
is
clinically
suspected,
heparin
should
be

stopped
immediately
and
treatment
with
an
alternative
anticoagulant,
waiting
for
laboratory
confirmation
may
be
catastrophic.
Early

diagnosis
of HIT will decrease the morbidity and mortality.