Abstract :
Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction caused by immunoglobulin G platelet-activating antibodies
against platelet factor 4 (PF4)/heparin complexes, leading to venous
and arterial thromboembolism (1). I read with keen interest the case
report describing a fatal case of probable HIT in a young man who
experienced pulmonary embolism (PE) and concomitant deep vein
thrombosis (2). The case of this patient with intracardiac thrombus
formation and severe ischemic stroke highlights the high risk of
thromboembolic events in patients with HIT despite anticoagulant
treatment with fondaparinux (5 mg/d), which was ineffective in case
of the patient even when the platelet count increased to 150.000/uL.
However, without any description of the patient’s weight, it remains
unclear whether the dosage of fondaparinux was appropriate. The
use of vitamin K antagonist (VKA) after normalization of the platelet
count, along with the administration of low-molecular-weight heparins or non-VKA oral anticoagulants immediately after the diagnosis of PE in a hemodynamically stable patient could lower the risk
of HIT development and significantly improve the prognosis (1, 3).
The rationale for choosing unfractionated heparin (UFH), the most
common cause of HIT, in the patient was not presented.