Delayed-onset HIT, in which thrombocytopenia and thrombosis occur after heparin has been withdrawn, is also described; however, the incidence is unknown [14, 15]


Delayed-onset HIT, in which thrombocytopenia and thrombosis occur after heparin has been withdrawn, is also described; however, the incidence is unknown [14, 15]. the complex of platelet factor 4 and heparin; PF4-H AB) and serotonin release assay (SRA) tests were sent. Because of the suspicion for HIT, she was started on bivalirudin with subsequent improvement in platelet count. Initial PF4-H AB and SRA tests were negative, bivalirudin was stopped, and heparin was restarted. Subsequently, her platelets trended down, again raising clinical suspicion of Nrp1 HIT. Repeat PF4-H AB and SRA testing resulted positive. Conclusions A positive SRA in the appropriate context is considered for the diagnosis of heparin-induced thrombocytopenia. This case report highlights that false-negative serological evaluation is possible early in the course of the disease. Repeat testing is recommended in patients with high clinical suspicion. 1. Background Mavoglurant racemate Heparin-induced thrombocytopenia (HIT) should be suspected in patients with sudden thrombocytopenia and signs of thrombosis after exposure to unfractionated or low-molecular weight heparin [1, 2]. The pathophysiology of HIT involves endogenous antibodies Mavoglurant racemate targeting platelet factor 4 complexed with heparin (PF4-H AB) that causes catastrophic platelet aggregation resulting in predominantly venous and rarely arterial thrombosis and embolism [3]. HIT is considered a rare etiology for ischemic stroke outside of the context of cerebral venous thrombosis [4, 5]. Once HIT is suspected, systemic hypercoagulability should be handled with nonheparin Mavoglurant racemate anticoagulants such as bivalirudin or argatroban. Serological evaluation of PF4-H Abdominal antibodies and SRA should be completed before restarting a heparin anticoagulant [1, 3]. The PF4-H Abdominal antibody is considered a Mavoglurant racemate very sensitive screening test, and together with a positive SRA in the correct medical context, it is definitely considered to be virtually diagnostic of heparin-induced thrombocytopenia [6C8]. False-negative PF4-H Abdominal and SRA are reported only early in the course of disease and in individuals receiving immunosuppression, massive blood transfusions, or plasmapheresis [8C12]. This manuscript shows false-negative early serological screening in HIT, stresses the importance of repeat serological screening if there is strong clinical suspicion, and provides a brief review of the relevant literature. 2. Case Demonstration A 75-year-old Caucasian woman with a history of hypertension and well-controlled type 2 diabetes mellitus was admitted after open reduction and internal fixation of an ankle fracture. She was treated with subcutaneous unfractionated heparin (5000 IU three times each day) for deep vein thrombosis (DVT) prophylaxis from day time 1. On day time 4, a DVT and pulmonary embolism (PE) workup was completed after she developed acute shortness of breath and tachycardia with hypoxemia. DVT and subocclusive saddle-shaped PE were both mentioned (Number 1), and she Mavoglurant racemate was started on a continuous heparin infusion. The following day time she developed sudden onset of left-sided weakness and rightward gaze deviation concerning acute ischemic stroke. CT angiogram of the head and neck and subsequent MRI brain exposed a stroke caused by right-sided common carotid artery occlusion with thrombus extending into the external and internal carotid arteries. A tandem occlusion of substandard branch of the right middle cerebral artery was also mentioned on cerebral angiography (Number 1). The patient underwent successful mechanical thrombectomy of the right carotid artery bifurcation thrombus. After the endovascular process, thrombocytopenia (153,000/ em /em L to 94,000/ em /em L) was mentioned. Clinical suspicion was raised for HIT and PF4-H Abdominal, and SRA checks were sent. Heparin infusion was halted, and she was started on continuous bivalirudin infusion. Transthoracic echocardiogram with bubble study exposed a patent foramen ovale (PFO) with right to remaining shunting, and the etiology of stroke was presumed a paradoxical embolism. On hospital day time 7, PF4-H Abdominal (optical denseness (OD)? ?0.103) and SRA checks resulted negative with uptrending platelet count (105,000/ em /em L) (Number 2). Bivalirudin was subsequently stopped, and the patient was restarted on restorative continuous heparin infusion due to reduced suspicion of HIT as a result of the bad serological checks. From day time 8, platelets started to downtrend to 36,000/ em /em L. Clinical re-emergence of HIT was suspected, and heparin infusion was held. Repeat PF4-H Abdominal antibody and SRA checks were sent and resulted positive. The patient was treated with bivalirudin and bridged successfully to warfarin with recovery of platelet count (205,000/ em /em L). She suffered no further thromboembolic events and was eventually discharged to an inpatient rehabilitation facility. Open in a separate window Number 1 (a, b) Computerized tomography.