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      Pseudo-Pulmonary Embolism as a Sign of Acute Heparin-Induced Thrombocytopenia in Hemodialysis Patients: Safety of Resuming Heparin after Disappearance of HIT Antibodies

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          Heparin-induced thrombocytopenia (HIT) is a syndrome caused by platelet-activating antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. Thrombocytopenia is the most common clinical feature of HIT. HIT can be considered as a hypercoagulable state, with a high risk of thrombosis. Another feature of HIT is an acute systemic reaction that characteristically begins 5–30 min after receiving an intravenous bolus of unfractionated heparin, such as is commonly given for hemodialysis (HD). Here we present 4 patients who developed acute HIT at or near the start of their chronic HD. All patients were anticoagulated with the low-molecular-weight heparin, nadroparin, for HD. Three of our patients underwent surgery approximately 1–2 weeks before developing HIT. All patients presented with an acute systemic reaction during HD. All patients were treated and further dialyzed with lepirudin. Under this treatment we observed a quick recovery of the platelet count, and patients remained symptom-free. Antibodies against the PF4-heparin complex were detected with a combination of a ‘quick test’ and an enzyme-linked immunosorbent assay test. The likelihood of having HIT previous to the detection of antibodies was estimated with the pre-test probability score criteria. The tests for PF4-heparin antibodies remained positive for an average of 165 days. Three patients underwent a rechallenge with nadroparin after disappearance of the HIT antibodies in their serum. All 3 remained symptomless when they were further hemodialyzed on nadroparin. Our observations indicate that nadroparin can be successfully reintroduced for HD anticoagulation once the patient’s HIT antibodies have disappeared.

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          Most cited references 11

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          An overview of the heparin-induced thrombocytopenia syndrome.

           T Warkentin (2004)
          Heparin-induced thrombocytopenia (HIT) is caused by heparin-dependent, platelet-activating IgG antibodies that increase thrombin generation in vivo, producing a prothrombotic phenotype. In addition to platelet activation, there is in vitro evidence that activation of endothelium and monocytes occurs, perhaps directly by HIT antibodies, but more likely through activated platelet (or microparticle)-endothelial-leukocyte interactions. Patients with cardiac disease receiving heparin present important diagnostic and therapeutic issues when unexpected thrombocytopenia arises. Concomitant vascular disease burden and intravascular catheter use further increase risk of HIT-associated arterial thrombosis in this patient population. Whether arterial thrombosis simply reflects the "hypercoagulability state" of HIT interacting with diseased or injured arteries, or whether arterial "white clots" reflect additional prothrombotic effects of HIT via endothelial and monocyte activation, remains uncertain. Patients with HIT can also develop deep-vein thrombosis, which can progress to limb loss if coumarin (warfarin) leads to severe protein C depletion (coumarin-induced venous limb gangrene). Therapy for patients strongly suspected to have HIT should focus on inhibiting thrombin (or its generation) pharmacologically. Two direct thrombin inhibitors (lepirudin, argatroban) are approved for treating HIT. When using these agents, coumarin anticoagulation should be delayed pending substantial resolution of thrombocytopenia, before cautiously introducing overlapping coumarin therapy.
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            Use of Heparin during Cardiopulmonary Bypass in Patients with a History of Heparin-Induced Thrombocytopenia

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              Heparin-induced thrombocytopenia in hemodialysis patients.

              This study was conducted to determine the incidence of heparin-induced thrombocytopenia (HIT), an important complication in heparin therapy, in 154 hemodialysis patients, with characterization of the subtypes using an enzyme-linked immunosorbent assay. The etiology of the immunologic type of HIT is suggested to involve the binding of a specific antibody for platelet factor 4-heparin complex to platelets and their consequent activation. The 154 consecutive patients were newly treated with hemodialysis due to chronic or acute renal failure between January 1993 and July 1995. Heparin-induced thrombocytopenia was suspected in six patients (3.9%), and its presence was confirmed by platelet aggregation testing. Five of the patients with HIT had anti-platelet factor 4-heparin complex antibody detected by the enzyme-linked immunosorbent assay and were diagnosed with immunologic HIT. The patient who did not have the antibody was thought to have another type of HIT.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                November 2006
                11 August 2006
                : 104
                : 4
                : c143-c148
                Department of Nephrology, Intensive Care, and Haematology of ZNA Stuivenberg, Antwerp, Belgium
                94959 Nephron Clin Pract 2006;104:c143–c148
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 20, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/94959
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