Plasmapheresis in heparin-induced thrombocytopenia and thrombosis.

Manzano, Luís; Yebra, M; Vargas, J.; Barbolla, L; Álvarez‐Mon, Melchor

doi:10.1161/str.21.8.1236b

Cited by 13 publications

(4 citation statements)

References 5 publications

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“…PE has also been used as a treatment in patients with thrombotic complications of HIT who have continued thrombosis and low platelet counts despite discontinuation of heparin therapy and anticoagulation with nonheparin anticoagulants. Multiple case reports (Table II) have shown elevated platelet counts, reduced antiheparin/PF4 antibodies or negative ELISA, and relief of symptoms in patients treated with PE [10–17]. The PE did not, however, reverse damage caused by thrombosis, and some of the reported patients still required amputations.…”

Section: Discussionmentioning

confidence: 99%

Use of plasma exchange in patients with heparin‐induced thrombocytopenia: A report of two cases and a review of the literature

Jaben

Torloni

Pruthi

et al. 2011

J of Clinical Apheresis

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Heparin-induced thrombocytopenia (HIT), which is characterized by thrombocytopenia and potentially serious thromboses, may develop in patients exposed to heparin anticoagulation. HIT is caused by antibodies to the heparin/platelet factor 4 (PF4) complex. Management of HIT involves discontinuation of heparin and anticoagulation with a nonheparin alternative such as a direct thrombin inhibitor (DTI). This poses a challenge in the management of patients who need to undergo cardiopulmonary bypass surgery (CPB), because CPB requires anticoagulation with heparin and standardized protocols for use of DTIs are not widely available. We report two patients with HIT who underwent successful CPB with heparin anticoagulation following plasma exchange (PE) to reduce heparin/PF4 antibody titers. Case 1 is a 46-year-old male with cardiac amyloidosis who needed urgent placement of a left ventricular assist device. Case 2 is a 34-year-old woman with acute myocarditis who needed placement of a biventricular assist device. Both patients had positive enzyme-linked immunosorbent assay assays for heparin/PF4 antibodies and clinical evidence of HIT before PE. Following PE and subsequent CPB, neither patient had clinical or laboratory evidence of HIT. The literature regarding the use of PE for the treatment of complications of HIT and as prophylaxis before CPB is reviewed.

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Section: Discussionmentioning

confidence: 99%

Use of plasma exchange in patients with heparin‐induced thrombocytopenia: A report of two cases and a review of the literature

Jaben

Torloni

Pruthi

et al. 2011

J of Clinical Apheresis

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“…TPE has been used in a limited number of patients with HIT in an effort to remove antibodies and/or PF4 from the circulation. Published reports have shown some potential benefit for TPE in two populations: (1) patients with HIT (or a recent history of HIT) who demonstrate circulating anti‐PF4/heparin antibodies and must undergo heparinization for cardiopulmonary bypass (CPB) and (2) patients with active (thrombotic) HITT not responding satisfactorily to standard therapy . The ASFA has designated the use of TPE prior to cardiac surgery in patients with HIT, or in patients with active thrombosis, as Category III, Grade 2C (optimal role not yet established, decision making should be individualized) .…”

Section: Use Of Tpe In Patients With Anti‐pf4/heparin Antibodiesmentioning

confidence: 99%

NHLBI state of the science symposium in therapeutic apheresis: Knowledge gaps and research opportunities in the area of hematology‐oncology

Karafin

Sachais

Connelly‐Smith

et al. 2015

J of Clinical Apheresis

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The National Heart Lung and Blood Institute (NHLBI) hosted a two-day state of the science symposium on therapeutic apheresis in Bethesda, MD on November 28th-29th, 2012. The purpose of the symposium was multifaceted, and included the following aims: (a) To discuss this state of research and key scientific questions in apheresis medicine; (b) To identify gaps in knowledge for relevant cardiovascular diseases, hematological and oncological diseases, infectious diseases and sepsis, renal diseases, and neurological diseases where there may be strong therapeutic rationale for the application of apheresis treatments; (c) To explore ways of coordinating therapeutic apheresis with other medical disciplines and treatment modalities; (d) To identify and prioritize the most important research questions to be answered in apheresis medicine; and (e) To offer NHLBI suggestions on how a structured research approach can be applied to the therapeutic apheresis research agenda in future years. The following document summarizes three such key proposals presented at the meeting for evaluating apheresis therapy for the treatment of pain in sickle cell disease, heparin induced thrombocytopenia, and leukostasis from acute myeloid leukemia. The challenges and limitations regarding apheresis therapy for each disease are discussed, and avenues for future investigation for each disease are outlined.

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“…Plasmapheresis has resulted in an improved outcome in severely affected HIT patients. 94,[99][100][101][102][103][104] Whether this is due to the removal of antigen complexes or specific antibodies or is at least partly due to the normalization of acquired plasma factor deficiencies 56 is unresolved.…”

Section: Plasmapheresis and Plasma Exchangementioning

confidence: 99%

Treatment of Heparin-Induced Thrombocytopenia

Greinacher¹

1999

Thromb Haemost

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IntroductionUnfractionated heparin (UFH) and low molecular weight heparin (LMWH) are the most widely used anticoagulants when parenteral anticoagulation with a short half-life is required. Both can be administered subcutaneously and intravenously, and both have been shown to be effective in a variety of clinical settings.1 UFH has several limitations. One is its poor bioavailability after subcutaneous injection and the marked variability in its anticoagulant response in patients with an acute thromboembolic complication.2,3 Another major issue associated with UFH is the induction of heparin-induced thrombocytopenia (HIT). Both limitations are closely linked,4 as the underlying cause is the high density of negative charges on the heparin molecule and its molecular weight. Both are responsible for the binding of heparin to plasma proteins other than antithrombin (AT), such as platelet factor 4 (PF4) and to several cell types. This leads to heparin-platelet interaction, the formation of HIT antigen (i.e., PF4/heparin complexes), and inhibition of the anticoagulant effect of heparin (aPTT-nonresponder).

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Plasmapheresis in heparin-induced thrombocytopenia and thrombosis.

Cited by 13 publications

References 5 publications

Use of plasma exchange in patients with heparin‐induced thrombocytopenia: A report of two cases and a review of the literature

Use of plasma exchange in patients with heparin‐induced thrombocytopenia: A report of two cases and a review of the literature

NHLBI state of the science symposium in therapeutic apheresis: Knowledge gaps and research opportunities in the area of hematology‐oncology

Treatment of Heparin-Induced Thrombocytopenia

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