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Open AccessArticle

Antiplatelet Antibodies Do Not Predict the Response to Intravenous Immunoglobulins during Immune Thrombocytopenia

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Service de Médecine Interne et Immunologie Clinique, Centre de Référence Constitutif des Cytopénies Auto-immunes de l’adulte, Centre Hospitalo-Universitaire Dijon Bourgogne, Université de Bourgogne Franche Comté, 21000 Dijon, France
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Laboratoire d’Hématologie et d’Immunologie Régional, Établissement Français du Sang (EFS) Bourgogne/Franche-Comté, 25000 Besançon, France
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Service de Médecine Interne, Centre Hospitalo-Universitaire, Université de Bourgogne Franche-Comté, 25000 Besançon, France
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Service de Médecine Interne, Centre Hospitalier, 89000 Auxerre, France
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Service de Médecine Interne, Centre Hospitalier William-Morey, 71100 Chalon/Saône, France
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Service d’Hématologie et Oncologie, Centre Hospitalier William-Morey, 71100 Chalon/Saône, France
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Service d’Hématologie, Centre Hospitalo-Universitaire Dijon Bourgogne, 21000 Dijon, France
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Service d’Hématologie, Centre Hospitalo-Universitaire, Université de Bourgogne Franche-Comté, 25000 Besançon, France
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2020, 9(6), 1998; https://doi.org/10.3390/jcm9061998
Received: 28 May 2020 / Revised: 19 June 2020 / Accepted: 24 June 2020 / Published: 25 June 2020
(This article belongs to the Section Hematology)
Immune thrombocytopenia (ITP) is a rare autoimmune disease due to autoantibodies targeting platelet glycoproteins (GP). The mechanism of platelet destruction could differ depending on the specificity of antiplatelet antibodies: anti-GPIIb/IIIa antibodies lead to phagocytosis by splenic macrophages, in a Fcγ receptor (FcγR)-dependent manner while anti-GPIb/IX antibodies induce platelet desialylation leading to their destruction by hepatocytes after binding to the Ashwell–Morell receptor, in a FcγR-independent manner. Considering the FcγR-dependent mechanism of action of intravenous immunoglobulins (IVIg), we assumed that the response to IVIg could be less efficient in the presence of anti-GPIb/IX antibodies. We conducted a multicentric, retrospective study including all adult ITP patients treated with IVIg who had antiplatelet antibodies detected between January 2013 and October 2017. Among the 609 identified, 69 patients were included: 17 had anti-GPIb/IX antibodies and 33 had anti-GPIIb/IIIa antibodies. The response to IVIg was not different between the patients with or without anti-GPIb/IX (88.2% vs. 73.1%). The response to IVIg was better in the case of newly diagnosed ITP (odds ratio (OR) = 5.4 (1.2–24.7)) and in presence of anti-GPIIb/IIIa (OR = 4.82 (1.08–21.5)), while secondary ITP had a poor response (OR = 0.1 (0.02–0.64)). In clinical practice, the determination of antiplatelet antibodies is therefore of little value to predict the response to IVIg. View Full-Text
Keywords: immune thrombocytopenia; antiplatelet antibodies; IVIg immune thrombocytopenia; antiplatelet antibodies; IVIg
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Rogier, T.; Samson, M.; Mourey, G.; Falvo, N.; Magy-Bertrand, N.; Ouandji, S.; Picque, J.-B.; Greigert, H.; Mausservey, C.; Imbach, A.; Ghesquière, T.; Voillat, L.; Caillot, D.; Deconinck, E.; Bonnotte, B.; Audia, S. Antiplatelet Antibodies Do Not Predict the Response to Intravenous Immunoglobulins during Immune Thrombocytopenia. J. Clin. Med. 2020, 9, 1998.

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