Fiche publication
Date publication
juin 2020
Journal
Journal of clinical medicine
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BONNOTTE Bernard
,
Dr CAILLOT Denis
,
Pr DECONINCK Eric
Tous les auteurs :
Rogier T, Samson M, Mourey G, Falvo N, Magy-Bertrand N, Ouandji S, Picque JB, Greigert H, Mausservey C, Imbach A, Ghesquière T, Voillat L, Caillot D, Deconinck E, Bonnotte B, Audia S
Lien Pubmed
Résumé
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.
Mots clés
IVIg, antiplatelet antibodies, immune thrombocytopenia
Référence
J Clin Med. 2020 Jun 25;9(6):
