Background: Autoantibody (AAb) induced platelet desialylation resulting in increased hepatic platelet clearance has previously been reported as pathomechanism in immune thrombocytopenia (ITP).

Methods: The platelet desialylation capacity of serum samples of well-characterized, adult primary ITP patients from the Vienna ITP Biobank (EC 1843/2016) was investigated. The exposure of beta-Galactose and N-Acetylglucosamine on platelets was analyzed as markers of platelet desialylation.

Results: Sera of 133 ITP patients (28% newly diagnosed, 72% persistent/chronic) were investigated, where sera of 38 patients (29%) induced platelet desialylation. Patients with desialylation capacity compared to those without more commonly had platelet-bound AAbs (n=19/46, 50% vs n=27/95, 28.4%, P=0.018), thrombopoietin levels >50 pg/mL (n=23/34, 67.6% vs n=37/38, 42.0%, P=0.011), and higher bleeding scores (median (IQR) 3.0 (1.0-5.0) vs 1.0 (0.0-4.0), P=0.043). While the bleeding score overall, and specifically the skin bleeding score, thrombopoietin >50 pg/mL, and the presence of AAbs showed a significant association in univariate analysis with desialylating AAbs, only positivity for antiplatelet AAbs remained significantly associated in multivariate binary logistic regression analysis. In contrast, no association of platelet desialylation capacity was seen with disease duration, ITP treatment, or previous splenectomy.

Conclusions: Platelet desialylation capacity was seen in a third of primary ITP patients and was associated with platelet-bound anti-GPIIbIIIa AAbs, although more studies are required to establish the linkage with anti-GPIb-IX AAb. Desialylation capacity was associated with a more severe bleeding phenotype, while in contrast to previous data, an association with platelet counts, disease duration, ITP treatment and splenectomy refractoriness was not confirmed.