Further studies on the pathogenic mechanisms leading to thrombocytopenia in systemic lupus erythematosus

BARONI PIETTO CM.; LEV PR.; GLEMBOTSKY AC.; GOMEZ G.; COLLADO V.; PISONI C.; GOMEZ R.; FLORES G.; HELLER PG.; GOETTE NP.; MARTA, RF.

Congreso; Reunión Anual de Sociedades de Biociencia y LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica.; 2019

We previously demonstrated increased platelet apoptosis and decreased proplatelet formation (PPF) as contributing causes of thrombocytopenia in patients with systemic lupus erythematosus (SLE). Here, we broaden the study evaluating platelet desialylation and megakaryopoiesis in the presence of SLE plasma. Twenty-five SLE patients with and without thrombocytopenia, healthy controls and healthy mothers from whom umbilical cord blood was obtained, signed the informed consent. Desialylation of normal platelets was observed in the presence of 67% SLE samples as assessed by Ricinus communis agglutinin I and peanut agglutinin binding (flow cytometry). Although not statistically significant, desialylation was more frequent in thrombocytopenic than non thrombocytopenic patients (77% vs 50%). 55% of SLE patients inducing desialylation also showed increased apoptosis and/or activation. To evaluate the effect of SLE plasma on megakaryopoiesis, normal CD34+ hematopoietic progenitors from cord blood were incubated with 10% SLE or control plasma for 12 days, The number of CD61+/CD42+ cells evaluated by flow cytometry was higher in the presence of SLE than control plasma (Mann-Whitney test p