Pathogenic mechanisms contributing to thrombocytopenia in patients with Systemic Lupus Erythematosus

LEV PR; GOMEZ G; GOMEZ R; HELLER PG; BARONI PIETTO MC; MARIN OYARZUN CP; PISONI C; GONZALES J; MARTA RF; GLEMBOTSKY AC; COLLADO V; GRODZIELSKI M; GOETTE NP

Milan

Congreso; International congress of Thrombosis and Haemostasis 2020; 2020

International Society of Thrombosis and Haemostasis ISTH

Systemic lupus erythematosus (SLE) is characterized by production of myriad of autoantibodies. Patients develop thrombocytopenia in 10-15% of cases. Here, we investigated possible causes of thrombocytopenia, including platelet apoptosis, desialylation and inhibition of platelet production in SLE. Twenty-five patients with and without thrombocytopenia were studied. Apoptosis assessed by phosphatidylserine exposure, loss of mitochondrial membrane potential, and active caspase 3 measurement, was found in platelets from 4 thrombocytopenic patients. Desialylation of normal platelet glycoproteins was induced by 67% SLE plasma samples (Ricinus communis agglutinin I and peanut agglutinin binding). Concerning desialylation, thrombocytopenic SLE plasma tended to be more harmful than non-thrombocytopenic samples.To evaluate the effect of SLE plasma on platelet production, megakaryopoiesis was studied in normal CD34+ hematopoietic progenitors incubated with 10% SLE plasma for 12 days. Additionally, normal mature megakaryocytes obtained after 12-days plasma-free culture of CD34+ cells were supplemented with 10% SLE or control plasma to evaluate proplatelet formation (PPF) at day 15. While megakaryopoiesis was increased, PPF was decreased in the presence of SLE plasma (both, Mann-Whitney test p