Digital Public Defence: Lamya Garabet
MD Lamya Garabet at Institute of Clinical Medicine will be defending the thesis "Effect of thrombopoietin receptor agonists on coagulation and fibrinolysis in patients with immune thrombocytopenia" for the degree of PhD (Philosophiae Doctor).
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture - time and place
- First opponent: Professor Riitta Lassila, University of Helsinki, Finland
- Second opponent: Senior Consultant Nora Butta, La Paz University Hospital, Madrid, Spain
- Third member and chair of the evaluation committee: Professor Emeritus Finn Wisløff, Faculty of Medicine, University of Oslo
Chair of defence
Associate Professor Tobias Gedde-Dahl, Institute of Clinical Medicine, University of Oslo
Vice-Rector Per Morten Sandset, University of Oslo
Immune thrombocytopenia (ITP) is an autoimmune disease characterized by low platelet count and increased bleeding risk. Treatment with thrombopoietin receptor agonists (TPO-RAs) is effective in increasing platelet count, however, an increase in thrombotic risk has been reported. Increased thrombotic risk has also been seen in ITP patients without TPO-RA treatment.
The aims of the thesis were to investigate the presence of a procoagulant state in ITP patients and evaluate the influence of TPO-RA treatment on this state by measuring various markers including markers of coagulation activation and fibrinolysis, platelet and endothelial cell activation, and neutrophil extracellular trap (NET) formation. We also assessed the procoagulant activity of the microvesicles (MVs) and measured thrombin generation.
ITP patients had increased coagulation activation and impaired fibrinolysis, increased endothelial cell activation and NET formation, all of which can contribute to a procoagulant state. TPO-RA treatment was associated with increased soluble P-selectin indicating increased platelet activation, increased phospholipid-dependent procoagulant activity of microvesicles and further impairment of fibrinolysis.
Overall, ITP patients have a procoagulant state and the initiation of TPO-RA treatment may lead to a more hypercoagulable state and thus increased thrombotic risk.
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