Thrombocytopenia is a clinical problem defined by a platelet count lower than 150×10⁹/L. It can be linked to various pathologies of central origin, such as decreased platelet production in the bone marrow, or peripheral origin with increased platelet destruction through autoimmune mechanisms, increased splenic sequestration, or excessive platelet consumption. Significant fatigue is often reported in association with thrombocytopenia, but its underlying pathophysiology remains unclear. One hypothesis is the role played by neurotrophic factors contained in platelets and released into the circulation following their activation, in particular the Brain-Derived Neurotrophic Factor (BDNF), which promotes the survival, growth, differentiation, and plasticity of neurons in both the central and peripheral nervous systems. Consequently, BDNF plays a key role in long-term memory, intellectual abilities, and neuroprotection.
In this context, this project aims to confirm whether platelet-origin neurotrophic biomarkers could explain the fatigue experienced by thrombocytopenic patients and whether it depends on the etiology of the thrombocytopenia.
Patients with constitutional or autoimmune (chronic or persistent ITP with last treatment administration ≥ 3 weeks) thrombocytopenia (platelet count < 150×109/L) already diagnosed
patient not being treated and not receiving serotonin reuptake inhibitor (SSRI) or norepinephrine (SNRI) or antithrombotic treatments (antiplatelet or anticoagulant) in the 10 days prior to inclusion
affiliation to social security (beneficiary or assignee)
patient followed in consultation in one of the recruiting haematology departments
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