Publications by authors named "F Cohen-Aubart"
Objectives: Lymphadenopathy is a classical manifestation of systemic lupus erythematosus (SLE) flare, occurring in approximately half of patients during the course of the disease. Lymphadenopathy in SLE is frequently associated with fever. Microbial infection may play a role in SLE onset and flares.
View Article and Find Full Text PDFThe immunosuppressive treatment of immune-mediated thrombotic thrombocytopenic purpura (iTTP) in patients with intolerance or refractoriness to the B-cell depleting monoclonal antibody rituximab remains debated. Daratumumab, a plasma cell-directed monoclonal antibody targeting CD38, represents a therapeutic option, but data are scarce. The French Thrombotic Microangiopathies Reference Center conducted a nationwide survey on iTTP patients treated with daratumumab.
View Article and Find Full Text PDFRationale: On the occasion of the General stage meeting of Internal Medicine, the National College of Internal Medicine Teachers (CEMI) conducted a survey on teaching activity among all French university hospital (HU) internal medicine specialists.
Method: The survey was carried out in September 2023 by sending an email to 101 hospital practitioners university professors (PU-PH) and 18 hospital practitioners assistant professors (MCU-PH) of internal medicine in subsection 53-01 of the National council of universities (CNU), as well as to the 11 HU internists working in immunology (subsection 47-01) or therapeutics (subsection 48-04).
Results: Seventy-three HUs (56.
Article Synopsis
- Langerhans cell Histiocytosis (LCH) and Erdheim-Chester disease (ECD) are linked to certain genetic mutations and pose a heightened risk for neurodegeneration, revealing microglia mutant clones in patients' brains.
- These mutant clones lead to symptoms like microgliosis and neuronal loss, notably affecting specific brain regions, with symptoms correlating to the disease's duration and the size of these clones.
- Research suggests that targeting these mutant microglia with a CSF1R-inhibitor could prevent neuronal loss, presenting a potential new treatment option distinct from current MAPK inhibitors.