Modification de l'homéostasie lymphoïde T dans la leucémie prolymphocytaire T

PARIS7-Bibliothèque centrale (751132105) / SudocSudocFranceF

Cyclic thrombocytopenia related to erythropoietin-dependent anti-platelet anti-GPIV/IIIb antibody in hemodialysis

International audienceWe describe herein the case of a 65-year-old patient on chronic hemodialysis with a medical history of idiopathic thrombocytopenia who experienced numerous episodes of severe thrombocytopenia with no specific diagnosis. Further analysis of the evolution of the platelet count showed that cyclic thrombocytopenia occurred after each injection of recombinant erythropoietin (rHu-EPO). Exploration of the involved mechanisms revealed the presence of a rHu-EPO-dependent anti-GPIV/IIIb antibody associated with a significant increase in GPIV/IIIb expression on her platelets after the addition of rHu-EPO. EPO was discontinued and the patient was treated with roxadustat with favorable results on her hemoglobin and platelet counts

New molecular basis associated with CD36 ‐negative phenotype in the sub‐Saharan African population

International audienceBackground: CD36 glycoprotein is expressed by various cell types, including platelets (PLTs), monocytes, and erythroid precursors, and is also the receptor for several ligands. However, absence of CD36 expression seems asymptomatic and is poorly described in Caucasians. In contrast, the frequency reaches 7% and 11% in African Caribbean and Asian persons, respectively. Lack of CD36 expression exposes to the risk of immunization in case of pregnancy or PLT transfusion. Two types of deficiency have been described: in Type I, PLTs and monocytes lack CD36 expression and the subjects are homozygous or compound heterozygous for CD36 mutations, whereas in Type II, only PLTs (Type IIa), and rarely also erythroid cells (Type IIb), are affected. Molecular events leading to Type II deficiency are poorly understood.Case report: An African girl, diagnosed with homozygous sickle cell disease and regularly transfused, was assessed for PLT CD36 expression by immunofluorescence microscopy. The deficiency was then confirmed by monoclonal antibody immobilization of PLT antigen (MAIPA) assay, and the subtype was assessed by flow cytometry. The underlying molecular basis was characterized by DNA sequencing. Furthermore, we tested the serum for possible anti-CD36 immunization.Results and conclusion: Flow cytometric analysis on the patient's blood samples allowed the diagnosis of Type I CD36 deficiency. CD36 antibodies, probably due to her past history of red blood cell transfusions, were identified by MAIPA and by Luminex technology assay. Interestingly, we identified through sequencing a new molecular basis involved in CD36 deficiency: two adenines were replaced by one guanine in Exon 4 (c.367_368delAAinsG) leading to a stop codon at Position 76

Molecular allelokaryotyping of T-cell prolymphocytic leukemia cells with high density single nucleotide polymorphism arrays identifies novel common genomic lesions and acquired uniparental disomy

T-cell prolymphocytic leukemia is a rare aggressive lymphoproliferative disease with a mature T-cell phenotype and characteristic genomic rearrangements of 14q11. This study identifies numerous new potential target genes in common breakpoints, deletions and regions of acquired uniparental disomy

Methylprednisolone-induced immune thrombocytopenia

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Methylprednisolone‐induced immune thrombocytopenia

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