12 research outputs found

    Case report: CAR-T cell therapy-induced cardiac tamponade

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    CD19-specific chimeric antigen receptor T (CAR-T) cell therapy has recently been shown to improve the prognosis of refractory diffuse large B-cell lymphoma (DLBCL). However, CAR-T cells may induce numerous adverse events, in particular cytokine release syndrome (CRS) which is frequently associated with cardiovascular manifestations. Among the latter, acute pericardial effusion represents less than 1% of cases and cardiac tamponade has only been reported once. The management and outcome of these severe complications are not well established. We report here, a case of cardiac tamponade associated with CRS in a context of CAR-T cell therapy, which required urgent pericardiocentesis.Case summaryA 65-year-old man with refractory DLBCL was treated with CAR-T cell therapy. He had a history of dilated cardiomyopathy with preserved ejection fraction and transient atrial fibrillation. A pericardial localization of the lymphoma was observed on the second relapse. One day after CAR-T cell infusion the patient was diagnosed with grade 1 CRS. Due to hypotension, he was treated with tocilizumab and dexamethasone, and then transferred to intensive care unit (ICU). Echocardiography performed at ICU admission showed acute pericardial effusion with signs of right ventricular heart failure due to cardiac tamponade. It was decided to perform pericardiocentesis despite grade IV thrombocytopenia in a context of aplasia. Analysis of pericardial fluid showed a large number of lymphoma cells and 73% of CAR-T cells amongst lymphocytes, a level that was similar in blood. Hemodynamic status improved after pericardiocentesis, and no recurrence of pericardial effusion was observed. The presence of a high count of activated CAR-T cells in the pericardial fluid as well as the short interval between CAR-T cells injection and the symptoms appear as potential arguments for a direct action of CAR-T cells in the mechanism of this adverse event. The patient was discharged from ICU after two days and initially exhibited a good response to DLBCL treatment. Unfortunately, he died fifty days after starting CAR-T cell therapy due to a new DLBCL relapse.ConclusionPatients with a pericardial localization of DLBCL should be assessed for a risk of cardiac tamponade if receiving CAR-T cell therapy and presenting CRS. In this case, cardiac tamponade seems directly related to CAR-T cell expansion. Pericardiocentesis should be considered as a feasible and effective treatment if the risk of bleeding is well controlled, in association with anti-IL6 and corticosteroids

    Étude de l'impact de la mise en place d'une checklist pour la prescription d'antibiothérapie en réanimation

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    Introduction : L'augmentation de la résistance microbienne est un enjeu de santé publique majeur. Des programmes de gestion responsable des antibiotiques se développent afin d’endiguer ce phénomène. Parmi eux, la checklist est un moyen intéressant que l’on peut utiliser en réanimation. Notre objectif était de déterminer si l'introduction d'une checklist pour la prescription d’antibiotiques en réanimation permettait d’augmenter le taux d’antibiothérapie appropriée. Méthodes : Nous avons réalisé une étude de type avant-après monocentrique dans le service de Médecine Intensive - Réanimation du centre hospitalier universitaire de Rouen (Normandie, France). Nous avons analysé des patients admis en réanimation bénéficiant d’une antibiothérapie curative pendant plus de 48 heures sur des périodes de neufs mois avant et après l'introduction de la checklist (respectivement de juin 2020 à février 2021 et de juin 2021 à février 2022). La checklist se présentait sous la forme d’un document papier compilant l’ensemble des données autour de la prescription d’antibiotique pour un patient, rempli chaque jour par le personnel médical. Nous avons évalué le taux d’antibiothérapie adaptée. Résultats : Aucune différence statistiquement significative n'a été constatée dans le pourcentage d’antibiothérapie appropriée entre les deux périodes (23% contre 22%, p=0,9). On a noté une augmentation significative du taux de posologie appropriée (81% contre 91%, p=0,006), du taux d’antibiothérapie ayant une durée respectant les recommandations (59% contre 69%, p=0,037) et de la réalisation d’un suivi thérapeutique des antibiotiques par l’augmentation de la réalisation de dosages (31% contre 49%, pConclusion : L'introduction d'une checklist spécifique aux antibiotiques en réanimation a été associée à une amélioration de certains marqueurs de qualité de la prescription antibiotique sans impact sur la sécurité des patients hospitalisés en réanimation

    Piercing et tatouage (réglementation en vigueur, pratiques actuelles et complications potentielles)

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    LIMOGES-BU Médecine pharmacie (870852108) / SudocLYON1-BU Santé (693882101) / SudocSudocFranceF

    Benchmark on the cracking simulation of reinforced concrete ties

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    International audienceThis contribution presents a part of the benchmark that was launched during the first year of the French na-tional project CEOS.FR. It consists in modeling the behavior of reinforced concrete ties and in simulating the evolution of the crack opening during loading. Different approaches are compared. The global mechani-cal behavior is generally well reproduced whereas the simulation of the crack evolution gives encouraging results (appropriate order of magnitude) but needs to be improve

    Neurological Syndromes Associated with Anti-GAD Antibodies

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    Glutamic acid decarboxylase (GAD) is an intracellular enzyme whose physiologic function is the decarboxylation of glutamate to gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter within the central nervous system. GAD antibodies (Ab) have been associated with multiple neurological syndromes, including stiff-person syndrome, cerebellar ataxia, and limbic encephalitis, which are all considered to result from reduced GABAergic transmission. The pathogenic role of GAD Ab is still debated, and some evidence suggests that GAD autoimmunity might primarily be cell-mediated. Diagnosis relies on the detection of high titers of GAD Ab in serum and/or in the detection of GAD Ab in the cerebrospinal fluid. Due to the relative rarity of these syndromes, treatment schemes and predictors of response are poorly defined, highlighting the unmet need for multicentric prospective trials in this population. Here, we reviewed the main clinical characteristics of neurological syndromes associated with GAD Ab, focusing on pathophysiologic mechanisms

    Quantitative brain imaging analysis of neurological syndromes associated with anti-GAD antibodies

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    International audienceNeurological disorders associated with anti-glutamic acid decarboxylase (GAD) autoimmunity are rare and include a variety of neurological syndromes: stiff-person syndrome, cerebellar ataxia or limbic encephalitis. The diagnosis remains challenging due to the variety of symptoms and normal brain imaging. The morphological MRI of 26 patients (T1-weighted and Fluid-attenuated inversion recovery (FLAIR)weighted images) was analyzed at the initial stage of diagnosis, matched by age and sex to 26 healthy subjects. We performed a vertex-wise analysis using a generalized linear model, adjusting by age, to compare the brain cortical thickness of both populations. In addition, we used a voxel-based morphometry of cerebellum thickness obtained by CEREbellum Segmentation (CERES), as well as the hippocampus volumetry comparison using HIPpocampus subfield Segmentation (HIPS). Finally, we extracted 62 radiomics features using LifeX to assess the classification performance using a random forest model to identify an anti-GAD related MRI. The results suggest a peculiar profile of atrophy in patients with anti-GAD, with a significant atrophy in the temporal and frontal lobes (adjusted p-value < 0.05), and a focal cerebellar atrophy of the V-lobule, independently of the anti-GAD phenotype. Finally, the MRIs from anti-GAD patients were correctly classified when compared to the control group, with an area under the curve (AUC) of 0.98. This study suggests a particular pattern of cortical atrophy throughout all anti-GAD phenotypes. These results reinforce the notion that the different neurological anti-GAD phenotypes should be considered as a continuum due to their similar cortical thickness profiles
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