JAK inhibition for CD3− CD4+ lymphocytic-variant ...
Document type :
Compte-rendu et recension critique d'ouvrage: Autre communication scientifique (congrès sans actes - poster - séminaire...)
Title :
JAK inhibition for CD3− CD4+ lymphocytic-variant hypereosinophilic syndrome
Author(s) :
Faguer, Stanislas [Auteur]
Institut des Maladies Métaboliques et Casdiovasculaires [UPS/Inserm U1297 - I2MC]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
Groh, Matthieu [Auteur]
Hôpital Foch [Suresnes]
Vergez, François [Auteur]
Institut National de la Santé et de la Recherche Médicale [INSERM]
Hunault-Berger, Mathilde [Auteur]
Centre de Recherche en Cancérologie et Immunologie Intégrée Nantes-Angers [CRCI2NA ]
Duployez, Nicolas [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Renaudineau, Yves [Auteur]
Institut Fédératif de Biologie (IFB)
Paul, Carle [Auteur]
Institut Toulousain des Maladies Infectieuses et Inflammatoires [Infinity]
Lefevre, Guillaume [Auteur]
Institute of Chemistry for Life and Health Sciences [iCLeHS]
Kahn, Jean-Emmanuel [Auteur]
Hôpital Ambroise Paré [AP-HP]
Institut des Maladies Métaboliques et Casdiovasculaires [UPS/Inserm U1297 - I2MC]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
Groh, Matthieu [Auteur]
Hôpital Foch [Suresnes]
Vergez, François [Auteur]
Institut National de la Santé et de la Recherche Médicale [INSERM]
Hunault-Berger, Mathilde [Auteur]
Centre de Recherche en Cancérologie et Immunologie Intégrée Nantes-Angers [CRCI2NA ]
Duployez, Nicolas [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Renaudineau, Yves [Auteur]
Institut Fédératif de Biologie (IFB)
Paul, Carle [Auteur]
Institut Toulousain des Maladies Infectieuses et Inflammatoires [Infinity]
Lefevre, Guillaume [Auteur]
Institute of Chemistry for Life and Health Sciences [iCLeHS]
Kahn, Jean-Emmanuel [Auteur]
Hôpital Ambroise Paré [AP-HP]
Journal title :
Clinical Immunology
Pages :
109275
Publisher :
Elsevier
Publication date :
2023-03
ISSN :
1521-6616
English keyword(s) :
Hypereosinophilic syndrome
JAK inhibition
Lymphocytic variant
Ruxolitinib
T-cell clone. Copyright © 2023. Published by Elsevier Inc.
JAK inhibition
Lymphocytic variant
Ruxolitinib
T-cell clone. Copyright © 2023. Published by Elsevier Inc.
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Alternatives are urgently needed in patients with CD3- CD4+ lymphocytic-variant hypereosinophilic syndrome (L-HES) requiring high-level steroids or who are unresponsive and/or intolerant to conventional alternative therapies. ...
Show more >Alternatives are urgently needed in patients with CD3- CD4+ lymphocytic-variant hypereosinophilic syndrome (L-HES) requiring high-level steroids or who are unresponsive and/or intolerant to conventional alternative therapies. We report five L-HES patients (44-66 years) with cutaneous involvement (n = 5) and persistent eosinophilia (n = 3) despite conventional therapies, who successfully received JAK inhibitors (tofacitinib n = 1, ruxolitinib n = 4). JAKi led to complete clinical remission in the first 3 months in all (with prednisone withdrawal in four). Absolute eosinophil counts normalized in cases receiving ruxolitinib, while reduction was partial under tofacitinib. After switch from tofacitinib to ruxolitinib, complete clinical response persisted despite prednisone withdrawal. The clone size remained stable in all patients. After 3-13 months of follow-up, no adverse event was reported. Randomized controlled trials are now mandatory to optimize the use of JAKi in L-HES.Show less >
Show more >Alternatives are urgently needed in patients with CD3- CD4+ lymphocytic-variant hypereosinophilic syndrome (L-HES) requiring high-level steroids or who are unresponsive and/or intolerant to conventional alternative therapies. We report five L-HES patients (44-66 years) with cutaneous involvement (n = 5) and persistent eosinophilia (n = 3) despite conventional therapies, who successfully received JAK inhibitors (tofacitinib n = 1, ruxolitinib n = 4). JAKi led to complete clinical remission in the first 3 months in all (with prednisone withdrawal in four). Absolute eosinophil counts normalized in cases receiving ruxolitinib, while reduction was partial under tofacitinib. After switch from tofacitinib to ruxolitinib, complete clinical response persisted despite prednisone withdrawal. The clone size remained stable in all patients. After 3-13 months of follow-up, no adverse event was reported. Randomized controlled trials are now mandatory to optimize the use of JAKi in L-HES.Show less >
Language :
Anglais
Popular science :
Non
Collections :
Source :