Mepolizumab Reduces Hypereosinophilic Syndrome Flares Irrespective of Blood Eosinophil Count and Interleukin-5.


Journal

The journal of allergy and clinical immunology. In practice
ISSN: 2213-2201
Titre abrégé: J Allergy Clin Immunol Pract
Pays: United States
ID NLM: 101597220

Informations de publication

Date de publication:
09 2022
Historique:
received: 09 11 2021
revised: 14 04 2022
accepted: 29 04 2022
pubmed: 15 5 2022
medline: 14 9 2022
entrez: 14 5 2022
Statut: ppublish

Résumé

Mepolizumab, an anti-interleukin-5 (IL-5) antibody, reduces disease flares in patients with hypereosinophilic syndrome (HES). Factors predicting treatment response are unknown. To assess mepolizumab efficacy by baseline blood eosinophil count (BEC) and serum IL-5 level in patients with HES. This post hoc analysis used data from the phase III study assessing mepolizumab in patients with HES (NCT02836496). Patients 12 years old or older, with HES for 6 or more months, 2 or more flares in the previous year, and BEC ≥1,000 cells/μL at screening were randomized (1:1) to 4-weekly subcutaneous mepolizumab (300 mg) or placebo, plus baseline HES therapy, for 32 weeks. The proportion of patients experiencing 1 or more flares (wk 32), annualized flare rate, and proportion of patients with change from baseline in Brief Fatigue Inventory (BFI) item 3 (wk 32), were analyzed by baseline BEC (<1500/≥1500 to <2500/≥2500 cells/μL). Flare outcomes were assessed by baseline serum IL-5 (<7.81/≥7.81 pg/mL). Across baseline BEC subgroups, mepolizumab reduced the proportion of patients experiencing 1 or more flares by 63% to 90% and flare rate by 58% to 84% (treatment-by-eosinophil interaction P = .76 and P = .90, respectively); patients had improved BFI item 3 score with mepolizumab versus placebo (cells/μL: <1,500: 54% vs 37%; ≥1,500 to <2,500: 47% vs 31%; ≥2,500: 61% vs 0%; treatment-by-eosinophil interaction P = .42). Most patients had undetectable baseline serum IL-5 levels; among these, mepolizumab versus placebo reduced the proportion of patients with 1 or more flares (77%) and flare rate (67%). Mepolizumab was efficacious in the patients with HES studied, irrespective of baseline BEC. Undetectable IL-5 levels should not preclude mepolizumab treatment.

Sections du résumé

BACKGROUND
Mepolizumab, an anti-interleukin-5 (IL-5) antibody, reduces disease flares in patients with hypereosinophilic syndrome (HES). Factors predicting treatment response are unknown.
OBJECTIVE
To assess mepolizumab efficacy by baseline blood eosinophil count (BEC) and serum IL-5 level in patients with HES.
METHODS
This post hoc analysis used data from the phase III study assessing mepolizumab in patients with HES (NCT02836496). Patients 12 years old or older, with HES for 6 or more months, 2 or more flares in the previous year, and BEC ≥1,000 cells/μL at screening were randomized (1:1) to 4-weekly subcutaneous mepolizumab (300 mg) or placebo, plus baseline HES therapy, for 32 weeks. The proportion of patients experiencing 1 or more flares (wk 32), annualized flare rate, and proportion of patients with change from baseline in Brief Fatigue Inventory (BFI) item 3 (wk 32), were analyzed by baseline BEC (<1500/≥1500 to <2500/≥2500 cells/μL). Flare outcomes were assessed by baseline serum IL-5 (<7.81/≥7.81 pg/mL).
RESULTS
Across baseline BEC subgroups, mepolizumab reduced the proportion of patients experiencing 1 or more flares by 63% to 90% and flare rate by 58% to 84% (treatment-by-eosinophil interaction P = .76 and P = .90, respectively); patients had improved BFI item 3 score with mepolizumab versus placebo (cells/μL: <1,500: 54% vs 37%; ≥1,500 to <2,500: 47% vs 31%; ≥2,500: 61% vs 0%; treatment-by-eosinophil interaction P = .42). Most patients had undetectable baseline serum IL-5 levels; among these, mepolizumab versus placebo reduced the proportion of patients with 1 or more flares (77%) and flare rate (67%).
CONCLUSIONS
Mepolizumab was efficacious in the patients with HES studied, irrespective of baseline BEC. Undetectable IL-5 levels should not preclude mepolizumab treatment.

Identifiants

pubmed: 35568330
pii: S2213-2198(22)00482-2
doi: 10.1016/j.jaip.2022.04.037
pii:
doi:

Substances chimiques

Antibodies, Monoclonal, Humanized 0
Interleukin-5 0
mepolizumab 90Z2UF0E52

Banques de données

ClinicalTrials.gov
['NCT02836496']

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2367-2374.e3

Investigateurs

Gabriel Ricardo García (GR)
Adriana Sosso (A)
Luis Wehbe (L)
Anahí Yañez (A)
Daniël Blockmans (D)
Florence Roufosse (F)
Martti Anton Antila (MA)
Daniela Blanco (D)
Sergio Grava (S)
Marina Andrade Lima (MA)
Andreia Luisa Francisco Pez (AL)
Stanislas Faguer (S)
Mohamed A Hamidou (MA)
Jean-Emmanuel Kahn (JE)
Guillaume Lefévre (G)
Knut Brockow (K)
Peter M Kern (PM)
Andreas J Reiter (AJ)
Bastian Walz (B)
Tobias Welte (T)
Fabrizio Pane (F)
Alessandro M Vannucchi (AM)
Ruth Cerino-Javier (R)
Alfredo Gazca-Aguilar (A)
Dante D Hernández-Colín (DD)
Héctor Glenn Valdéz-López (HG)
Izabela R Kupryś-Lipińska (IR)
Jacek Musial (J)
Witold Prejzner (W)
Eniko Mihaly (E)
Viola Popov (V)
Mihnea Tudor Zdrenghea (MT)
Sergey V Gritsaev (SV)
Vladimir Ivanov (V)
Nikolay Tsyba (N)
Aránzazu Alonso (A)
Maria Cinta Cid Xutgla (MC)
Maria Laura Fox (ML)
Regina Garcia Delgado (RG)
Jesús María Hernández Rivas (JM)
Guillermo Sanz Santillana (GS)
Ana Isabel González (AI)
Andrew J Wardlaw (AJ)
Praveen Akuthota (P)
Joseph H Butterfield (JH)
Geoffrey L Chupp (GL)
John B Cox (JB)
Gerald J Gleich (GJ)
Devi Jhaveri (D)
Marc E Rothenberg (ME)

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Marc E Rothenberg (ME)

Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, and the Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio.

Florence Roufosse (F)

Department of Internal Medicine, Erasmus Hospital, Free University of Brussels, Brussels, Belgium.

Stanislas Faguer (S)

Department of Nephrology and Organ Transplantation, Reference Center for Rare Kidney Diseases, Rangueil Hospital, Toulouse University Hospital, Toulouse, France.

Gerald J Gleich (GJ)

Departments of Dermatology and Medicine, School of Medicine, University of Utah, Salt Lake City, Utah.

Jonathan Steinfeld (J)

Respiratory Research & Development, GSK, Collegeville, Pa.

Steven W Yancey (SW)

Respiratory Therapeutic Area, GSK, Research Triangle Park, NC.

Eleni Mavropoulou (E)

Clinical Statistics, GSK, Uxbridge, Middlesex, UK.

Namhee Kwon (N)

Respiratory Research & Development, GSK, Brentford, Middlesex, UK. Electronic address: namhee.n.kwon@gsk.com.

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