Gastrointestinal Eosinophil Responses in a Longitudinal, Randomized Trial of Peanut Oral Immunotherapy.


Journal

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775

Informations de publication

Date de publication:
06 2021
Historique:
received: 06 04 2020
accepted: 01 05 2020
pubmed: 21 5 2020
medline: 20 8 2021
entrez: 21 5 2020
Statut: ppublish

Résumé

Gastrointestinal side effects are common during oral immunotherapy (OIT) and eosinophilic esophagitis (EoE) is a potential complication. We aimed to characterize eosinophilic gastrointestinal responses to peanut OIT, in which peanut protein is given orally, with incremental increases in dose over time. Twenty adults with IgE-mediated peanut allergy were randomly assigned to groups given peanut OIT (n = 15) or placebo (n = 5); 1 additional subject withdrew before randomization. Serial gastrointestinal biopsies were collected at baseline (n = 21, 0 weeks), following dose escalation (n = 10, 52 weeks), and during the maintenance phase (n = 11, 104 weeks). Endoscopic findings were characterized using the EoE endoscopic reference score. Biopsies were assessed for eosinophils per high-power field (eos/hpf) and other pathology features using EoE histologic scoring system scores. We performed immunohistochemical analyses of eosinophil peroxidase deposition, quantified using automated image analysis. At baseline, no subjects reported current gastrointestinal symptoms. However, 3 of the 21 subjects (14%) had esophageal peak eosinophil counts ≥15 eos/hpf and all subjects had dilated intercellular spaces (DIS). OIT induced or exacerbated esophageal eosinophilia (EE) at 52 weeks in most subjects (peak eosinophil counts >5 eos/hpf in 6 of 7 patients [86%]; peak eosinophil counts ≥15 eos/hpf in 4 of 7 patients [57%]). One subject met clinicopathologic criteria for EoE and withdrew; no significant changes in esophageal peak eosinophil counts were observed in the placebo group. EE in the OIT group corresponded with significant increases in EoE histologic scoring system scores and deposition of eosinophil peroxidase. In 4 of 6 participants (67%), OIT-induced EE and gastrointestinal eosinophilia resolved by the end of the maintenance phase. Gastrointestinal symptoms were not clearly associated with EE or gastrointestinal eosinophilia. In this pilot study, we found that peanut OIT-induced EE and gastrointestinal eosinophilia are usually transient and are not always associated with gastrointestinal symptoms. Clinicaltrials.gov no: NCT02103270.

Sections du résumé

BACKGROUND & AIMS
Gastrointestinal side effects are common during oral immunotherapy (OIT) and eosinophilic esophagitis (EoE) is a potential complication. We aimed to characterize eosinophilic gastrointestinal responses to peanut OIT, in which peanut protein is given orally, with incremental increases in dose over time.
METHODS
Twenty adults with IgE-mediated peanut allergy were randomly assigned to groups given peanut OIT (n = 15) or placebo (n = 5); 1 additional subject withdrew before randomization. Serial gastrointestinal biopsies were collected at baseline (n = 21, 0 weeks), following dose escalation (n = 10, 52 weeks), and during the maintenance phase (n = 11, 104 weeks). Endoscopic findings were characterized using the EoE endoscopic reference score. Biopsies were assessed for eosinophils per high-power field (eos/hpf) and other pathology features using EoE histologic scoring system scores. We performed immunohistochemical analyses of eosinophil peroxidase deposition, quantified using automated image analysis.
RESULTS
At baseline, no subjects reported current gastrointestinal symptoms. However, 3 of the 21 subjects (14%) had esophageal peak eosinophil counts ≥15 eos/hpf and all subjects had dilated intercellular spaces (DIS). OIT induced or exacerbated esophageal eosinophilia (EE) at 52 weeks in most subjects (peak eosinophil counts >5 eos/hpf in 6 of 7 patients [86%]; peak eosinophil counts ≥15 eos/hpf in 4 of 7 patients [57%]). One subject met clinicopathologic criteria for EoE and withdrew; no significant changes in esophageal peak eosinophil counts were observed in the placebo group. EE in the OIT group corresponded with significant increases in EoE histologic scoring system scores and deposition of eosinophil peroxidase. In 4 of 6 participants (67%), OIT-induced EE and gastrointestinal eosinophilia resolved by the end of the maintenance phase. Gastrointestinal symptoms were not clearly associated with EE or gastrointestinal eosinophilia.
CONCLUSIONS
In this pilot study, we found that peanut OIT-induced EE and gastrointestinal eosinophilia are usually transient and are not always associated with gastrointestinal symptoms. Clinicaltrials.gov no: NCT02103270.

Identifiants

pubmed: 32434067
pii: S1542-3565(20)30676-5
doi: 10.1016/j.cgh.2020.05.019
pmc: PMC8445108
mid: NIHMS1597021
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT02103270']

Types de publication

Journal Article Randomized Controlled Trial Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1151-1159.e14

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI125567
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI147462
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI104209
Pays : United States

Informations de copyright

Copyright © 2021 AGA Institute. Published by Elsevier Inc. All rights reserved.

Références

Arch Dis Child. 2017 Sep;102(9):825-829
pubmed: 28404554
Am J Gastroenterol. 2007 Jun;102(6):1301-6
pubmed: 17531015
Mucosal Immunol. 2015 Jul;8(4):930-42
pubmed: 25563499
Ann Allergy Asthma Immunol. 2014 Dec;113(6):624-9
pubmed: 25216976
J Allergy Clin Immunol. 2018 Jul;142(1):10-23
pubmed: 29980278
Ann Allergy Asthma Immunol. 2018 Mar;120(3):237-240.e4
pubmed: 29397272
Lancet. 2019 Oct 19;394(10207):1437-1449
pubmed: 31522849
J Allergy Clin Immunol. 2018 Jan;141(1):1-9
pubmed: 29307409
Dis Esophagus. 2017 Feb 1;30(3):1-8
pubmed: 26857345
J Allergy Clin Immunol. 2018 Dec;142(6):1843-1855
pubmed: 29729938
Clin Exp Allergy. 2016 Nov;46(11):1431-1440
pubmed: 27388929
Gastroenterology. 2016 Mar;150(3):581-590.e4
pubmed: 26584601
N Engl J Med. 2018 Nov 22;379(21):1991-2001
pubmed: 30449234
Allergy. 2016 Jun;71(6):889-900
pubmed: 26970242
J Allergy Clin Immunol. 2017 Jan;139(1):173-181.e8
pubmed: 27522159
J Exp Med. 2014 Jul 28;211(8):1657-72
pubmed: 25071163
J Immunol. 2017 Jun 15;198(12):4672-4681
pubmed: 28515279
Lancet Gastroenterol Hepatol. 2018 Feb;3(2):85-94
pubmed: 29242014
Am J Gastroenterol. 2005 Mar;100(3):543-8
pubmed: 15743349
J Allergy Clin Immunol Pract. 2020 Jan;8(1):125-131
pubmed: 31382040
Am J Gastroenterol. 2014 Apr;109(4):515-20
pubmed: 24445569
J Allergy Clin Immunol. 2011 Mar;127(3):654-60
pubmed: 21377034
Nat Med. 2013 Aug;19(8):1005-13
pubmed: 23872715
Immunity. 2014 Apr 17;40(4):582-93
pubmed: 24745334
Front Immunol. 2018 Nov 22;9:2624
pubmed: 30524424
Lancet. 2019 Jun 1;393(10187):2222-2232
pubmed: 31030987
Can J Gastroenterol Hepatol. 2016;2016:1980686
pubmed: 27446827
Gastroenterology. 2013 Dec;145(6):1230-6.e1-2
pubmed: 23954315
J Allergy Clin Immunol Pract. 2017 Mar - Apr;5(2):369-375
pubmed: 28042003
J Allergy Clin Immunol Pract. 2015 Jan-Feb;3(1):123-4
pubmed: 25577634
Gut. 2013 Apr;62(4):489-95
pubmed: 22619364
Clin Exp Allergy. 2010 Apr;40(4):563-75
pubmed: 20447076
Lancet. 2014 Apr 12;383(9925):1297-1304
pubmed: 24485709
J Exp Med. 2015 Apr 6;212(4):513-24
pubmed: 25779634
J Pediatr Gastroenterol Nutr. 2014 Nov;59(5):589-93
pubmed: 25023586

Auteurs

Benjamin L Wright (BL)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona; Division of Pulmonology, Phoenix Children's Hospital, Phoenix, Arizona.

Nielsen Q Fernandez-Becker (NQ)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Neeraja Kambham (N)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California; Department of Pathology, Stanford University School of Medicine, Stanford, California.

Natasha Purington (N)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Shu Cao (S)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Dana Tupa (D)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Wenming Zhang (W)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Sayantani B Sindher (SB)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Matthew A Rank (MA)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona; Division of Pulmonology, Phoenix Children's Hospital, Phoenix, Arizona.

Hirohito Kita (H)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona; Department of Immunology, Mayo Clinic Arizona, Scottsdale, Arizona.

David A Katzka (DA)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.

Kelly P Shim (KP)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona; Division of Pulmonology, Phoenix Children's Hospital, Phoenix, Arizona.

Bryan J Bunning (BJ)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

Alfred D Doyle (AD)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona.

Elizabeth A Jacobsen (EA)

Division of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona; Department of Immunology, Mayo Clinic Arizona, Scottsdale, Arizona.

Mindy Tsai (M)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California; Department of Pathology, Stanford University School of Medicine, Stanford, California.

Scott D Boyd (SD)

Division of Pulmonology, Phoenix Children's Hospital, Phoenix, Arizona; Department of Pathology, Stanford University School of Medicine, Stanford, California.

Monali Manohar (M)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California.

R Sharon Chinthrajah (RS)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, California. Electronic address: schinths@stanford.edu.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH