Masked bolus gluten challenge low in FODMAPs implicates nausea and vomiting as key symptoms associated with immune activation in treated coeliac disease.


Journal

Alimentary pharmacology & therapeutics
ISSN: 1365-2036
Titre abrégé: Aliment Pharmacol Ther
Pays: England
ID NLM: 8707234

Informations de publication

Date de publication:
01 2020
Historique:
received: 16 08 2019
revised: 18 09 2019
accepted: 01 10 2019
pubmed: 27 11 2019
medline: 28 7 2020
entrez: 27 11 2019
Statut: ppublish

Résumé

In patients with coeliac disease, FODMAPs in gluten-containing foods, and participant anticipation of a harmful ('nocebo') effect, may contribute to acute symptoms after gluten challenge. To establish acute gluten-specific symptoms linked to immune activation in coeliac disease METHODS: We included 36 coeliac disease patients on a gluten-free diet receiving placebo in the RESET CeD trial. Double-blind, bolus vital wheat gluten (~6-g gluten protein) and sham challenges low in FODMAPs were consumed 2 weeks apart. Assessments included daily Coeliac Disease Patient Reported Outcome (CeD PRO) symptom scores (0-10), adverse events and serum interleukin-2 (baseline and 4 hours). Median CeD PRO score for nausea increased most (sham: 0 vs gluten: 5.5; P < .001). Apart from tiredness (1 vs 4, P = .005) and headache (0 vs 2, P = .002), changes in other symptoms were small or absent. Only nausea increased significantly in occurrence with gluten (11% vs 69%, P < .001). Without nausea, only tiredness and flatulence were common after gluten. Nausea (6% vs 61%, P < .001; median onset: 1:34 hours) and vomiting (0% vs 44%, P < .001; 1:51 hours) were the only adverse events more common with gluten than sham. Interleukin-2 was always below the level of quantitation (0.5 pg/mL) at baseline, and after sham. Interleukin-2 was elevated after gluten in 97% of patients (median fold-change: 20), and correlated with severity of nausea (r Nausea and vomiting are relatively specific indicators of acute gluten ingestion, and correlate with immune activation. IBS-like symptoms without nausea are unlikely to indicate recent gluten exposure.

Sections du résumé

BACKGROUND
In patients with coeliac disease, FODMAPs in gluten-containing foods, and participant anticipation of a harmful ('nocebo') effect, may contribute to acute symptoms after gluten challenge.
AIM
To establish acute gluten-specific symptoms linked to immune activation in coeliac disease METHODS: We included 36 coeliac disease patients on a gluten-free diet receiving placebo in the RESET CeD trial. Double-blind, bolus vital wheat gluten (~6-g gluten protein) and sham challenges low in FODMAPs were consumed 2 weeks apart. Assessments included daily Coeliac Disease Patient Reported Outcome (CeD PRO) symptom scores (0-10), adverse events and serum interleukin-2 (baseline and 4 hours).
RESULTS
Median CeD PRO score for nausea increased most (sham: 0 vs gluten: 5.5; P < .001). Apart from tiredness (1 vs 4, P = .005) and headache (0 vs 2, P = .002), changes in other symptoms were small or absent. Only nausea increased significantly in occurrence with gluten (11% vs 69%, P < .001). Without nausea, only tiredness and flatulence were common after gluten. Nausea (6% vs 61%, P < .001; median onset: 1:34 hours) and vomiting (0% vs 44%, P < .001; 1:51 hours) were the only adverse events more common with gluten than sham. Interleukin-2 was always below the level of quantitation (0.5 pg/mL) at baseline, and after sham. Interleukin-2 was elevated after gluten in 97% of patients (median fold-change: 20), and correlated with severity of nausea (r
CONCLUSIONS
Nausea and vomiting are relatively specific indicators of acute gluten ingestion, and correlate with immune activation. IBS-like symptoms without nausea are unlikely to indicate recent gluten exposure.

Identifiants

pubmed: 31769533
doi: 10.1111/apt.15551
doi:

Substances chimiques

Dietary Carbohydrates 0
Placebos 0
Glutens 8002-80-0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

244-252

Subventions

Organisme : This study was funded by ImmusanT, Inc
Pays : International

Investigateurs

A Adams (A)
J Andrews (J)
C Behrend (C)
G Brown (G)
Alfred Hospital (A)
S Chen Yi Mei (S)
A Coates (A)
A J M Daveson (AJM)
A DiMarino (A)
H Ee (H)
D Elliott (D)
R Epstein (R)
B Feyen (B)
R Fogel (R)
K Friedenberg (K)
R Gearry (R)
M Gerdis (M)
M Goldstein (M)
V Gupta (V)
R Holmes (R)
G Holtmann (G)
S Idarraga (S)
G James (G)
T King (T)
T Klein (T)
S Kupfer (S)
B Lebwohl (B)
J Lowe (J)
J Murray (J)
E Newton (E)
D Quinn (D)
D Radin (D)
T Ritter (T)
H Stacey (H)
C Strout (C)
R Stubbs (R)
S Thackwray (S)
V Trivedi (V)
J Tye-Din (J)
J Weber (J)
S Wilson (S)

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Références

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Auteurs

A James M Daveson (AJM)

Faculty of Medicine, University of Queensland, Brisbane, Qld, Australia.

Jason A Tye-Din (JA)

Immunology Division, The Walter and Eliza Hall Institute, Parkville, Vic., Australia.
Department of Medical Biology, University of Melbourne, Parkville, Vic., Australia.
Department of Gastroenterology, The Royal Melbourne Hospital, Parkville, Vic., Australia.
Centre for Food & Allergy Research, Murdoch Children's Research Institute, Parkville, Vic., Australia.

Gautam Goel (G)

ImmusanT, Inc., Cambridge, MA, USA.

Kaela E Goldstein (KE)

ImmusanT, Inc., Cambridge, MA, USA.

Holly L Hand (HL)

ImmusanT, Inc., Cambridge, MA, USA.

Kristin M Neff (KM)

ImmusanT, Inc., Cambridge, MA, USA.

Leslie J Williams (LJ)

ImmusanT, Inc., Cambridge, MA, USA.

Kenneth E Truitt (KE)

ImmusanT, Inc., Cambridge, MA, USA.

Robert P Anderson (RP)

ImmusanT, Inc., Cambridge, MA, USA.

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