Utilizing both IgA tissue transglutaminase and IgG-deamidated gliadin peptide antibodies offers accurate celiac disease diagnosis without duodenal biopsy.

Celiac disease Non-biopsy diagnosis Serologic diagnosis

Journal

Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
ISSN: 1878-3562
Titre abrégé: Dig Liver Dis
Pays: Netherlands
ID NLM: 100958385

Informations de publication

Date de publication:
28 Oct 2024
Historique:
received: 11 08 2024
revised: 22 09 2024
accepted: 06 10 2024
medline: 30 10 2024
pubmed: 30 10 2024
entrez: 29 10 2024
Statut: aheadofprint

Résumé

Gastroenterologists still raise concerns about adopting a non-biopsy strategy for diagnosing celiac disease (CeD) in adults. To assess the performance of the concurrent detection of two autoantibodies targeting two independent antigens, tissue transglutaminase (tTG) and deamidated gliadin peptides (DGP). This prospective, multicenter, binational study collected consecutive patients with a high pre-test probability for CeD. Between 2018 and 2020, adults were enrolled at four Italian and one Argentinian center. Serology was also blindly analyzed by a central laboratory (Werfen, San Diego, USA) for tTG IgA and DGP IgG by Aptiva Particle-based multi-analyte technology (PMAT) assays. CeD diagnosis required histological confirmation of Marsh 3 damage. 181 adult patients with suspected CeD were enrolled (134 with histological diagnosis of CeD and 47 not histologically confirmed as CeD). Patients positive for both tTG IgA and DGP IgG (double positive) were predictive of CeD in 92.5 % of patients at >1x upper limit of normal (ULN). Double positivity for tTG IgA and DGP IgG, both at >10x ULN, had a 100 % positive predictive value for the presence of Marsh 3 histology. Incorporating DGP IgG alongside tTG IgA in a single-step approach can be considered a valid confirmatory strategy for definitive non-biopsy diagnosis of CeD.

Sections du résumé

BACKGROUND BACKGROUND
Gastroenterologists still raise concerns about adopting a non-biopsy strategy for diagnosing celiac disease (CeD) in adults.
AIM OBJECTIVE
To assess the performance of the concurrent detection of two autoantibodies targeting two independent antigens, tissue transglutaminase (tTG) and deamidated gliadin peptides (DGP).
METHODS METHODS
This prospective, multicenter, binational study collected consecutive patients with a high pre-test probability for CeD. Between 2018 and 2020, adults were enrolled at four Italian and one Argentinian center. Serology was also blindly analyzed by a central laboratory (Werfen, San Diego, USA) for tTG IgA and DGP IgG by Aptiva Particle-based multi-analyte technology (PMAT) assays. CeD diagnosis required histological confirmation of Marsh 3 damage.
RESULTS RESULTS
181 adult patients with suspected CeD were enrolled (134 with histological diagnosis of CeD and 47 not histologically confirmed as CeD). Patients positive for both tTG IgA and DGP IgG (double positive) were predictive of CeD in 92.5 % of patients at >1x upper limit of normal (ULN). Double positivity for tTG IgA and DGP IgG, both at >10x ULN, had a 100 % positive predictive value for the presence of Marsh 3 histology.
CONCLUSIONS CONCLUSIONS
Incorporating DGP IgG alongside tTG IgA in a single-step approach can be considered a valid confirmatory strategy for definitive non-biopsy diagnosis of CeD.

Identifiants

pubmed: 39472176
pii: S1590-8658(24)01055-7
doi: 10.1016/j.dld.2024.10.010
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest FZ served as a speaker for Werfen and a consultant for Takeda. CC served as a speaker for Werfen and Takeda. GLN was employee of Werfen at time of study. JCB was consultant for Takeda. All other authors declared no conflict of interest.

Auteurs

Fabiana Zingone (F)

Department of Surgery, Oncology, Gastroenterology, University of Padua, Padua, Italy; Gastroenterology Unit, Azienda Ospedale Università di Padova, Padua, Italy.

Gary L Norman (GL)

Research and Development, Headquarters & Technology Center Autoimmunity, Werfen, San Diego, CA, USA.

Edgardo Smecuol (E)

Small Bowel Section, Dr. C. Bonorino Udaondo Gastroenterology Hospital, Buenos Aires, Argentina.

Daria Maniero (D)

Department of Surgery, Oncology, Gastroenterology, University of Padua, Padua, Italy.

Antonio Carroccio (A)

Unit of Internal Medicine, PROMISE Department, Villa Sofia Cervello United Hospitals - University of Palermo, Palermo, Italy.

Federico Biagi (F)

Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy; Gastroenterology Unit of Pavia Institute, Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy.

Juan P Stefanolo (JP)

Small Bowel Section, Dr. C. Bonorino Udaondo Gastroenterology Hospital, Buenos Aires, Argentina.

Sonia Niveloni (S)

Small Bowel Section, Dr. C. Bonorino Udaondo Gastroenterology Hospital, Buenos Aires, Argentina.

Geoffrey Holmes (G)

Department of Gastroenterology, Royal Derby Hospital, Derby, UK.

Vincenzo Villanacci (V)

Institute of Pathology, Spedali Civili, University of Brescia, Brescia, Italy.

Antonella Santonicola (A)

Department of Medicine, Surgery, Dentistry, Scuola Medica; Salernitana, University of Salerno, Baronissi (SA), Italy; Center for Celiac disease AOU San Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy.

Julio C Bai (JC)

Small Bowel Section, Dr. C. Bonorino Udaondo Gastroenterology Hospital, Buenos Aires, Argentina; Research Institute, Universidad del Salvador, Buenos Aires, Argentina.

Carolina Ciacci (C)

Institute of Pathology, Spedali Civili, University of Brescia, Brescia, Italy; Center for Celiac disease AOU San Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy. Electronic address: cciacci@unisa.it.

Classifications MeSH