» Articles » PMID: 36959611

Role of Age in Dynamics of Autoantibodies in Pediatric Celiac Disease

Overview
Journal Ital J Pediatr
Publisher Biomed Central
Specialty Pediatrics
Date 2023 Mar 24
PMID 36959611
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Celiac disease (CD) is characterized by elevated serum titers of autoantibodies IgA anti-tissue transglutaminase 2 (TGA-IgA) and IgA anti-endomysial (EMA), with small bowel mucosa atrophy. We evaluated age differences between CD children exhibiting variable antibody titers at diagnosis.

Methods: CD children diagnosed between January 2014 and June 2019, according to 2012 ESPGHAN guidelines were studied. All had EMA and TGA-IgA measurements, while a proportion of them underwent esophagogastroduodenoscopy (EGD). Patients were grouped based on serum TGA-IgA titers normalized to the upper limit of normal (ULN) and differences in median age (years) assessed by analysis of variance (ANOVA) and creation of orthogonal contrasts.

Results: CD was diagnosed in 295 subjects (median age: 4.4 [IQR: 2.60-8.52]) with a biopsy sparing protocol (high titer: ≥ 10xULN) and in 204 by EGD biopsy. Of the latter, 142 (median age: 8.5 [IQR: 5.81-11.06]) and 62 (median age: 9.5 [IQR: 6.26-12.76]) had a low (< 5xULN) and a moderate (≥ 5 < 10xULN) TGA-IgA titer, respectively. Potential CD was diagnosed in 20 patients (median age: 3.6 [IQR: 2.47-6.91]). The median age was significantly lower in the no-biopsy group (ANOVA: F = 25.98, p < .001) than in low- and moderate titer groups (p < 0.0001), while there was no statistical difference between biopsy-sparing and potential CD groups.

Conclusion: CD patients with greatly elevated antibody titers (≥ 10xULN) were diagnosed at an earlier age than those with lower titers. This may indicate that an increase in TGA-IgA is independent of age and suggests a polarization of autoimmunity in younger individuals with higher serum antibody levels.

Citing Articles

Oxidative stress-related markers as prognostic factors for patients with primary sclerosing cholangitis in Japan.

Oyama A, Takaki A, Adachi T, Wada N, Takeuchi Y, Onishi H Hepatol Int. 2023; 17(5):1215-1224.

PMID: 37493884 PMC: 10522747. DOI: 10.1007/s12072-023-10557-2.

References
1.
Ciszewski C, Discepolo V, Pacis A, Doerr N, Tastet O, Mayassi T . Identification of a γc Receptor Antagonist That Prevents Reprogramming of Human Tissue-resident Cytotoxic T Cells by IL15 and IL21. Gastroenterology. 2019; 158(3):625-637.e13. PMC: 7861144. DOI: 10.1053/j.gastro.2019.10.006. View

2.
Auricchio R, Mandile R, Del Vecchio M, Scapaticci S, Galatola M, Maglio M . Progression of Celiac Disease in Children With Antibodies Against Tissue Transglutaminase and Normal Duodenal Architecture. Gastroenterology. 2019; 157(2):413-420.e3. DOI: 10.1053/j.gastro.2019.04.004. View

3.
Tiberti C, Montuori M, Panimolle F, Trovato C, Anania C, Valitutti F . Screening for Type 1 Diabetes-, Thyroid-, Gastric-, and Adrenal-Specific Humoral Autoimmunity in 529 Children and Adolescents With Celiac Disease at Diagnosis Identifies as Positive One in Every Nine Patients. Diabetes Care. 2016; 40(2):e10-e11. DOI: 10.2337/dc16-2095. View

4.
Oberhuber G, Granditsch G, Vogelsang H . The histopathology of coeliac disease: time for a standardized report scheme for pathologists. Eur J Gastroenterol Hepatol. 1999; 11(10):1185-94. DOI: 10.1097/00042737-199910000-00019. View

5.
Ludvigsson J, Leffler D, Bai J, Biagi F, Fasano A, Green P . The Oslo definitions for coeliac disease and related terms. Gut. 2012; 62(1):43-52. PMC: 3440559. DOI: 10.1136/gutjnl-2011-301346. View