Predictors of slow responsiveness and partial mucosal recovery in adult patients with celiac disease.
Celiac disease
Gluten free diet
Mucosal healing
Mucosal recovery
Tissue transglutaminase
Journal
Gastroenterology and hepatology from bed to bench
ISSN: 2008-2258
Titre abrégé: Gastroenterol Hepatol Bed Bench
Pays: Iran
ID NLM: 101525875
Informations de publication
Date de publication:
2023
2023
Historique:
received:
16
01
2023
accepted:
12
03
2023
medline:
9
8
2023
pubmed:
9
8
2023
entrez:
9
8
2023
Statut:
ppublish
Résumé
The present study aims to determine the rate of mucosal recovery and predictors of persistent mucosal damage after gluten free diet (GFD). Celiac disease (CD) is a complex multi-systemic autoimmune disease triggered by exposure to dietary gluten in genetically predisposed individuals. There is still little evidence on the best method for assessing GFD adherence and mucosal recovery during treatment. The retrospective study included only adult patients (age≥18 years old), with biopsy-proven CD evaluated at a tertiary referral centre between 2016 and 2021. We performed a logistic regression analysis to identify factors associated with partial mucosal recovery (MR) after GFD. We included in the multivariate analysis parameters available at the time of CD diagnosis. A total of 102 patients were enrolled, two thirds were females, median age of 39 years (yrs). The initial biopsy analysis showed different stages of villous atrophy (VA) in 79 (77.4%) cases, while in 23(22.5%) cases showed mild enteropathy (Marsh 1, 2). After at least 12 months of GFD, 26 (25.5%) patients had persistent VA despite good or excellent adherence to GFD. Younger patients (< 35yrs), who showed severe mucosal damage (Marsh 3c lesions) and who had increased anti-gliadin antibody (AGA) levels were at risk for failure to obtain mucosal recovery (MR). Logistic regression analysis demonstrated that complete mucosal atrophy (P=0.007) and high AGA antibody levels (cutoff 129 U/ml, P=0.001) were independent risk factors for lack of mucosal improvement after at least 12 months of GFD. Interestingly, genotype, tTG-IgA antibody levels, or duration of GFD levels did not influence the occurrence of MR. Although AGA seropositivity has lost much of their diagnostic significance in recent years due to the introduction of the more sensitive and specific antibody tests, our study reported that patients aged < 35 yrs, who showed severe mucosal damage (Marsh 3c lesions) and who had increased AGA antibody levels at diagnosis were at risk for failure to obtain MR. The elevated AGA levels at diagnosis could be used as a prognostic tool for assessing MR.
Sections du résumé
Aim
UNASSIGNED
The present study aims to determine the rate of mucosal recovery and predictors of persistent mucosal damage after gluten free diet (GFD).
Background
UNASSIGNED
Celiac disease (CD) is a complex multi-systemic autoimmune disease triggered by exposure to dietary gluten in genetically predisposed individuals. There is still little evidence on the best method for assessing GFD adherence and mucosal recovery during treatment.
Methods
UNASSIGNED
The retrospective study included only adult patients (age≥18 years old), with biopsy-proven CD evaluated at a tertiary referral centre between 2016 and 2021. We performed a logistic regression analysis to identify factors associated with partial mucosal recovery (MR) after GFD. We included in the multivariate analysis parameters available at the time of CD diagnosis.
Results
UNASSIGNED
A total of 102 patients were enrolled, two thirds were females, median age of 39 years (yrs). The initial biopsy analysis showed different stages of villous atrophy (VA) in 79 (77.4%) cases, while in 23(22.5%) cases showed mild enteropathy (Marsh 1, 2). After at least 12 months of GFD, 26 (25.5%) patients had persistent VA despite good or excellent adherence to GFD. Younger patients (< 35yrs), who showed severe mucosal damage (Marsh 3c lesions) and who had increased anti-gliadin antibody (AGA) levels were at risk for failure to obtain mucosal recovery (MR). Logistic regression analysis demonstrated that complete mucosal atrophy (P=0.007) and high AGA antibody levels (cutoff 129 U/ml, P=0.001) were independent risk factors for lack of mucosal improvement after at least 12 months of GFD. Interestingly, genotype, tTG-IgA antibody levels, or duration of GFD levels did not influence the occurrence of MR.
Conclusion
UNASSIGNED
Although AGA seropositivity has lost much of their diagnostic significance in recent years due to the introduction of the more sensitive and specific antibody tests, our study reported that patients aged < 35 yrs, who showed severe mucosal damage (Marsh 3c lesions) and who had increased AGA antibody levels at diagnosis were at risk for failure to obtain MR. The elevated AGA levels at diagnosis could be used as a prognostic tool for assessing MR.
Identifiants
pubmed: 37554747
doi: 10.22037/ghfbb.v16i2.2734
pmc: PMC10404835
doi:
Types de publication
Journal Article
Langues
eng
Pagination
194-202Déclaration de conflit d'intérêts
The authors declare no conflict of interests.
Références
Turk J Gastroenterol. 2019 May;30(5):389-397
pubmed: 31060993
Gut. 1990 Jan;31(1):111-4
pubmed: 2180789
Nutrients. 2017 Jan 06;9(1):
pubmed: 28067823
Nutrients. 2021 Jun 30;13(7):
pubmed: 34209138
Foods. 2022 May 10;11(10):
pubmed: 35626950
PLoS One. 2017 Nov 2;12(11):e0187526
pubmed: 29095937
Aliment Pharmacol Ther. 2017 Nov;46(9):894-895
pubmed: 29023879
Dig Dis. 2015;33(2):236-243
pubmed: 25925929
Aliment Pharmacol Ther. 2014 Feb;39(4):407-17
pubmed: 24392888
BMC Gastroenterol. 2014 Feb 13;14:28
pubmed: 24524430
Am J Gastroenterol. 2010 Jun;105(6):1412-20
pubmed: 20145607
Clin Gastroenterol Hepatol. 2008 Feb;6(2):186-93; quiz 125
pubmed: 18096440
Front Nutr. 2020 May 29;7:73
pubmed: 32548124
Clin Exp Gastroenterol. 2021 Nov 16;14:451-456
pubmed: 34815686
Nutrients. 2022 Sep 07;14(18):
pubmed: 36145072
United European Gastroenterol J. 2019 Jun;7(5):583-613
pubmed: 31210940
World J Gastroenterol. 2022 Jan 7;28(1):154-175
pubmed: 35125825
Indian J Med Res. 2019 Jan;149(1):18-25
pubmed: 31115370
Aliment Pharmacol Ther. 2013 Feb;37(3):332-9
pubmed: 23190299
Int J Mol Sci. 2022 Dec 01;23(23):
pubmed: 36499446
BMC Med. 2019 Jul 23;17(1):142
pubmed: 31331324
J Clin Gastroenterol. 2016 Sep;50(8):619-23
pubmed: 27003856
Clin Gastroenterol Hepatol. 2009 May;7(5):530-6, 536.e1-2
pubmed: 19268725
Eur J Pediatr. 2021 Jan;180(1):263-269
pubmed: 32772154
J Pediatr Gastroenterol Nutr. 2020 Jan;70(1):37-41
pubmed: 31599818
Aliment Pharmacol Ther. 2017 Oct;46(7):681-687
pubmed: 28782118
J Pediatr Gastroenterol Nutr. 2017 Feb;64(2):286-291
pubmed: 28112686
Aliment Pharmacol Ther. 2022 Mar;55(5):514-527
pubmed: 35043426
J Clin Lab Anal. 2016 Jan;30(1):65-70
pubmed: 25385391
Gastroenterology. 2019 Mar;156(4):885-889
pubmed: 30578783
Aliment Pharmacol Ther. 2022 Jul;56 Suppl 1:S49-S63
pubmed: 35815829
Scand J Gastroenterol. 2016 Dec;51(12):1439-1446
pubmed: 27534885
Aliment Pharmacol Ther. 2014 Sep;40(6):639-47
pubmed: 25066096
Nat Med. 1997 Jul;3(7):797-801
pubmed: 9212111