Objectives: Our objective was to determine the rate of mucosal recovery in pediatric patients with celiac disease on a gluten-free diet. We also sought to determine whether immunoglobulin A tissue transglutaminase (tTG) correlates with mucosal damage at the time of a repeat endoscopy with duodenal biopsy in these patients.
Methods: We performed a retrospective chart review of 103 pediatric patients, younger than 21 years, with a diagnosis of celiac disease defined as Marsh 3 histology, and who underwent a repeat endoscopy with duodenal biopsy at least 12 months after initiating a gluten-free diet.
Results: We found that 19% of pediatric patients treated with a gluten-free diet had persistent enteropathy. At the time of the repeat biopsy, tTG was elevated in 43% of cases with persistent enteropathy and 32% of cases in which there was mucosal recovery. Overall the positive predictive value of the autoantibody tTG was 25% and the negative predictive value was 83% in patients on a gluten-free diet for a median of 2.4 years.
Conclusions: Nearly 1 in 5 children with celiac disease in our population had persistent enteropathy despite maintaining a gluten-free diet and immunoglobulin A tTG was not an accurate marker of mucosal recovery. Neither the presence of symptoms nor positive serology were predictive of a patient's histology at the time of repeat biopsy. These findings suggest a revisitation of monitring and management criteria of celiac disease in childhood.
*Department of Pediatric Gastroenterology and Nutrition, MassGeneral Hospital for Children
†Celiac Research Program, Harvard Medical School
‡Division of Gastroenterology and Nutrition
§Clinical Research Center, Boston Children's Hospital
||Department of Medicine, Massachusetts General Hospital, Boston, MA
¶University of Manitoba, Winnipeg, Manitoba, Canada.
Address correspondence and reprint requests to Maureen M. Leonard, MD, Department of Pediatrics/Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Massachusetts General Hospital for Children, 175 Cambridge St, CPZ-575 Boston, MA 02114 (e-mail: firstname.lastname@example.org).
Received 5 February, 2016
Accepted 28 October, 2016
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was conducted with support from the Harvard Digestive Disease Center HDDC (NIH/NIDDK, 5 P30 DK34854) and the Harvard Catalyst | The Harvard Clinical and Translational Science Center (NCRR and NCATS, NIH Award UL1 TR001102) and financial contributions from Harvard University and its affiliated academic health care centers.
Drs Leonard and Weir contributed equally to the article.
Alessio Fasano, MD, Alba Therapeutics: Co-founder and stockholder; Mead Johnson Nutrition: Sponsored research; Inova Diagnostics: Sponsored research; Regeneron: Sponsored research; Pfizer: Consultant. The remaining authors report no conflicts of interest.