Pediatric autoimmune gastritis: An international, multicentric study

Abstract

Objectives: Autoimmune gastritis (AIG) has been poorly described in childhood. We sought to identify the patterns of manifestations of pediatric AIG at onset and to describe its laboratory, clinical, and histopathological features.

Methods: This was a retrospective, longitudinal, multicenter, cohort study enrolling histologically proven AIG patients with an onset in the pediatric age (<18 years old). We retrieved laboratory and clinical data at the time of onset and at last follow-up when available. Differences between Helicobacter pylori-exposed versus H. pylori-naïve, and anti-parietal cell antibody (PCA)-positive versus PCA-negative patients were investigated.

Results: Overall, 51 pediatric AIG patients (median age: 13 years, interquartile range: 11-16; F:M ratio 1.7:1) were included. Most patients were diagnosed with the overt type of AIG (47; 92.1%), while four (7.8%) were still in the potential phase. Atopic dermatitis (9.8%), rhinitis (7.8%), and asthma (5.9%) were common comorbidities, suggesting a link with T helper 2 (Th2) disorders. Two patients (3.9%) were found to have had previous or concurrent eosinophilic esophagitis, and five (9.8%) had eosinophilic gastritis. Notably, four patients (7.8%) presented with collagenous gastritis. On histological examination, the majority of patients were negative for H. pylori infection, except for 1 case out of 51 (2.0%) who had an active infection.

Conclusions: AIG may affect pediatric patients and lead to complications in this population. At presentation, the disease may exhibit histologic patterns attributed to collagenous and/or eosinophilic gastritis. Moreover, a possible association between AIG and Th2 disorders has been observed, warranting further research.

Keywords: Helicobacter pylori; anemia; gastric atrophy; neuroendocrine neoplasm; vitamin B12.

Figure 1

Histopathological specimen of the gastric corpus of a patient who was diagnosed with collagenous gastritis (A, B) and subsequently evolved into autoimmune gastritis (C, D) after roughly 2 years. In (A), the hematoxylin and eosin staining shows increased eosinophil infiltration of the mucosa with a thickening of the subepithelial collagen, better noticed with the Masson‐trichrome staining (B); a very mild glandular atrophy can be noticed. In (C and D), after 2 years, typical features of autoimmune gastritis are noticed with hematoxylin and eosin staining, namely mucosal atrophy; the subepithelial collagen band is not clearly evident anymore.