We have read with interest the article published in the Images in Pediatrics section titled “Gastric outlet obstruction secondary to Helicobacter pylori”, which describes a case of gastric outlet obstruction in a toddler aged 2 years with evidence of pyloric stenosis on endoscopy treated with dilation, in which analysis of biopsy specimens led to diagnosis of gastritis associated with H. pylori infection and foveolar hyperplasia.1 We appreciate the contribution, given the rarity of the presentation, and for reporting an effective endoscopic treatment option. Nevertheless, we would like to offer some constructive comments regarding the direct causality attributed in the article.

The authors propose that obstruction secondary to H. pylori is associated with duodenogastric reflux (DGR) secondary to antral dysmotility and that prolonged exposure to biliary acids can cause mucosal injury through inflammation, resulting in edema, foveolar hyperplasia and vascular congestion. In our opinion, what the authors describe in their reasoning is consistent with reactive/chemical gastropathy associated with DGR. In fact, the association of DGR with features such as foveolar hyperplasia, edema and congestion has been previously described in the pediatric population.2 Still, this does not prove that H. pylori is the main cause of DGR or that the infection alone explains the obstruction.

Furthermore, the association between DGR and H. pylori is complex and not unidirectional. Although it has been hypothesized that H. pylori could promote the development of DGR due to the changes in antral and duodenal motility, a pediatric study on the subject cited by the authors themselves reported results in the opposite direction: lower prevalence of DGR in H. pylori-positive compared to H. pylori-negative patients (8.7% vs 19.5%) and a lower prevalence of H. pylori in the group with DGR compared to controls (26.7% vs 48%).3 Therefore, the cooccurrence of H. pylori and a histology compatible with reactive gastropathy is not sufficient to infer direct causality. It would be more prudent to refer to coocurrence or association, an interpretation further supported by the high population prevalence of H. pylori in children and adolescents (35.1% in 2015–2022).4

Finally, since this patient was outside the typical age range for hypertrophic pyloric stenosis, we believe that, in order to support a causal attribution (gastroduodenal reflux or H. pylori) for gastric outlet stenosis/obstruction, it is important to explicitly document the exclusion of other organic causes, both intrinsic and extrinsic (eg, antral web or ring, annular pancreas, extrinsic compression, or intramural lesions). In this regard, in addition to ultrasound, an upper gastrointestinal series or cross-sectional imaging techniques, when indicated, could provide key information.