The patient was successfully treated with a proton pump inhibitor (omeprazole), sucralfate, and antibiotics (amoxycillin, metronidazole) for 4 weeks with complete resolution of symptoms. Endoscopic reevaluation 3 weeks after the completion of treatment revealed the absence of both the ulcer and spiral shaped bacterial colonies in biopsy samples.
The patient remained well during a one-year follow-up with no ulcer recurrence.
Gastric and duodenal ulcer disease occurs far less frequently in children than in adults. H. pylori infection has been established as a major etiologic factor in the development of peptic ulcer disease in adults (11) and children (2,12). H. pylori infection was found in 90% of children with duodenal ulcers and in 25% of children with gastric ulcers (13). In spite of a high prevalence of H. pylori infection worldwide, the incidence of duodenal ulcer disease in children is low (5). Primary gastric ulcers in childhood are very rare in comparison with the incidence of secondary ulcers (critically ill children, NSAID). Their etiology remains unclear and a hereditary predisposition has not been established.
Indeed, according to a review of recent publications in adults in developed countries involving peptic ulceration, up to 40% of the duodenal ulceration, and up to 50% of gastric ulceration, may be unrelated to H. pylori infection or other identifiable etiology such as NSAID intake, steroids use, or Crohn disease (3,4,14). Very little is known about the prevalence of non-H. pylori, non-NSAID peptic ulceration in the pediatric population. Hassal et al. described four children with duodenal ulceration with neither H. pylori infection nor NSAID intake (6). Others have documented 10 children with duodenal ulceration where H. pylori was detected in only 3 of them, and among 3 children with gastric ulceration, none had H. pylori infection (5). Oderda et al. identified 5 H. pylori negative children with duodenal ulceration (7). It is becoming increasingly clear that there might be yet unknown risk factors, other than H. pylori or drugs, in a significant proportion of gastric and duodenal ulcers in childhood.
Our case report allows us to identify a new agent that can play a role in the development of gastric ulceration in children.
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