Helicobacter pylori Infection in Children and Adolescents: Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition

Helicobacter pylori–induced gastritis causing mucosal ulceration either in the stomach or the proximal duodenum is a relatively uncommon event in children compared with adults. When H. pylori–associated ulcers occur in children, duodenal ulceration is much more frequently identified than gastric ulcers. In children younger than 6 to 10 years of age, peptic ulcers are usually due to noxious agents (such as corticosteroids and nonsteroidal antiinflammatory agents) or after major stresses (for example, burns, head injury, systemic illness). In these settings, upper gastrointestinal tract hemorrhage, vomiting, or perforation are frequent presenting features. The ulcers tend not to recur after healing if either the offending agent or underlying disease predisposing to mucosal ulceration can be removed. In older children and adolescents, the clinical presentation and natural history of peptic ulcers are more comparable to those observed in adults. The ulcers present as epigastric and nocturnal abdominal pain in teenagers with a positive family history of peptic ulceration. In this setting, despite healing of the acute ulceration, the natural history is for the ulcer to recur. It is now clear that such ulcers are not related to a genetic predisposition to hyperpepsinogenemia but to infection of the stomach with the pathogen H. pylori. Recurrences of H. pylori–associated peptic ulceration are markedly reduced by treatment directed at eradicating the gastric infection. For example, duodenal ulcer recurrence rates in H. pylori–infected children have been reported to be reduced from 65% recurrence at 1 year of follow-up if ulcers are healed with acid suppressive agents alone compared with 1-year ulcer recurrence rates below 5% if the gastric pathogen is eradicated. This intervention therefore results in reduced global health care costs. Historical Perspective Peptic ulcer disease has been considered to arise as a result of an imbalance between mucosal defenses and aggressive factors, including acid and pepsin. Mucosal defenses against acid and pepsin include mucus and bicarbonate, mucosal blood flow, prostaglandins, trefoil peptides, and epidermal growth factor. Primary peptic ulcers are usually duodenal, chronic, and related to H. pylori, whereas secondary ulcers are gastric, acute, and unrelated to infection status. It is clear that marked overproduction of gastric acid, such as occurs in the Zollinger-Ellison syndrome and, more commonly in children, antral G cell hyperplasia (also referred to as pseudo-Zollinger Ellison syndrome) can cause duodenal ulceration. However, excess acid production does not account for the overwhelming majority of peptic ulcers in children. It has been known for many years that recurrent peptic ulcer disease in humans is accompanied by a chronicactive gastritis. In 1983, Drs. Barry Marshall and Robin Warren in Perth, Australia provided the explanation for the cause of the gastritis and accompanying peptic ulcer disease when they successfully cultured H. pylori from the gastric antrum of humans. Subsequent studies in children confirmed the findings first reported in adults. There is specificity to the infection, the infection is associated with previously unexplained recurrent peptic ulcers, and both gastritis and ulcers resolve when the infection is successfully eradicated (1). Although there is general consensus worldwide to treat H. pylori infection when there is endoscopic evidence of peptic ulceration, whether to intervene in other more frequently encountered clinical settings remains uncertain. Increasing knowledge of the natural history of the infection, routes of transmission in human populations, and potential environmental reservoirs will help to clearly define why, when, and in whom to treat H. pylori. Journal of Pediatric Gastroenterology and Nutrition 35:S128–S133 © August 2002 Lippincott Williams & Wilkins, Inc., Philadelphia