Introduction

Peptic ulcer disease in the pediatric population is relatively uncommon with an annual incidence of approximately 5.4 per 100,000 [1]. Most patients can be treated medically since the advent of H₂ blocker and proton pump inhibitor pharmaceuticals and surgery is required only in a minority of cases. Cases of ulcer disease can be subcategorized into primary and secondary.

Primary peptic ulcer disease is caused by infection with Helicobacter pylori. H.pylori is a Gram negative organism implicated in the pathogenesis of peptic ulcer disease by Marshall and Warren in 1984 [2] - a discovery for which they were awarded the 2005 Nobel Prize in Physiology or Medicine. It has since been identified as a risk factor for other gastroduodenal diseases including gastric mucosa associated lymphoid tissue (MALT) lymphoma and distal gastric cancer [3][4]. Infection prevalence varies by geographic location. Although infection rates have fallen below ten percent in Europe and North America, the prevalence remains high in Asia and developing countries where studies have shown over 65% of patients testing positive by their teenage years [5][6][7][8]. Infection is typically acquired in the first year of life with transmission often occurring from mother to child. Older children and teens are diagnosed more often with primary peptic ulcers while children under ten years are more likely to have secondary peptic ulcers.

Secondary peptic ulcer disease is attributable to other underlying disorders such as antral G cell hyperplasia, antral G cell hyperfunction and Zollinger-Ellison syndrome (ZES) [1][9][10]. ZES patients with gastrinoma who also carry a diagnosis of multiple endocrine neoplasia type I (MEN I) frequently become symptomatic in childhood. Other disorders of acid hypersecretion include hyperparathyroidism and chronic renal disease. Gastric ulcers can be seen in patients with Crohn disease and distinguishing this disease from other reasons for gastric ulcers requires a certain index of suspicion. Primary hyperparathyroidism or parathyroid hyperplasia are included in both MEN-I and MEN-IIa. The associated gastric ulcers are a result of increased acid secretion from hypercalcemia. Chronic renal disease is associated with increased serum histamine concentration which also stimulates acid production. Ménétrier disease, Crohn disease, eosinophilic gastroenteritis, lymphocytic gastritis and autoimmune gastritis are also associated with gastric ulcers. Nonsteroidal anti-inflammatory medications, aspirin and ethanol use can also lead to development of gastric ulcer disease. Stress ulcers arise in the face of sepsis, shock, injury, hypoxia and burns.

Content in this topic is referenced in SCORE Peptic Ulcer Disease overview