Peptic Ulcer Disease in Children

1. Gisela Chelimsky, MD* 2. Steven Czinn, MD† 1. 2. *Department of Pediatrics. 3. 4. †Chief, Division of Pediatric Gastroenterology, Department of Pediatrics, Rainbow Babies and Children’s Hospital and Case Western Reserve University, Cleveland, OH. Objectives After completing this article, readers should be able to: 1. Describe the different mechanisms involved in the pathogenesis of peptic ulcer disease. 2. Recognize the presenting symptoms of peptic ulcer disease and the differential diagnosis of those symptoms in children. 3. Clarify the role of endoscopic procedures in pediatric peptic ulcer disease. 4. Describe the role of Helicobacter pylori in the pathogenesis of peptic ulcer disease. 5. Review the medications and dosages commonly used in the treatment of peptic ulcer disease and H pylori infection in children. During the past decade, it has been estimated that peptic ulcer disease has affected more than 4 million people in the United States annually. For much of the last century, the pathogenesis of this disease was believed to be due to a number of predisposing factors, the most important of which was the hypersecretion of gastric acid. The development of pediatric flexible fiberoptic endoscopes that allowed the gastroenterologist to obtain gastric biopsies and identification of the microorganism Helicobacter pylori have changed our understanding of gastritis in children. Acid-peptic inflammation is believed to occur when there is an imbalance between cytotoxic and cytoprotective factors in the upper gastrointestinal tract. The toxic mechanisms include acid, pepsin, medications such as aspirin and nonsteroidal anti-inflammatory drugs, bile acids, and infection with H pylori . The defensive or cytoprotective mechanisms include the mucous layer, local bicarbonate secretion, and mucosal blood flow. Acid secretion from the parietal cells can be stimulated by three secretagogues: histamine via the paraendocrine pathway, acetylcholine via the neuroendocrine pathway, and gastrin via the endocrine pathway. Each employs a different mode of delivery to its target, the oxyntic cell. Acethylcholine is released at the vagal cholinergic terminals near the oxyntic cells (or parietal cell). Gastrin is released by the G cells in the antral and duodenal mucosa and is …