|Year : 2015 | Volume
| Issue : 2 | Page : 263-264
Peptic ulcer disease in children
Bharat Bhushan Dogra
Department of Surgery, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre Pimpri, Pune, Maharashtra, India
|Date of Web Publication||13-Mar-2015|
Bharat Bhushan Dogra
Dr. D. Y. Patil Medical College, Hospital, Pimpri, Pune - 411 018, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Dogra BB. Peptic ulcer disease in children. Med J DY Patil Univ 2015;8:263-4
Peptic ulcer disease (PUD) is uncommon in children with an estimated frequency of one case in 3000 hospital admissions.  Ulcers may be primary or secondary in nature depending on the underlying pathology. Primary ulcers usually occur in duodenal region and the vast majority of primary duodenal ulcers are associated with Helicobacter pylori infection of the gastric antral mucosa. Although H. pylori is almost always acquired in childhood, peptic ulceration is rare under the age of 10 years. Secondary ulcers occur more often in younger children. They have a worse prognosis and are usually associated with stress and systemic illness such as sepsis, head trauma, burns, sickle cell disease, type I diabetes, systemic lupus erythematosus and drug therapy. Secondary ulceration may be gastric or duodenal and may be life threatening in the acute phase due to the risk of perforation. , Goldman reported a case of a 12-month-old child with perforated duodenal ulcer in association with malaria.  Under normal circumstances, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and thus, peptic ulcer occurs when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory agents (NSAIDs), H. pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. H. pylori happens to be the major cause of gastritis in children and adults. Studies in children have demonstrated a specific association between H. pylori and primary gastritis. H. pylori colonization has been observed in the gastric mucosa in cases of duodenal ulcer disease. Duodenal ulcers do not appear to relapse if H. pylori is cleared from the gastric mucosa.  However, incidence of duodenal ulcer disease in children is low, and no specific symptoms have been associated with the presence of H. pylori gastritis in children. H. pylori gastritis as such may be an asymptomatic condition in the majority of infected children. On September 1-2, 1998, a group of pediatric gastroenterologists, mainly from Europe, and other specialists working in the field met in Budapest to discuss the management of H. pylori infection in children and consensus was achieved  that:
- H. pylori infection causes chronic gastritis in children.
- H. pylori infection is associated with gastric and duodenal ulcer disease in children.
- Eradication of H. pylori leads to healing of chronic gastritis.
- Eradication of H. pylori leads to long-term healing of duodenal ulcer disease.
Guariso and Gasparetto in their update on peptic ulcers in pediatric age published in 2012 also noted that common cause of peptic ulcers in the pediatric age is H. pylori infection, though the use of NSAIDs, like aspirin and ibuprofen, represents a significant cause of ulcers as well.  Other stressful events (i.e., shock, sepsis, burnings, major trauma, intracranial hypertension, surgical procedures, and chronic diseases) can provoke acute gastric ulcers, in the pediatric age. Lesions generally appear 3-6 days after the event and the main related symptoms are bleeding and abdominal pain. Most of the times, multiple lesions involving any part of the stomach are observed. 
Helicobacter pylori related ulcers are treated with a course of antibiotics to eradicate the bacterium from the gastrointestinal (GI) tract, as well as with drugs to reduce stomach acid and protect the stomach lining. Standard triple therapy consisting of proton pump inhibitor (1-2 mg/kg/day), ampicillin (50 mg/kg/day), clarithromicin (20 mg/kg/day), or metronidazole (20 mg/kg/day) is administered with very good results. NSAIDs related ulcers are treated by stopping the causative medications, and by administering drugs that promote healing of the stomach lining. Stress ulcers, erosions of the stomach and duodenum, and upper GI bleeding are well-known complications of critical illness in children admitted to pediatric intensive care units. Severe illness and a decreased gastric pH are, in fact, related to an increased risk of gastric ulceration and hemorrhage. Emergency GI endoscopy for upper-GI hemorrhage leads to the identification of the bleeding lesion in more than 80% of cases. The endoscopic assessment should ideally be performed within 6-12 h after stabilization of the patient. In pediatric patients, gastric and duodenal ulcers are the main indications for endoscopic treatment of nonvariceal GI hemorrhage. 
Stress ulcers, erosions of the stomach and duodenum, and upper-GI bleeding are well-known complications of critical illness in children admitted to pediatric intensive care units. Adequate prophylactic regimens have shown to reduce the risk of gastric and duodenal ulcers and should, therefore, be routinely administered in such patients.  Endoscopic hemostasis of bleeding peptic ulcer is effective and safe in children. Laparoscopic patch repair of the perforation can be employed safely in most pediatric patients. Morrison et al. also observed that perforation from PUD is adequately treated with primary closure, omental buttress, and medical management of the underlying etiology  Eradication of H. pylori and subsequent antiulcer medication are indicated in the management of complicated PUD. 
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