Background. Peptic ulcer disease (PUD) in children is reported worldwide, although it is relatively rare as compared with adults. Helicobacter pylori (HP) infection is a common cause of PUD in the pediatric age. Other risk factors include the use of nonsteroidal anti-inflammatory agents (NSAIDs), steroids, immunosuppressive drugs, and stressful events. Aim. To critically review the evidence on epidemiology, diagnostic management, and available treatments for PUD in the pediatric age. Methods. A MEDLINE search was performed indicating keywords as “Peptic Ulcer Disease,” “Epidemiology,” “Pediatric,” “Helicobacter pylori,” “Gastric ulcer,” “Bulbar Ulcer,” and “Upper Gastrointestinal Bleeding.” A selection of clinical trials, systematic reviews, and meta-analyses within the time period 2002–2012 was performed. Results. PUD in children is reported worldwide with an estimated frequency of 8.1% in Europe and of 17.4% in the US. When the underlying cause of PUD is addressed, the prognosis is excellent. Standard triple therapy, bismuth-based quadruple therapy, and the sequential therapy represent the current recommended treatments for HP related ulcers. NSAIDs related ulcers are treated by stopping the causative medications and by administration of proton-pump inhibitors or antisecretory drugs. Conclusions. PUD still represents a major concern in the paediatric age. A careful differential diagnosis and an adequate treatment constitute an excellent prognosis. 1. Introduction Peptic ulcers are discontinuities of the gastric or duodenal mucosa with penetration to the muscularis mucosae and exposure of the submucosa [1, 2]. Primitive ulcers are caused by alterations of the gastric function (i.e., increased HCl production and pepsin function); they are mainly single lesions and are usually found at the small gastric curve and at the antrum. Secondary ulcers, on the contrary, are caused by extragastric pathogenic events, that is, stress or drugs. They can be multiple and can have a spread localization within the stomach. More than 20% of patients have a family history of duodenal ulcers. In up to one third of patients with duodenal ulcers, basal acid output (BAO) and maximal acid output are increased. A study by Schubert and Peura [3] attested that individuals are at especially high risk those with a basal acid production (BAP) greater than 15？mEq/h. In addition to the increased gastric and duodenal acidity observed in some patients with duodenal ulcers, accelerated gastric emptying is also often present. A common cause of peptic ulcers in the pediatric age is
References
[1]
C. De Giacomo, P. L. Bacchini, M. Lombardi, et al., “La patologia gastrica,” in L'endoscopia Digestiva in età Pediatrica e Giovanile, G. L. De Angelis, Ed., pp. 49–68, EMSI, Rome, Italy, 2002.
[2]
C. Imrie, M. Rowland, B. Bourke, and B. Drumm, “Is Helicobacter pylori infection in childhood a risk factor for gastric cancer?” Pediatrics, vol. 107, no. 2, pp. 373–380, 2001.
[3]
M. L. Schubert and D. A. Peura, “Control of gastric acid secretion in health and disease,” Gastroenterology, vol. 134, no. 7, pp. 1842–1860, 2008.
[4]
N. Gallo, C. F. Zambon, F. Navaglia et al., “Helicobacter pylori infection in children and adults: a single pathogen but a different pathology,” Helicobacter, vol. 8, no. 1, pp. 21–28, 2003.
[5]
U. Blecker and B. D. Gold, “Gastritis and peptic ulcer disease in childhood,” European Journal of Pediatrics, vol. 158, no. 7, pp. 541–546, 1999.
[6]
M. Gasparetto, M. Pescarin, and G. Guariso, “Helicobacter pylori eradication therapy: current availabilities,” ISRN Gastroenterology, vol. 2012, Article ID 186734, 8 pages, 2012.
[7]
A. Capretta, L. Da Dalt, T. Zangardi, et al., “Upper gastrointestinal bleeding after ingestion of Ibuprofen. National Congress SIGENP Abstracts,” Digestive and Liver Disease, vol. 39, article A75, 2007.
[8]
L. Bak-Romaniszyn, S. Wojtuń, J. Gil, and I. P？aneta-Ma？ecka, “Peptic ulcer disease etiology, diagnosis and treatment,” Polski Merkuriusz Lekarski, vol. 17, no. 1, pp. 128–132, 2004.
[9]
W. D. Chey and B. C. Y. Wong, “American College of Gastroenterology guideline on the management of Helicobacter pylori infection,” American Journal of Gastroenterology, vol. 102, no. 8, pp. 1808–1825, 2007.
[10]
G. Guariso, D. Basso, C. F. Bortoluzzi et al., “GastroPanel: evaluation of the usefulness in the diagnosis of gastro-duodenal mucosal alterations in children,” Clinica Chimica Acta, vol. 402, no. 1-2, pp. 54–60, 2009.
[11]
D. Basso, C. F. Zambon, D. P. Letley et al., “Clinical Relevance of Helicobacter pylori cagA and vacA gene polymorphisms,” Gastroenterology, vol. 135, no. 1, pp. 91–99, 2008.
[12]
S. Koletzko, N. L. Jones, K. J. Goodman et al., “Evidence-based guidelines from ESPGHAN and NASPGHAN for Helicobacter pylori infection in children,” Journal of Pediatric Gastroenterology and Nutrition, vol. 53, no. 2, pp. 230–243, 2011.
[13]
W. Heldwein, J. Schreiner, J. Pedrazzoli, and P. Lehnert, “Is the Forrest classification a useful tool for planning endoscopic therapy of bleeding peptic ulcers?” Endoscopy, vol. 21, no. 6, pp. 258–262, 1989.
[14]
H. Shu-Ching, S. Bor-Shyang, L. Shui-Cheng, et al., “East etiology and treatment of childhood peptic ulcer disease in taiwan: a single center 9-year experience,” African Medical Journal, vol. 86, no. 3, pp. 100–109, 2009.
[15]
N. Kalach, P. Bontems, S. Koletzko, et al., “Frequency and risk factors of gastric and duodenal ulcers or erosions in children: a prospective 1-month European multicenter study,” European Journal of Gastroenterology & Hepatology, vol. 22, no. 10, pp. 1174–1181, 2010.
[16]
K. Brown, P. Lundborg, J. Levinson, et al., “Incidence of peptic ulcer bleeding in the US pediatric population,” Journal of Pediatric Gastroenterology and Nutrition, vol. 54, no. 6, pp. 733–736, 2012.
[17]
R. Egbaria, A. Levine, A. Tamir, and R. Shaoul, “Peptic ulcers and erosions are common in Israeli children undergoing upper endoscopy,” Helicobacter, vol. 13, no. 1, pp. 62–68, 2008.
[18]
M. I. El Mouzan and A. M. Abdullah, “Peptic ulcer disease in children and adolescents,” Journal of Tropical Pediatrics, vol. 50, no. 6, pp. 328–330, 2004.
[19]
A. Sawada, “Peptic ulcer in children,” Nippon Rinsho, vol. 62, no. 3, pp. 546–550, 2004.
[20]
W. Fischbach, P. Malfertheiner, J. C. Hoffmann et al., “S3-guideline “Helicobacter pylori and gastroduodenal ulcer disease” of the German Society for Digestive and Metabolic Diseases (DGVS) in cooperation with the German Society for hygiene and microbiology, society for pediatric gastroenterology and nutrition e.V., German Society for rheumatology,” Zeitschrift für Gastroenterologie, vol. 47, no. 12, pp. 1230–1263, 2009.
[21]
M. U？ra？ and E. Pehlivano？lu, “Helicobacter pylori infection and peptic ulcer in eastern Turkish children: is it more common than known?” Turkish Journal of Pediatrics, vol. 53, no. 6, pp. 632–637, 2011.
[22]
J. Sykora and M. Rowland, “Helicobacter pylori in pediatrics,” Helicobacter, vol. 16, supplement 1, pp. 59–64, 2011.
[23]
S. H. Berezin, H. E. Bostwick, M. S. Halata, J. Feerick, L. J. Newman, and M. S. Medow, “Gastrointestinal bleeding in children following ingestion of low-dose ibuprofen,” Journal of Pediatric Gastroenterology and Nutrition, vol. 44, no. 4, pp. 506–508, 2007.
[24]
B. Velayos, L. Fernández-Salazar, F. Pons-Renedo, et al., “Accuracy of urea breath test performed immediately after emergency endoscopy in peptic ulcer bleeding,” Digestive Diseases and Sciences, vol. 57, no. 7, pp. 1880–1886, 2012.
[25]
P. Y. Hung, Y. H. Ni, H. Y. Hsu, and M. H. Chang, “Portal hypertension and duodenal ulcer in children,” Journal of Pediatric Gastroenterology and Nutrition, vol. 39, no. 2, pp. 158–160, 2004.
[26]
A. Levine, S. Domanov, I. Sukhotnik, T. Zangen, and R. Shaoul, “Celiac-associated peptic disease at upper endoscopy: how common is it?” Scandinavian Journal of Gastroenterology, vol. 44, no. 12, pp. 1424–1428, 2009.
[27]
S. Sarkar, G. Selvaggi, N. Mittal et al., “Gastrointestinal tract ulcers in pediatric intestinal transplantation patients: etiology and management,” Pediatric Transplantation, vol. 10, no. 2, pp. 162–167, 2006.
[28]
E. Lionetti, R. Francavilla, M. Ruggieri, V. Di Stefano, M. B. Principi, and L. Pavone, “Recurrent peptic ulcer disease in a pediatric patient with type 1 neurofibromatosis and primary ciliary dyskinesia,” Minerva Pediatrica, vol. 61, no. 5, pp. 557–559, 2009.
[29]
M. Bardou, M. Youssef, Y. Toubouti, et al., “Newer endoscopic therapies decrease both re- bleeding and mortality in high risk patients with acute peptic ulcer bleeding : a series of meta-analyses,” Gastroenterology, vol. 123, article A239, 2003.
[30]
K. C. Lai, S. K. Lam, K. M. Chu et al., “Lansoprazole reduces ulcer relapse after eradication of Helicobacter pylori in nonsteroidal anti-inflammatory drug users—a randomized trial,” Alimentary Pharmacology and Therapeutics, vol. 18, no. 8, pp. 829–836, 2003.
[31]
L. Reveiz, R. Guerrero-Lozano, A. Camacho, L. Yara, and P. A. Mosquera, “Stress ulcer, gastritis, and gastrointestinal bleeding prophylaxis in critically ill pediatric patients: a systematic review,” Pediatric Critical Care Medicine, vol. 11, no. 1, pp. 124–132, 2010.
[32]
T. E. Araujo, S. M. G. Vieira, and P. R. A. Carvalho, “Stress ulcer prophylaxis in pediatric intensive care units,” Jornal de Pediatria, vol. 86, no. 6, pp. 525–530, 2010.
[33]
Y. Y. Wu, “Efficacy and safety of famotidine for the treatment of stress ulcers in neonates,” Chinese Journal of Contemporary Pediatrics, vol. 10, no. 5, pp. 593–595, 2008.
[34]
N. M. Tofil, K. W. Benner, M. P. Fuller, and M. K. Winkler, “Histamine 2 receptor antagonists vs intravenous proton pump inhibitors in a pediatric intensive care unit: a comparison of gastric pH,” Journal of Critical Care, vol. 23, no. 3, pp. 416–421, 2008.
[35]
J. F. Mougenot, D. Belli, and S. Cadranel, “Endoscopic therapy for nonvariceal bleeding,” in Pediatric Gastrointestinal Endoscopy Textbook and Atlas, H. S. Winter, M. S. Murphy, J. F. Mougenot, et al., Eds., pp. 137–141, BC Decker, Hamilton, Canada, 2006.
[36]
J. C. Dakubo, S. B. Naaeder, and J. N. Clegg-Lamptey, “Gastro-duodenal peptic ulcer perforation,” Zhongguo Dang dai er ke Za Zhi, vol. 10, no. 5, pp. 593–595, 2008.
[37]
B. P. Y. Wong, N. S. Y. Chao, M. W. Y. Leung, K. W. Chung, W. K. Kwok, and K. K. W. Liu, “Complications of peptic ulcer disease in children and adolescents: minimally invasive treatments offer feasible surgical options,” Journal of Pediatric Surgery, vol. 41, no. 12, pp. 2073–2075, 2006.
