Therapy With Gastric Acidity Inhibitors Increases the Risk of Acute Gastroenteritis and Community-Acquired Pneumonia in Children

• Published in: Pediatrics (Evanston) 2006-05, Vol.117 (5), p.e817-e820
• Main Authors: Canani, Roberto Berni, Cirillo, Pia, Roggero, Paola, Romano, Claudio, Malamisura, Basilio, Terrin, Gianluca, Passariello, Annalisa, Manguso, Francesco, Morelli, Lorenzo, Guarino, Alfredo, Working Group on Intestinal Infections of Italian Society of Pediatric Gastroenterology, Hepatology and Nutrition (SIGENP)
• Format: Article
• Language: English
• Subjects: Achlorhydria - chemically induced; Acute Disease; Anti-Ulcer Agents - adverse effects; Anti-Ulcer Agents - therapeutic use; Child, Preschool; Community-Acquired Infections; Gastroenteritis - etiology; Gastroesophageal Reflux - complications; Gastroesophageal Reflux - drug therapy; Helicobacter pylori; Histamine H2 Antagonists - adverse effects; Histamine H2 Antagonists - therapeutic use; Humans; Infant; Omeprazole - adverse effects; Omeprazole - therapeutic use; Pneumonia - etiology; Proton Pump Inhibitors; Ranitidine - adverse effects; Ranitidine - therapeutic use; Risk Factors
• ISSN: 0031-4005; 1098-4275
• DOI: 10.1542/peds.2005-1655

Gastric acidity (GA) inhibitors, including histamine-2 receptor antagonists (H2 blockers) and proton pump inhibitors (PPIs), are the mainstay of gastroesophageal reflux disease (GERD) treatment. A prolonged GA inhibitor-induced hypochlorhydria has been suggested as a risk factor for severe gastrointestinal infections. In addition, a number of papers and a meta-analysis have shown an increased risk of pneumonia in H2-blocker-treated intensive care patients. More recently, an increased risk of community-acquired pneumonia associated with GA inhibitor treatment has been reported in a large cohort of adult patients. These findings are particularly relevant to pediatricians today because so many children receive some sort of GA-blocking agent to treat GERD. To test the hypothesis that GA suppression could be associated with an increased risk of acute gastroenteritis and pneumonia in children treated with GA inhibitors, we conducted a multicenter, prospective study. The study was performed by expert pediatric gastroenterologists from 4 pediatric gastroenterology centers. Children (aged 4-36 months) consecutively referred for common GERD-related symptoms (for example, regurgitation and vomiting, feeding problems, effortless vomiting, choking), from December 2003 to March 2004, were considered eligible for the study. Exclusion criteria were a history of GA inhibitors therapy in the previous 4 months, Helicobacter pylori infection, diabetes, chronic lung or heart diseases, cystic fibrosis, immunodeficiency, food allergy, congenital motility gastrointestinal disorders, neuromuscular diseases, or malnutrition. Control subjects were recruited from healthy children visiting the centers for routine examinations. The diagnosis of GERD was confirmed in all patients by standard criteria. GA inhibitors (10 mg/kg ranitidine per day in 50 children or 1 mg/kg omeprazole per day in 50 children) were prescribed by the physicians for 2 months. All enrolled children were evaluated during a 4-month follow-up. The end point was the number of patients presenting with acute gastroenteritis or community-acquired pneumonia during a 4-month follow-up study period. We obtained data in 186 subjects: 95 healthy controls and 91 GA-inhibitor users (47 on ranitidine and 44 on omeprazole). The 2 groups were comparable for age, gender, weight, length, and incidence of acute gastroenteritis and pneumonia in the 4 months before enrollment. Rate of subjects presenting with acute gastroenteritis and