Search

Twenty-three children with Helicobacter (Campylobacter) pylori-associated chronic gastritis are reported. Family history of peptic disease, previous digestive procedures, and nonspecific epigastric pain were the most frequently encountered clinical features. Antral nodularity at endoscopy and histologic evidence of follicular gastritis were characteristic morphological aspects. Rapid urease tests suggested the diagnosis in 90 of patients. Significant increases of serum IgG and IgA against Helicobacter pylori allowed the identification of infected children with 95 cumulative sensitivity. Treatment with amoxicillin and bismuth subcitrate eradicated the infection and improved gastritis in 13 of 19 children. These findings provide further evidence for the etiologic role of Helicobacter pylori in chronic antral gastritis in children.

Twenty-three children with Helicobacter (Campylobacter) pylori-associated chronic gastritis are reported. Family history of peptic disease, previous digestive procedures, and nonspecific epigastric pain were the most frequently encountered clinical features. Antral nodularity at endoscopy and histologic evidence of follicular gastritis were characteristic morphological aspects. Rapid urease tests suggested the diagnosis in 90% of patients. Significant increases of serum IgG and IgA against Helicobacter pylori allowed the identification of infected children with 95% cumulative sensitivity. Treatment with amoxicillin and bismuth subcitrate eradicated the infection and improved gastritis in 13 of 19 children. These findings provide further evidence for the etiologic role of Helicobacter pylori in chronic antral gastritis in children.