ASSOCIATION OF GASTRIC METAPLASIA AND DUODENITIS WITH HELICOBACTER-PYLORI INFECTION IN CHILDREN

Helicobacter pylori infection causes chronic-active gastritis and is associated with peptic ulceration. However, the link between gastric H pylori colonization and duodenal ulcers is not well understood. Therefore, a retrospective, case-controlled study was conducted to determine whether H pylori infection is associated with gastric metaplasia and mucosal inflammation in the duodenum. Biopsy specimens from the duodenal bulb were obtained from 31 of 47 children with H pylori-induced gastritis. Two control groups, matched for age and sex, consisted of 33 children with normal antral histologic evaluation and 33 with H pylori-negative gastritis. Coded duodenal sections were stained with periodic acid-Schiff, hematoxylin-eosin, and silver to examine for gastric metaplasia, mucosal inflammation, and Helicobacter-like organisms, respectively. Thirteen of 31 (42%) H pylori-infected children had gastric metaplasia, in contrast to 1 of 33 with normal histologic characteristics (P < .0001) and 2 of 33 with H pylori-negative gastritis (P < .001). H pylori was detected overlying ectopic gastric mucose in only 2 of 13 cases. Duodenal ulcers were identified endoscopically in 10 of 13 children with gastric metaplasia and 9 of 18 H pylori-infected subjects without metaplasia (P = NS). Twenty-four of 31 (77%) children with H pylori gastritis had duodenitis compared with 4 of 33 (12%) with H pylori-negative gastritis (P < .001) and 2 of 33 (6%) with a normal antrum (P < .001). Duodenitis was present in 14 of 19 children with H pylori infection and duodenal ulcers and 10 of 12 infected patients without mucosal ulceration (P not significant). These findings demonstrate a higher frequency of both gastric metaplasia and mucosal inflammation in the proximal small intestine H pylori-infected children. However, there was a lack of correlation between the presence of duodenal ulceration and both gastric metaplasia and duodenitis.