Favorable Long‐term Outcome After Isolated Liver Transplantation in a Child With Short Bowel Syndrome

To the Editor: We wish to comment on the paper by Ozturk et al. (1.) on intestinal metaplasia (IM) and gastric atrophy in children with Helicobacter pylori gastritis. They reported various degrees of gastric atrophy and IM in 72% to 77% of patients with H. pylori. They concluded that the high incidence was a result of the prolonged duration of infection in Turkish children and recommended that children with H. pylori should be followed more carefully in high incidence regions. We would like to add our experience in a larger population to that of Ozturk et al. We evaluated 255 children (median age, 12 years; range, 4–18 years) who had upper intestinal endoscopy for abdominal pain or dyspeptic symptoms. The diagnosis of H. pylori gastritis was based on CLOtest (Delta West Bertley, Australia) and histologic evaluation of tissue stained with hematoxylin-and-eosin (H&E) and Toluidine-O. H. pylori was found in 163 of 255 children (63.7%), and chronic antral gastritis in 64 (25%). IM was diagnosed in H&E stained sections. Sections were also stained with periodic acid-Schiff–Alcian blue (pH 2.5) for sialomucin and high iron diamine (HID). Five of 64 patients had IM with chronic antral gastritis. One of 64 patients with H. pylori had atrophic gastritis. The incidences of IM and gastric atrophy were 1.56% and 7.8%, respectively, in patients with H. pylori. IM was observed in 2.15% (n = 2) of patients who tested negative for H. pylori. The World Health Organization International Agency of Research on Cancer classified H. pylori as a carcinogen in 1994 (2.). Although H. pylori infection carries a 4-9 fold risk of precancerous gastric conditions, especially when infection starts in childhood, (3.) it should be stressed that most patients with H. pylori gastritis do not develop gastric cancer, and that up to 20% percent of patients with gastric cancer are seronegative for H. pylori. Recently, Atisook et al. (4.) in a nationwide study in Thailand, found that the rate of IM in infected patients less than 30 years was 3.6%, and atrophic changes occurred in 5%. The incidence of IM and atrophic gastritis increased with age. Infection with H. pylori during childhood is thought to increase the risk for gastric carcinoma in adult life; however, the presence of IM and atrophic gastritis in children with H. pylori infection and the relationship between these lesions and gastric carcinoma are matters of controversy. Gallo et al. (5.) evaluated 307 consecutive children with H. pylori infection and did not find IM or atrophic gastritis in any. Among our patients IM was found in 7.8%. Our results are different from those of Ozturk et al., even though the studies were performed in the same region of western Turkey. It is not clear why gastric atrophy and IM are low in children from this high prevalence area. Differences in the strain of H. pylori, host factors, and food habits could be important (3., 6.). For reasons that are poorly understood, chronic H. pylori infection gives rise to different types of lesions in different people. Whether host or environmental factors, such as diet and lifestyle as well as bacterial virulence factors, lead to the development of a given type of mucosal lesion is a matter of speculation (3., 7.). Chronic infection with H. pylori appears to follow two distinct pathways (6.). Some infected patients develop diffuse antral gastritis (DAG), and others develop multifocal atrophic gastritis (MAG). DAG is a superficial chronic active gastritis that involves the antrum. It is believed that DAG does not predispose individuals to intestinal metaplasia, dysplasia, or cancer. In our series, most of the children had DAG. This may be an explanation for the low incidence of atrophy and IM in our patients. Another possibility is that gastric atrophy and IM would be found more frequently if multiple biopsy specimens providing an accurate survey of the gastric mucosa were always taken. A set of four biopsy specimens (2 corpus and 2 antral biopsy specimens) is believed to underestimate IM in about 25% of the cases (3.). A more significant underdiagnosis might be expected as a result of the limited random sampling usually performed in routine practice. Underdiagnosis by pathologists is another possible cause of the low prevalence of IM and atrophy. Although there is reasonable concordance in the diagnosis of IM, poor interobserver agreement in the evaluation of atrophy is notorious (8.). Limiting factors include the lack of a uniform definition of atrophy and the difficulty in accurate assessment in the presence of chronic inflammation and lymphoid hyperplasia. It has been speculated that atrophy represents a point of no return for gastric mucosa and it is controversial whether return to normal histology is possible with therapy. (9., 10.). We observed regression of IM after eradication of H. pylori in two of our five patients. Thus, although we have not found a high incidence of IM in our patients, H. pylori eradication seemed to prevent progression of pathologic changes in the gastric mucosa. Additional studies with larger populations are needed to explore this issue and the overall outcome of persistent H. pylori infection in childhood. *Cigdem Arikan *Funda Özgenç *Gökhan Tümgör †Basak Doganavsargil *Sema Aydoğdu *Raşit Vural Yağci