Relationship between persistence of Helicobacter pylori and dysplasia, intestinal metaplasia, atrophy, inflammation, and cell proliferation following partial gastrectomy.

Abstract

Helicobacter pylori and partial gastric resection are risk factors for gastric cancer. Our aims were to investigate the presence of H. pylori in postgastrectomy patients and to correlate that with alterations in mucosal architecture and cell proliferation. One hundred fifty-one endoscopic biopsies from 22 patients, (15-47 years of age, mean 29.2 years) following partial gastrectomy with Billroth II reconstruction for peptic ulcer disease, were examined for the presence of H. pylori using Giemsa staining. Sections were scored for grade of hyperplasia, intestinal metaplasia, dysplasia, inflammation, and atrophy. Immunohistochemistry for proliferative cell nuclear antigen (PCNA) was used to characterize cell proliferation. H. pylori was observed in 17/22 (77.3%) of patients or in 57/151 (37.7%) of biopsies. Metaplasia was seen in 18/22, chronic atrophic gastritis in 20/22, and cystic glandular dilation in 21/22 patients. The highest type of metaplasia in each patient was: four Type I, five Type IIA and nine Type IIB. Dysplasia was present in 16 biopsies from nine patients. H. pylori was more prevalent in intestinal metaplasia type I (44.8% of biopsies), than in type IIA (32.7%) or type IIB (25%). No H. pylori was detected in regions showing dysplasia or cystic glandular dilation. H. pylori colonization was associated with degree of inflammation (P = 0.00001) and cell proliferation (P = 0.0001). In conclusion, H. pylori is commonly seen many years after gastrectomy, it is associated with an increased epithelial cell proliferation, and it is not present in areas of histologic markers of premalignancy (type IIB metaplasia and dysplasia).