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

Helicobacter pylori and partial gastric resection are risk factors for gast ric cancer. Our aims were to investigate the presence of H. pylori in postg astrectomy patients and to correlate that with alterations in mucosal archi tecture and cell proliferation. One hundred fifty-one endoscopic biopsies f rom 22 patients, (15-47 years of age, mean 29.2 years) following partial ga strectomy with Billroth II reconstruction for peptic ulcer disease, were ex amined for the presence of H. pylori using Giemsa staining. Sections were s cored for grade of hyperplasia, intestinal metaplasia, dysplasia, inflammat ion, and atrophy. Immunohistochemistry for proliferative cell nuclear antig en (PCNA) was used to characterize cell proliferation. H. pylori was observ ed in 17/22 (77.3%) of patients or in 57/151 (37.7%) of biopsies. Metaplasi a was seen in 18/22, chronic atrophic gastritis in 20/22, and cystic glandu lar dilation in 21/22 patients. The highest type of metaplasia in each pati ent was: four Type I, five Type IIA and nine Type IIB. Dysplasia was presen t in 16 biopsies from nine patients. H. pylori was more prevalent in intest inal metaplasia type I (44.8% of biopsies), than in type IIA (32.7%) or typ e IIB (25%). No H. pylori was detected in regions showing dysplasia or cyst ic glandular dilation. H. pylori colonization was associated with degree of inflammation (P = 0.00001) and cell proliferation (P = 0.0001). In conclus ion, H. pylori is commonly seen many years after gastrectomy, it is associa ted with an increased epithelial cell proliferation, and it is not present in areas of histologic markers of premalignancy (type IIB metaplasia and dy splasia).