One hundred eighty-seven patients (138 were male and 49 were female) who had received gastric resection for peptic duodenal ulcer (group 1; n = 131) or advanced gastric cancer (group 2; n = 56) were included in this prospective study. All patients were asked for and granted their informed consent for inclusion. Reconstruction of the digestive tract consisted of a Billroth I gastroduodenostomy (n = 14) or a Billroth II gastrojejunostomy (n = 173). All 187 patients underwent upper digestive tract endoscopy between April 1, 2000, and March 31, 2006, at the endoscopic units of the departments of Surgery Pietro Valdoni and Medical Therapy of the University of Rome La Sapienza, First Medical School. All endoscopies were performed in the setting of postgastrectomy surveillance. None of these patients had received eradicating therapy for HP infection, antibiotics, nonsteroidal anti-inflammatory drugs, or chemotherapy in the 4 weeks before the diagnostic procedure. Endoscopic examination of the esophagus, gastric stump, anastomosis, and anastomosed small bowel for approximately 20 cm was routinely performed. A rapid urease test on gastric biopsy specimens from 37 cases, belonging to both groups, was performed at the beginning of the study. However, this test was later abandoned to reduce the number of total biopsy specimens because findings overlapped with the histological results in 36 of 37 cases. Histological microscopic examination was always performed. Most of the study patients had undergone the initial operation in other institutions and had not received any assessment of the HP status before our endoscopy. In any case, to the best of our knowledge, no patient had received any eradicating therapy after surgery. However, we prescribed antibiotic eradicating therapy to any patient we discovered to have positive findings for HP infection (HP positive), with no further HP status assessment at a later stage. Ten to 12 biopsy specimens were routinely taken from the stoma and the peristomal areas, from other areas of residual gastric mucosa along the lesser and greater curvatures, and from any areas showing erythema, erosion, or friability. Biopsy specimens were fixed in 10% formalin and embedded in paraffin. Sections were stained with hematoxylin-eosin. Additional sections of biopsy specimens were examined using Giemsa stain for HP detection. All histological slides were blindly reviewed by an experienced gastrointestinal pathologist (I.P.). The histological findings were classified as normal mucosa (NM; no changes in the mucosa), chronic nonatrophic gastritis (NAG; inflammatory cells in the lamina propria, but no loss of glands), CAG (loss of glands of any grade and stromal proliferation between the glands), IM (absorption, goblet, and Paneth cells in the superficial epithelium), and dysplasia (secretive, nuclear, and cytoplasmic abnormalities, excluding reactive, nondysplastic conditions). Helicobacter pylori infection, any histological mucosal changes, and inflammation1 (presence of chronic inflammatory cells in the lamina propria, such as lymphocytes, plasma cells, macrophages, and histiocytes) and its activity1 (presence of neutrophil granulocyte infiltration in the lamina propria or in intraepithelial foci) were recorded as present or absent. When more histological lesions were present, the case was classified according to increasing severity in the following order: NM, NAG, CAG, IM, and dysplasia. The last 3 (CAG, IM, and dysplasia) were all included in the GCPL group, which was the main focus of our study.