title: Histologic and serum risk markers for noncardia early gastric cancer.
abstract: Corpus dominant gastritis and intestinal metaplasia (IM) are considered markers of increased risk of gastric carcinoma. The aim of our study was to determine serum and histologic risk markers of gastric cancer. Antral and corpus histology, pepsinogen and gastrin 17 levels were compared among patients with history of endoscopic mucosal resection (EMR) for early gastric cancer and controls. Serum pepsinogen (PG) and gastrin 17 levels were measured by RIA. There were 53 gastric cancer patients and 75 controls. The scores for IM in each region and atrophy at the lesser curvature of the corpus were significantly higher in the cancer group than in the H. pylori-positive control group. IM at the greater curvature of the corpus and atrophy at the lesser curvature of the corpus were associated with multiple malignant lesions. Although corpus gastritis was associated with an increased risk of gastric cancer (odds ratio [OR] = 3.4; 95% confidence interval [CI] 1.6-7.0) (p = 0.001), the most important marker was the presence of IM at the lesser curvature of the corpus (OR = 15.1; 95% CI 4.3-52.6) (p < 0.001)). The best cut-off points of serum markers for gastric cancer were a PG I concentration of 45 ng/mL or less and a gastrin 17 >60 pg/mL (sensitivity = 83%; specificity = 68%). IM at the lesser curvature of the corpus and the combination of serum gastrin 17 and PG I identified a group at high risk for development of gastric cancer. Annual endoscopic follow-up is warranted for patients with IM found at the greater curvature of the corpus.
authors.affiliation: Health Administration Center, Wakayama University, Wakayama City, Japan. shiotani@center.wakayama-u.ac.jp <shiotani@center.wakayama-u.ac.jp>
authors.forename: Akiko
authors.initials: A
authors.lastname: Shiotani
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Iishi
authors.forename: Noriya
authors.initials: N
authors.lastname: Uedo
authors.forename: Mitutaka
authors.initials: M
authors.lastname: Kumamoto
authors.forename: Yukinori
authors.initials: Y
authors.lastname: Nakae
authors.forename: Shingo
authors.initials: S
authors.lastname: Ishiguro
authors.forename: Masaharu
authors.initials: M
authors.lastname: Tatsuta
authors.forename: David Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D004724:Endoscopy; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005755:Gastrins / Q000097:blood*; D016481:Helicobacter Infections / Q000276:immunology; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D007413:Intestinal Mucosa / Q000276:immunology / Q000473:pathology; D008297:Male; D008679:Metaplasia / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D020116:Pepsinogen A / Q000097:blood*; D020115:Pepsinogen C / Q000097:blood*; D011706:Pyloric Antrum / Q000473:pathology; D013274:Stomach Neoplasms / Q000097:blood / Q000175:diagnosis* / Q000209:etiology
chemical_list: D015415:Biomarkers; D005755:Gastrins; C013550:gastrin 17; D020115:Pepsinogen C; D020116:Pepsinogen A