Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer.
VacA was histochemically stained in biopsy specimen and was intracellularly and mainly located in fundic gland area. It is recognized gastric atrophy was observed in the H. pylori-positive patients with intracellular VacA compared with others. The aim of study is to understand the relationship between intracellular VacA and the progression of gastric atrophy that is associated with gastric cancer. Biopsy specimens and sera were obtained from 364 people in their 50s and 60s without gastric cancer diagnosed at first endoscopy undergoing diagnostic endoscopy, for H. pylori infection, histology, and the histochemical status of intracellular VacA using anti-VacA Ab during the follow-up period (mean, 7.3 years). Three hundred eleven of 364 enrolled patients were H. pylori positive and 53 patients were H. pylori negative at first endoscopy. VacA was intracellularly stained with vacuolation and cell destruction in the fundic gland in 98 of 311 H. pylori-positive patients and not stained in another 213 H. pylori-positive patients plus 53 H. pylori-negative patients at first endoscopy. Gastric atrophy has significantly progressed in the H. pylori-positive patints with intracellular VacA with gastric ulcers compared with the others and six gastric cancers have developed in this group during the follow-up period (mean, 7.3 years). Intracellular VacA is a valuable marker to predict whether Helicobacter pylori induces progressive atrophic gastritis that is associated with the development of gastric cancer.
Karita
Mikio
M
Internal Medicine, Hofu-Onsen Hospital, 1640, Daidou, Houfu-shi, Yamaguchi-ken, Japan. makarita@ymg.urban.ne.jp
Teramukai
Satoshi
S
Matsumoto
Satoru
S
Shibuta
Hidemi
H
D000368:Aged; D000942:Antigens, Bacterial / Q000378:metabolism; D001426:Bacterial Proteins / Q000097:blood* / Q000378:metabolism; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D005748:Gastric Fundus / Q000378:metabolism / Q000473:pathology; D005757:Gastritis, Atrophic / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007425:Intracellular Membranes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017027:Protein Tyrosine Phosphatases / Q000378:metabolism; D054633:Receptor-Like Protein Tyrosine Phosphatases, Class 5; D013274:Stomach Neoplasms / Q000382:microbiology*; D013276:Stomach Ulcer / Q000378:metabolism / Q000382:microbiology
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; C516895:PTPRZ1 protein, human; D017027:Protein Tyrosine Phosphatases; D054633:Receptor-Like Protein Tyrosine Phosphatases, Class 5