切除胃全割切片によるHelicobacter pyloriと化生性病変の分布についての免疫組織化学的研究

摘要

Chronic active gastritis caused by Helicobacter pylori (H pylori) infection tends to progress to atrophic gastritis and is often associated with intestinal metaplasia of the foveolar epithelia and pseudopyloric gland metaplasia in the fundic gland area. To determine the relationship between H pylori infection and metaplastic changes in the gastric mucosa, whole-mucosal step sectioning studies were performed using 10 surgically resected stomach specimens that histologically showed H pylori attached to the foveolar epithelial cells as well as chronic active gastritis. The 10 specimens were obtained from 5 cases of gastric or duodenal ulcers, 3 cases of early gastric carcinoma, and 2 cases of advanced gastric carcinoma. All formalin-fixed stomachs were sectioned into numerous tissue blocks and embedded in paraffin. A series of 5 μm-thick serial paraffin sections were made from every tissue block and stained as follows: (1) haematoxylin and eosin stain, (2) immunostaining for H pylori (HP), and (3) double-staining using human gastric mucin (M1) immunostaining and alcian blue (AB). After each section was histologically evaluated, 5 staining properties were selected and the positively stained areas were plotted on photographic copies showing the stomach specimens. The five staining properties were as follows: (1) HP+, (2) IM・AB+ (compatible with complete intestinal metaplasia), (3) IM・AB+M1+ (compatible with incomplete intestinal metaplasia), (4) Fov・AB+M1+ (foveolar epithelia without obvious intestinal metaplasia but with an intestinalized phenotype), and (5) PM・AB+ (pseudopyloric gland metaplasia, mucous neck cells or pyloric glands with an intestinalized phenotype). The 10 stomach specimens were then classified into three types according to the distribution of these 5 staining properties: type I, showing HP+ IM+ PM+ (5 cases); type II, showing HP+ IM- PM- (2 cases); and type III, showing HP+ IM- PM+ (3 cases). In type I, the distributions of H pylori and the metaplastic changes, especially pseudopyloric gland metaplasia, overlapped. In types II and III, the distributions of H pylori and the metaplastic changes, especially intestinal metaplasia, did not overlap. In 4 out of 5 type I cases, H pylori was observed in areas of incomplete intestinal metaplasia epithelia (IM・AB+M1+). Type II and III cases generally showed higher degrees of mucosal inflammation and atrophy of proper glands than type I cases. Four out of 5 type II and III cases were associated with carcinoma, whereas only 1 type I case was associated with carcinoma. The other cases were associated with ulcer lesions. In conclusion, areas of pseudopyloric gland metaplasia with mild intestinal metaplasia may include areas of H pylori infection, as observed in type I stomach specimens. This condition may induce ulcers. On the other hand, areas of marked intestinal metaplasia associated with severe inflammation, as observed in type II and III specimens, do not contain areas of H pylori infection but may increase the risk of carcinogenesis.