幽门螺杆菌与化生性病变在胃黏膜中的分布

Distribution of Helicobacter pylori and metaplastic lesions in gastric mucosa

目的：探讨在胃黏膜中幽门螺杆菌(Hpylori)与化生性病变的分布及其相关性.方法：Hpylori感染的胃病患者10例(胃或十二指肠溃疡5例,癌症病例5例),手术切除胃标本做全胃取材,把所有标本做连续切片做(1)HE染色；(2)Hpylori免疫组化染色,(3)人胃黏蛋白(human gastric mucin,M1)做免疫组化染色后用奥新蓝(alcian blue,AB)做双重染色,把染色结果画在取材图上.结果：根据(1)Hpylori；(2)完全性肠上皮化生；(3)不完全性肠上皮化生及(4)奥新蓝阳性的假幽门腺化生和/或颈黏液细胞(PM)的分布结果,全部病例分为3型；在Ⅰ型(HP^+IM^+PM^+)以假幽门腺化生为主,Hpylori与化生性病变的分布重复,Ⅱ型(HP^+IM^-PM^-)和Ⅲ型(HP^+IM^- PM^+)是以肠上皮化生为主,与Hpylori的分布不重复,呈相反.Ⅰ型5例中4例在不完全性肠上皮化生细胞上见Hpylori感染.Ⅱ型和Ⅲ型的炎症细胞浸润及萎缩程度比Ⅰ型重.Ⅱ型和Ⅲ型5例均是癌症病例,Ⅰ型5例中仅有1例是癌症病例,其余4例是溃疡病例.结论：Ⅰ型胃黏膜中的假幽门腺化生和伴H pylori感染的轻度肠上皮化生,可能与诱发溃疡性病变有关；Ⅱ,Ⅲ型的肠上皮化生,加上严重的炎症持续,可能增加癌发生的危险性.

AIM： To investigate the distribution of Helicobacter pylori and metaplastic lesions as well as their correlations in gastric mucosa. METHODS： Whole-mucosal step sectioning were performed using 10 surgically resected stomach specimens （5 cases of gastric or duodenal ulcers, 5 of gastric carcinoma） that histologically showed H pylori infection. Serial paraffin sections were prepared and stained as follows： （1） hematoxylin and eosin staining; （2） immunohistochemical staining for H pylori, and （3） immunohistochemical and alcian blue （AB） doublestaining for human gastric mucin （M1）. After each section was histologically evaluated, the positively stained areas were plotted on photographic copies showing the stomach specimens. RESULTS： The staining properties were as follows： （1）H pylori＋; （2） complete intestinal metaplasia （IM）; （3） incomplete intestinal metaplasia, and （4） pseudopyloric gland metaplasia （PM） and mucous neck cells. The 10 stomach specimens were then classified into three types： In type Ⅰ （H pylori＋IM＋PM＋）, the distributions of H pylori and the metaplastic changes, especially PM, overlapped. In types Ⅱ （H pylori＋IM-PM） and Ⅲ（H pylori＋IMPM＋）, the distributions of H pylori and the metaplastic changes, especially IM, did not overlap. In 4 out of 5 type Ⅰ cases, H pylori was observed in the areas of incomplete IM epithelia. 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 In cases were associated with carcinoma, whereas only 1 type Ⅰ case was associated with carcinoma. The other cases were associated with ulcer lesions. CONCLUSION： In conclusion, areas of PM with mild IM may include areas of H pylori infection, as observed in type Ⅰ stomach specimens, which may associated with the induction of ulcers. On the other hand, areas of marked IM associated with severe inflammation, as observed in type Ⅱ and Ⅲ specimens, do not contain areas of H pylori infection, which may increase the risk of carcinogenesis.