幽门螺杆菌感染对胃病细胞动力学的影响

Effect of Hp infection on gastric epithelial cell kinetics in stomach diseases

目的 观察 Ｈｐ 感染在正常粘膜演变为胃癌过程中对细胞增殖动力学的影响，以探讨 Ｈｐ 的致癌机制．方法 研究对象为正常胃粘膜的消化不良患者（ ＮＳ，ｎ ＝ １４） 及慢性浅表性胃炎（ ＣＳＧ， ｎ ＝ ５６） 、慢性萎缩性胃炎（ ＣＡＧ，ｎ ＝ ２０） 、慢性萎缩性胃炎伴肠上皮化生（ＣＡＧＩＭ ，ｎ ＝ １６） 、不典型增生（Ｄｙｓ ，ｎ ＝ １８） 、胃癌（ ＧＣ，ｎ ＝ １７） Ｈｐ 阳性与阴性患者．应用Ｋｉ６７ 免疫组化技术评价胃幽门窦上皮细胞增生，并用标记指数百分率（ＬＩ％ ） 来表示．结果 Ｈｐ 阳性患者（ ｎ ＝ ７５） 的Ｋｉ６７ ＬＩ％ 为１７ ±５ ， Ｈｐ 阴性患者（ ｎ ＝ ５２ ） 的 Ｋｉ６７ ＬＩ％ 为 １３ ±６ ， 差异有 显著 性（ Ｐ＜ ０－０５） ；伴有 Ｈｐ 感染的ＣＳＧ 与ＮＳ 或 Ｈｐ 阴性的ＣＳＧ 患者相比ＬＩ％ 增加（ Ｐ＜ ０－０１） ；ＣＡＧ，ＣＡＧＩＭ ，Ｄｙｓ ，ＧＣ 的 Ｈｐ 阳性与阴性患者的ＬＩ％ 相比无显著差异；五种胃病无论 Ｈｐ 阳性或阴性患者与正常者相比，ＬＩ％ 明显增加（ Ｐ＜ ０－０１） ． ＬＩ％ 与胃粘膜炎症程度无关．结论 Ｈｐ 感染促进胃上皮细胞过度增殖主要发生在胃粘膜病变的早期。

AIM To investigate the effect of Helicobacter pylori (Hp) infection on the gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma and the mechanisms of Hp causing gastric maligancy. METHODS By using immunohistochemical technique, the Ki 67 labelling index (LI%) was used to assess the gastric antral epithelial cell proliferation in bioptic gastric mucosa specimens of normal gastric mucosa dyspeptic subjects (NS, n =14 ) and five groups of patients (chronic superficial gastritis, CSG, n =56 ; chronic atrophic gastritis, CAG, n =20 ; chronic atrophic gastritis with intestinal metaplasia, CAGIM, n =16 ; dysplasia, Dys, n =18 ; gastric cancer, GC, n =17 ). Each was comprised of Hp positive and negative patients. RESULTS Ki 67 labelling index (LI%) was 17±5 in seventy five Hp positive patients, significantly higher than 13±6 in fifty two Hp negative patients ( P <0 05). CSG with Hp infection showed higher LI% than NS or CSG without Hp infection. There was no significant difference between the patients with or without Hp infection of CAG, CAGIM, Dys and GC. Five groups of patients had increased LI% compared with normal control, regardless of Hp infection. There was no correlation between LI% and the severity of gastritis. CONCLUSION Hp infection plays a role in the hyperproliferation of gastric epithelial cell predominantly in the early stage of gastric mucosa lesion, but not influcences the increased cell proliferation seen in precancerous lesion or GC. This provides further evidences that Hp infection may be an initiating step in the progression from normal mucosa to gastric carcinoma.