论文部分内容阅读
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Ｋｉ６７ 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Ｋｉ６７ ＬＩ％ 为１７ ±５ ， Ｈｐ 阴性患者（ ｎ ＝ ５２ ） 的 Ｋｉ６７ 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，并不影响在癌前病变或胃癌患者中所
Objective To investigate the effect of Hp infection on the proliferation kinetics of normal gastric mucosa during gastric carcinogenesis and to explore the mechanism of Hp carcinogenesis. Methods Patients with dyspepsia (NS, n = 14), chronic superficial gastritis (CSG, n = 56), chronic atrophic gastritis (CAG, n = 20), and chronic atrophic gastritis Epithelial metaplasia (CAGIM, n = 16), dysplasia (Dys, n = 18), gastric cancer (GC, n = 17) were positive and negative in Hp. The application of Ki 67 immunohistochemical evaluation of gastric pyloric sinusoidal epithelial cell proliferation, and with the index of the percentage (LI%) to represent. Results The Ki-67 LI% of Hp-positive patients (n = 75) was 17 ± 5, and the Ki-67 LI% of Hp-negative patients was 13 ± 6 (P <0-05) (P <0-01). There was no significant difference in the Hp positive rate between CAG, CAGIM, Dys, GC and LI negative patients with CSG with Hp infection and NS or Hp negative CSG patients; The five gastric diseases showed a significant increase in LI% (P <0-01) in both Hp-positive and -negative patients compared with the normal controls. LI% and gastric mucosal inflammation has nothing to do. Conclusion Hp infection can promote gastric epithelial cell hyperproliferation mainly occurs in the early stage of gastric mucosal lesions, does not affect in precancerous lesions or gastric cancer patients