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目的研究幽门螺杆菌（Ｈｐ）诱生的胃粘膜相关淋巴组织（ＭＡＬＴ）增生与萎缩关系及Ｈｐ根除后淋巴滤泡（ＬＦ）消失情况．方法光镜观察２５８例Ｈｐ阳性的慢性胃炎三联（奥美拉唑、克拉霉素、痢特灵，７ｄ）药治疗前后（１ｍｏ及１ａ）及正常胃粘膜２５例的ＬＦ检出率和聚集强度．结果慢性胃炎ＬＦ总检出率为７２５％；萎缩性胃炎＞浅表性胃炎，而正常胃粘膜ＬＦ检出率为４％；慢性胃炎ＬＦ聚集强度与粘膜炎症程度呈正相关（ｒ＝０６５，Ｐ＜００１）；但与粘膜萎缩程度呈负相关（ｒ＝－０６９，Ｐ＜００１）；治疗后慢性胃炎ＬＦ检出率和聚集强度明显减低（Ｐ＜００１）；腺上皮萎缩与ＬＦ形成关系密切．结论胃ＭＡＬＴ增生及相伴的免疫反应，可能是引起Ｈｐ相关性胃炎出现胃粘膜萎缩的重要原因之一．
Objective To study the relationship between the proliferation and atrophy of gastric mucosa-associated lymphoid tissue (MALT) induced by Helicobacter pylori (Hp) and the disappearance of lymphoid follicles (LF) after Hp eradication. Methods The LF detection rate and aggregation intensity of 258 cases of Hp-positive chronic gastritis triple therapy (omeprazole, clarithromycin, furazolidone, 7d) before and after treatment (1mo and 1a) and normal gastric mucosa . Results The total detection rate of LF in chronic gastritis was 725%; atrophic gastritis> superficial gastritis, while the detection rate of normal gastric mucosa was 4%. The concentration of LF in chronic gastritis was positively correlated with the degree of mucosal inflammation (r = 0 65, P <001), but negatively correlated with mucosal atrophy (r = -069, P <001). The detection rate and aggregation intensity of chronic gastritis were significantly decreased after treatment 01); gland epithelial atrophy and the formation of LF is closely related. Conclusion MALT hyperplasia and accompanying immune response may be one of the important causes of gastric mucosal atrophy in Hp-related gastritis.