幽门螺杆菌感染与胃粘膜淋巴组织增生  

HELICOBACTERPYLORIINFECTIONANDGASTRICMUCOSA┐ASSOCIATEDLYMPHOIDTISSUEHYPERPLASIA

作　　者：黄自平[1,2] 梁扩寰[1,2] 

机构地区：[1]上海市第一人民医院消化科 [2]同济医科大学附属同济医院内科

出　　处：《中华内科杂志》1996年第9期609-611,共3页Chinese Journal of Internal Medicine

摘　　要：应用６种方法检测２５６例胃粘膜活检标本的幽门螺杆菌（Ｈｐ），总检出率为７０．７０％，其顺序为活动性胃炎＞非活动性胃炎＞正常胃粘膜，慢性萎缩性胃炎＞浅表－萎缩性胃炎＞慢性浅表性胃炎＞正常胃粘膜。胃粘膜淋巴滤泡检出率为４３．３６％，其顺序与Ｈｐ检出率相同。有淋巴滤泡形成者Ｈｐ检出率显著高于无淋巴滤泡形成者（８１．４８％比６５．４９％，Ｐ＜０．００１）；淋巴滤泡形成与腺上皮萎缩和肠上皮化生关系密切。结果提示，Ｈｐ感染诱导的胃粘膜淋巴组织增生及其伴随的免疫反应可能是Ｈｐ相关性胃炎出现胃粘膜腺体萎缩的主要机制。TheassociationofHelicobacterpylori(Hp)infectionwithmucosa-associatedlymphoidtissue(MALT)hyperplasiaingastricmucosawasinvestigated.TheresultsshowedthattheincidenceofHpinfectionincreasedasthedegreeofthemucosalinjurywasaggravated,buttheprevalenceoflym-phoidfoliclesinthemucosawithatrophicantritiswasmuchmorethaninthemucosawithouttheat-rophicandthefrequencyofdetectingHpandintestinalmetaplasiainthemucosawithlymphoidfoliclessignificantlyincreased,ascomparedwiththemucosawithoutit.ThesefindingssuggestthatgastricMALThyperplasiainducedbyHpinfectionmayleadtodestructionofgastricglandsthroughhypersen-sitivity.

关 键 词：胃炎 幽门螺杆菌 胃粘膜增生 

分 类 号：R573.302[医药卫生—消化系统]