幽门螺杆菌感染儿童的胃化生与十二指肠溃疡病
Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.
作者信息
Gormally S M, Kierce B M, Daly L E, Bourke B, Carroll R, Durnin M T, Drumm B
机构信息
Department of Paediatrics, University College, Dublin, Ireland.
出版信息
Gut. 1996 Apr;38(4):513-7. doi: 10.1136/gut.38.4.513.
BACKGROUND
Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained.
AIMS
To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori.
PATIENTS
All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland.
METHODS
Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia.
RESULTS
Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent.
CONCLUSION
The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.
背景
胃黏膜幽门螺杆菌感染在十二指肠溃疡病发病机制中至关重要。幽门螺杆菌仅定植于胃上皮，因此其与十二指肠疾病的关联难以解释。
目的
确定十二指肠中的胃化生是否会增加幽门螺杆菌感染儿童患十二指肠溃疡病的风险。
患者
爱尔兰一家儿童医院20个月内接受上消化道内镜检查的所有儿童。
方法
从胃窦黏膜获取两份活检标本，从十二指肠第一部获取两份活检标本。一份胃窦活检标本用于快速尿素酶试验（Clo Test）。活检切片用苏木精和伊红染色，还用甲酚紫染色以鉴定幽门螺杆菌。进行过碘酸希夫（PAS）染色以鉴定胃化生区域。
结果
从148例患者（男:女为1:2:1）获取了胃和十二指肠活检标本。25名儿童（17%）患有幽门螺杆菌阳性胃炎。34名儿童（23%）十二指肠存在胃化生。8岁以下儿童中9%有胃化生，12岁及以上儿童中这一比例为38%（p<0.005）。7名儿童患有十二指肠溃疡病。7例十二指肠溃疡病儿童中有6例（86%）存在胃化生，而141例无溃疡病儿童中有28例（20%）存在胃化生（p<0.001）。虽然幽门螺杆菌和胃化生都是十二指肠溃疡病的重要危险因素，但两者同时存在与十二指肠溃疡病显著增加相关。幽门螺杆菌感染和胃化生两者皆有的儿童中超过50%发生了十二指肠溃疡病。相比之下，两者皆无的儿童未发生十二指肠疾病（100例中0例）。
结论
十二指肠中胃化生的存在是幽门螺杆菌定植患者患十二指肠溃疡病的主要危险因素。
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