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目的探讨广州地区2~12岁儿童胃幽门螺杆菌(H·pylori)感染的临床及病理学特点。方法对广州地区2~12岁具有消化道症状的儿童1186例进行胃镜检查,取胃窦部黏膜进行快速尿素酶试验,用ELISA检测血清H·pylori抗体,并对其中528例同时取胃黏膜进行病理组织学检查。结果胃镜检查为胃十二指肠疾病者1010例,阳性率为85·2%(1010/1186);发现幽门螺杆菌感染301例,阳性率25·38%,各年龄组幽门螺杆菌的检出率为2~3岁14·38%(21/146),4~5岁为19·31%(39/202),6~7岁为24·01%(67/279),8~9岁为28·87%(82/284),10~12岁为33·45%(92/275);组织学改变为胃黏膜上皮变性,腺体上皮脱落坏死,发生坏死的腺体有淋巴细胞的广泛浸润及聚集灶,感染严重的病例可找到生发中心的淋巴小结。在变性的黏膜表面与坏死的腺体内可找到幽门螺杆菌。结论H·pylori感染在广州地区2~12岁有消化道症状的儿童中并不少见,并随年龄的增加有上升趋势。H·pylori感染的病理改变全部为慢性炎症表现,炎症程度重,表现为胃黏膜上皮细胞和腺体的变性坏死,固有层淋巴细胞浸润,多形白细胞浸润较少。
Objective To investigate the clinical and pathological features of H. pylori infection in children aged 2 ~ 12 years in Guangzhou. Methods A total of 1186 children aged 2 ~ 12 years with gastrointestinal symptoms were enrolled in this study. Gastric mucosa was taken for rapid urease test. Serum H · pylori antibody was detected by ELISA. Gastric mucosa was taken from 528 of them Histopathological examination. Results The gastroscopy was diagnosed as gastroduodenal disease in 1010 cases, the positive rate was 85.2% (1010/1186). 301 cases of H. pylori infection were found, the positive rate was 25.38%. Helicobacter pylori was detected in all age groups The rates were 14.38% (21/146) of 2 ~ 3 years old, 19.31% (39/202) of 4-5 years old, 24.01% (67/279) of 6 ~ 7 years old, 8-9 The age was 28.87% (82/284), and the age ranged from 10 to 12 years old was 33.45% (92/275). Histological changes were gastric mucosal epithelial degeneration, glandular epithelium exfoliated and necrotic, necrotic glands had lymphocytes The extensive infiltration and aggregation lesions, severe cases of infection can find the germinal center lymph nodes. Helicobacter pylori can be found on the surface of degenerative mucosal membranes and necrotic glands. Conclusions H · pylori infection is not uncommon in children with gastrointestinal symptoms of 2 ~ 12 years old in Guangzhou area, and it is increasing with age. H · pylori infection pathological changes are all chronic inflammation, inflammation, manifested as gastric mucosal epithelial cells and glandular degeneration and necrosis, lamina propria lymphocyte infiltration, polymorphonuclear leukocyte infiltration less.