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目的 探讨幽门螺杆菌 (Hp)毒素与儿童胃十二指肠疾病的关系及Hp毒素参与胃十二指肠粘膜病变的机制 ,并评价Hp毒素抗体检测的临床意义。方法 采用免疫印迹法测定 39例Hp阳性和 32例Hp阴性患儿血清多种Hp毒素抗体。观察胃十二指肠粘膜病理变化。结果 Hp阳性患儿 ,Hp毒素抗体相对分子质量为 116 0 0 0、30 0 0 0、2 6 5 0 0、195 0 0和现症感染标志 (CIM)的阳性率均为10 0 %。相对分子质量为 890 0 0、6 10 0 0、5 80 0 0、370 0 0和 35 0 0 0的阳性率分别为 94 9%、87 2 %、5 3 9%、87 2 %和 46 2 %。HpⅠ型菌株占 94 9% ,未检出Ⅱ型菌株。Hp阴性患儿各抗体的检出率为0 %～ 2 8 1%。各种抗体在不同疾病之间的检出率无显著差异。细胞毒素相关蛋白 (CagA)、空泡细胞毒素 (VacA)和尿素酶A、D、E抗体阳性者胃十二指肠粘膜无一例正常 ,中重度炎症发生率为 94 9%～97 3%。尿素酶B抗体阳性者胃粘膜中性粒细胞浸润比阴性者多见 ,差异有显著性。结论 本地区儿童主要感染HpⅠ型毒力菌株 ,引起的胃十二指肠粘膜炎症较严重。尿素酶B抗体阳性提示胃粘膜有活动性炎症。CagA、VacA等Hp毒素抗体可能不是儿童十二指肠溃疡的特异标志物
Objective To investigate the relationship between Helicobacter pylori (Hp) toxin and gastroduodenal diseases in children and the mechanism of Hp toxin involvement in the pathogenesis of gastroduodenal mucosa and to evaluate the clinical significance of Hp toxin antibody detection. Methods The serum Hp toxin antibodies of 39 cases of Hp positive and 32 cases of Hp negative children were detected by immunoblotting. Observe the pathological changes of gastroduodenal mucosa. Results The positive molecular weight of Hp toxin antibody in Hp positive children was 116 0 0 0 0 0 0 0, 2 65 0 0, 195 0 0 and the positive sign of infection (CIM) was 100%. The positive rates of relative molecular masses of 890 0 0, 6 10 0 0, 5 80 0 0, 370 0 0 and 35 0 0 0 were 94 9%, 87 2%, 53 9%, 87 2% and 46 2 %. Hp type Ⅰ strains accounted for 94 9%, no type Ⅱ strains were detected. The detection rate of each antibody in Hp-negative children was 0% -281%. There was no significant difference in the detection rate of various antibodies between different diseases. No positive cases of gastroduodenal mucosa were found in CagA, VacA and urease A, D and E antibodies. The incidence of moderate and severe inflammation was 94.9% ~ 97.3%. Urease B antibody positive gastric mucosal neutrophil infiltration were more common, the difference was significant. Conclusion The children in this area are mainly infected with Hp Ⅰ virulent strains and cause more severe gastroduodenal mucosal inflammation. Positive urease B antibody gastric mucosa prompted active inflammation. Hp toxin antibodies such as CagA and VacA may not be specific markers of childhood duodenal ulcer