幽门螺杆菌细胞毒素相关蛋白A在特发性血小板减少性紫癜发病机制中的作用

目的目前,认为幽门螺杆菌(helicobacter pylori,Hp)感染是引起特发性血小板减少性紫癜(idiopathic thrombo-cytopenic purpura,ITP)的病因之一。研究幽门螺杆菌细胞毒素相关基因蛋白A(cytotoxin-associated gene protein,cagA)与特发性血小板减少性紫癜的血小板相关IgG抗体(platelet associated IgG,PA-IgG)及血小板数量变化的关系有助于探索Hp感染引起ITP的机制。文中通过检测ITP患者血清中cagA、PA-IgG和PLT数量,分析Hp感染与ITP发生的关系。方法快速尿素酶试验(rapid urease test,RUT)及14C尿素呼气试验(UBT)检测Hp。60例ITP患者分为Hp-、Hp+cagA-及Hp+cagA+3组,酶联免疫法测定外周血cagA、PA-IgG,用血细胞仪测定血小板计数,并比较抗Hp治疗前后的变化。结果 Hp+cagA+组的PA-IgG水平与Hp-和Hp+cagA-组比较明显升高(P<0.05),血小板计数与Hp-和Hp+cagA-组比较明显降低(P<0.05)。Hp+cagA-组的PA-IgG水平及血小板计数与Hp-组相比无统计学意义显著性差异(P>0.05)。Hp+cagA-组抗Hp治疗后PA-IgG水平下降及血小板计数上升不明显(P>0.05)。Hp+cagA+组抗Hp治疗后PA-IgG水平下降及血小板计数上升明显(P<0.01)。结论 Hp感染者可能由于其cagA导致PA-IgG升高而使血小板计数降低,参与ITP的发病机制。

Role of cytotoxin associated protein A in the pathogenesis of idiopathic thrombocytopenic purpura

Objective Helicobacter Pylori(Hp) infection is now considered one of the causes of idiopathic thrombocytopenic purpura(ITP).This study aimed to explore the mechanism of Hp infection causing ITP by investigating the relation of cytotoxin associated protein A of Hp with the PA-IgG level and PLT count in ITP patients.Methods We detected Hp using the rapid urease test(RUT) and 14C urea breath test(14C UBT).We divided 60 patients with ITP into three groups,Hp-,Hp+ cagA-,and Hp+ cagA+,determined the PLT counts and levels of cagA and PA-IgG before and after anti-Hp therapy,and compared them among the three groups.Results The PA-IgG level was significantly higher(P<0.05) while the PLT count markedly lower(P<0.05) in the Hp+ cagA+ group than in the Hp-and Hp+ cagA-groups,but neither showed significant difference between the latter two(P>0.05).Compared with the baseline,the PA-IgG level was significantly decreased and PLT count remarkably increased in the Hp+ cagA+ group(P<0.01),but neither exhibited statistical significance in the Hp+ cagA-group(P>0.05).Conclusion Helicobacter pylori increases the PA-IgG level and reduces the PLT count in ITP patients,which may be associated with cagA and involved the pathogenesis of ITP.