核因子κB及幽门螺杆菌和细胞毒素相关基因A在特发性血小板减少性紫癜发病中的临床意义

Clinical significance of NF-κB,H.pylori and CagA in onset of idiopathic thrombocytopenic purpura

目的探究核因子κB(NF-κB)、幽门螺杆菌(H.pylori)及幽门螺杆菌细胞毒素相关基因A(CagA)在特发性血小板减少性紫癜(ITP)发病中的临床意义。方法抽取168例ITP患者(ITP组),另选择50例健康志愿者(对照组)。均通过14 C呼气试验检测H.pylori,以酶联免疫法检测血清NF-κB水平及Hp-CagA-IgG抗体表达,并测定血小板计数及血小板相关IgG抗体(PAIgG)、PAIgM。结果与对照组相比,ITP组除了初诊时血小板计数显著低及PAIgG、PAIgM含量显著高(P<0.05)以外,其血清NF-κB水平明显高(P<0.05),H.pylori、CagA阳性率明显高(P<0.05)。ITP患者NF-κB、H.pylori、CagA与血小板计数负相关,与PAIgG、PAIgM含量正相关(P<0.05)。轻度ITP患者初诊时血小板计数>中度ITP者>重度ITP者,PAIgG、PAIgM及NF-κB<中度ITP者<重度ITP者,H.pylori、CagA阳性率<中度ITP者<重度ITP者,差异均有统计学意义(P<0.05)。ITP患者中H.pylori阴性者血小板计数>H.pylori阳性且CagA阴性者>H.pylori、CagA均阳性者,PAIgG、PAIgM及NF-κB<H.pylori阳性且CagA阴性者<H.pylori、CagA均阳性者,比较差异均有统计学意义(P<0.05)。结论H.pylori感染可能直接通过CagA蛋白参与ITP的发病,或H.pylori感染促使CagA激活NF-κB而影响免疫应答导致PAIgG、PAIgM升高及血小板降低。

Objective To explore the clinical significance of nuclear factor(NF)-κB,Helicobacter pylori(H.pylori)and H.pylori cytotoxin associated gene A(CagA)in the pathogenesis of idiopathic thrombocytopenic purpura(ITP).Methods A total of 168 patients with ITP were enrolled as the ITP group.And 50 healthy volunteers were enrolled as the control group.H.pylori was detected by 14 C breath test.Serum NF-κB level and Hp-CagA-IgG antibody expression were detected by enzyme-linked immunosorbent assay.The platelet count,platelet-associated IgG antibody(PAIgG)and PAIgM were determined.Results Compared with the control group,platelet count was significant decreased,and PAIgG and PAIgM were significantly increased in ITP group when first visit(P<0.05).Serum NF-κB of ITP group was significantly increased(P<0.05),and positive rates of H.pylori and CagA were significantly higher(P<0.05).NF-κB,H.pylori and CagA were negatively correlated with platelet count,but positively correlated with PAIgG and PAIgM in ITP patients(P<0.05).Platelet count of mild ITP patients was the highest at first visit,followed by moderate ITP patients and severe ITP patients.The order of PAIgG,PAIgM and NF-κB is completely reversed.The corresponding order of H.pylori and CagA positive rate from low to high were mild ITP,moderate ITP and severe ITP(P<0.05).In ITP group,platelet count in patients without H.pylori was higher than that in patients with H.pylori-positive and CagA-negative,the platelet count in patients with H.pylori-positive and CagA-negative was higher than that in patients with H.pylori-positive and CagA-positive.The PAIgG,PAIgM and NF-κB in patients without H.pylor i were lower than those in patients with H.pylori,and the PAIgG,PAIgM and NF-κB in patients with H.pylori-positive and CagA-negative were lower than those in H.pylori-positive and CagA-positive patients(P<0.05).Conclusion H.pylori infection may be directly involved in the pathogenesis of ITP through the CagA protein.Or H.pylori infection prompts CagA to activate NF-κB,which influences immune response,and causes PAIgG,PAIgM elevation and thrombocytopenia decline.