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特发性血小板减少性紫癜(ITP)由多种原因引起,近年来有学者发现幽门螺杆菌(Hp)感染和ITP有一定关系。研究表明,Hp感染导致ITP的可能机制:一是分子模拟学说,即Hp抗体与血小板糖抗原有交叉反应,而导致血小板破坏较少。Hp提高噬菌血小板作用或诱导血小板聚集加速血小板破坏。二是细胞因子改变,Hp感染诱发了Th1为主的免疫反应,而产生的相应细胞因子可能促使ITP发展。但也有学者认为Hp和ITP没有关系,引起这些研究差异的原因是宿主遗传背景不同、Hp株差异性导致抗Hp治疗疗效不同以及研究的地理位置的差异。
Idiopathic thrombocytopenic purpura (ITP) caused by a variety of reasons, in recent years, some scholars have found that the relationship between Helicobacter pylori (Hp) infection and ITP. Studies have shown that Hp infection leads to possible mechanisms of ITP: First, the molecular simulation theory that Hp antibodies and platelet glycoprotein cross-reaction, resulting in less platelet destruction. Hp increases phagocytosis or induces platelet aggregation to accelerate platelet destruction. Second, changes in cytokines, Hp infection induced Th1-based immune response, and the resulting cytokine may promote the development of ITP. However, some scholars think that there is no relationship between Hp and ITP. The reason for these differences is that the host genetic background is different, Hp strain differences lead to different anti-Hp therapies and geographical differences.