Takahashi Toru, Yujiri Toshiaki, Shinohara Kenji, Inoue Yusuke, Sato Yutaka, Fujii Yasuhiko, Okubo Masashi, Zaitsu Yuzuru, Ariyoshi Koichi, Nakamura Yukinori, Nawata Ryouhei, Oka Yoshitomo, Shirai Mutsunori, Tanizawa Yukio
Department of Bio-Signal Analysis, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Br J Haematol. 2004 Jan;124(1):91-6. doi: 10.1046/j.1365-2141.2003.04735.x.
The eradication of Helicobacter pylori often leads to platelet recovery in patients with chronic idiopathic thrombocytopenic purpura (cITP). Although this clinical observation suggests the involvement of H. pylori, little is known about the pathogenesis of cITP. We initially examined the effect of H. pylori eradication on platelet counts in 20 adult Japanese cITP patients. Then, using platelet eluates as the probe in immunoblot analyses, we examined the role of molecular mimicry in the pathogenesis of cITP. Helicobacter pylori infection was detected in 75% (15 of 20) of cITP patients. Eradication was achieved in 13 (87%) of the H. pylori-positive patients, seven (54%) of which showed increased platelet counts within the 4 months following treatment. Completely responsive patients also showed significant declines in platelet-associated immunoglobulin G (PAIgG) levels. Platelet eluates from 12 (nine H. pylori-positive and three H. pylori-negative) patients recognized H. pylori cytotoxin-associated gene A (CagA) protein, and in three completely responsive patients, levels of anti-CagA antibody in platelet eluates declined after eradication therapy. Cross-reactivity between PAIgG and H. pylori CagA protein suggests that molecular mimicry by CagA plays a key role in the pathogenesis of a subset of cITP patients.
根除幽门螺杆菌通常会使慢性特发性血小板减少性紫癜（cITP）患者的血小板恢复正常。尽管这一临床观察结果提示幽门螺杆菌参与其中，但关于cITP的发病机制却知之甚少。我们首先检测了20例成年日本cITP患者根除幽门螺杆菌对血小板计数的影响。然后，以血小板洗脱液作为免疫印迹分析的探针，研究分子模拟在cITP发病机制中的作用。在75%（20例中的15例）的cITP患者中检测到幽门螺杆菌感染。13例（87%）幽门螺杆菌阳性患者实现了根除，其中7例（54%）在治疗后的4个月内血小板计数升高。完全缓解的患者血小板相关免疫球蛋白G（PAIgG）水平也显著下降。12例患者（9例幽门螺杆菌阳性和3例幽门螺杆菌阴性）的血小板洗脱液可识别幽门螺杆菌细胞毒素相关基因A（CagA）蛋白，在3例完全缓解的患者中，根除治疗后血小板洗脱液中的抗CagA抗体水平下降。PAIgG与幽门螺杆菌CagA蛋白之间的交叉反应表明，CagA介导的分子模拟在一部分cITP患者的发病机制中起关键作用。
