Department of Neurology, Clinical Hospital Dubrava, Avenija Gojka Šuška 6, 10000, Zagreb, Croatia.
J Neurol. 2011 May;258(5):753-61. doi: 10.1007/s00415-010-5824-9. Epub 2010 Nov 18.
Citotoxin-associated gene-A (CagA)-positive Helicobacter pylori strains have been associated with occurrence and destabilization of coronary atherosclerotic plaques. However, data on the relationship between CagA-positive H. pylori infection and carotid artery instability are lacking. Thus, the role of CagA antigen in patients with symptomatic and asymptomatic carotid atherosclerotic plaques was investigated. A total of 64 patients with advanced carotid artery stenosis, including 33 patients with symptomatic and 31 patients with asymptomatic internal carotid artery stenosis, verified by duplex ultrasound, all undergoing carotid endarterectomy, were studied. The control group consisted of 65 subjects without a history or presence of vascular diseases. Serology for H. pylori and CagA antigen was assessed in all participants. Specimens of atherosclerotic plaques obtained from all patients during carotid endarterectomy were analyzed immunohistochemically using anti-CagA monoclonal antibodies. The ultrasonographic plaque characteristics were also estimated. CagA antibody titers were significantly higher in symptomatic patients (8.8; range, 5.8-32.7) compared to asymptomatic patients (4.7; range, 2.1-8.8; P = 0.005) and the control group (5.0; range 2.2-7.9; P < 0.001). There was significant difference in echolucency (≥ 25% soft material) between the symptomatic and asymptomatic groups (P = 0.034) by ultrasonographic evaluation. Positive immunoreactivity between monoclonal CagA antibodies and antigens within atherosclerotic specimens was significantly higher among symptomatic patients compared to asymptomatic patients (97.0 vs. 74.2%; P = 0.009). H. pylori may play a role in the pathogenesis of the atherosclerotic process due to autoimmune mechanisms and even contribute to destabilization of carotid atherosclerotic plaques.
细胞毒素相关基因 A(CagA)阳性幽门螺杆菌菌株与冠状动脉粥样硬化斑块的发生和不稳定有关。然而,关于 CagA 阳性 H. pylori 感染与颈动脉不稳定性之间的关系的数据尚缺乏。因此,研究了 CagA 抗原在有症状和无症状颈动脉粥样硬化斑块患者中的作用。共有 64 例颈动脉狭窄进展的患者,包括 33 例有症状和 31 例无症状颈内动脉狭窄患者,经双功超声证实,并均接受颈动脉内膜切除术。对照组由 65 例无血管疾病史或无血管疾病的患者组成。所有参与者均进行 H. pylori 和 CagA 抗原的血清学检查。在所有患者进行颈动脉内膜切除术时,从所有患者的粥样硬化斑块标本中提取标本,并用抗 CagA 单克隆抗体进行免疫组织化学分析。还评估了超声斑块特征。与无症状患者(4.7;范围,2.1-8.8;P=0.005)和对照组(5.0;范围,2.2-7.9;P<0.001)相比,有症状患者的 CagA 抗体滴度明显更高(8.8;范围,5.8-32.7)。超声评估显示,两组之间的回声不透明度(≥25%软物质)存在显著差异(P=0.034)。与无症状患者相比,在有症状患者中,单克隆 CagA 抗体和动脉粥样硬化标本内抗原之间的阳性免疫反应性显著更高(97.0 对 74.2%;P=0.009)。由于自身免疫机制,H. pylori 可能在动脉粥样硬化过程的发病机制中起作用,甚至导致颈动脉粥样硬化斑块的不稳定。