Pieniazek P, Karczewska E, Duda A, Tracz W, Pasowicz M, Konturek S J
Department of Physiology, Jagiellonian University, Cracow, Poland.
J Physiol Pharmacol. 1999 Dec;50(5):743-51.
The role of Helicobacter pylori (HP) as the main etiological factor in gastritis and peptic ulcer disease is undisputable. Gastric mucosal damage caused by HP involves various bacterial and host-dependent toxic substances that have been recently associated with an increased risk of coronary artery disease (CAD), possibly through the activation acute phase response and of procoagulant hemostatic factors. Recent studies showed a close and strong correlation between plasma increments of some cytokines such as IL-6 or TNFalpha and cardiovascular diseases. HP infection induces platelet activation and aggregation that could be the pathogenic explanation of the association between HP infection and CAD. The aim of this study was to determine the seroprevalence of HP infection and antibodies to CagA, an antigen that is expressed by the most virulent HP strains inducing an enhanced gastric inflammatory response, in patients undergoing routine coronary artery examination. We studied 76 patients with CAD and 81 healthy controls patients without significant change in coronary circulation. Angiograms were read by two independent experienced cardiologists blinded to the results of HP status. The presence of serum IgG antibodies to HP and to CagA and plasma interleukin-8 (IL-8) levels was measured by ELISA. In addition plasma C-reactive protein fibrinogen, total cholesterol and lipids levels were measured in all studied patients. Seropositivity to HP was found in 81.5 % of cases and in 51% of controls and the difference in prevalence was statistically significant, the odds ratio being 4.3 for Hp patients. Antibody to CagA protein was detected in 47.3% of CAD but only in 28% of healthy controls (OR = 2.3 vs OR = 10). C-reactive protein, plasma fibrinogen and total cholesterol were, respectively higher in patients with CAD than in controls. Present data show that there is significant link between CAD and HP infection. The HP infection significantly increases the risk of CAD, especially when both the anti-HP IgG and anti-CagA IgG are considered. Higher prevalence of cytotoxic HP strains might enhance the atherosclerotic process by inducing a persistent, low grade inflammatory response in arterial wall with enhanced synthesis of acute phase reactants.
幽门螺杆菌（HP）作为胃炎和消化性溃疡病的主要病因，其作用是无可争议的。HP引起的胃黏膜损伤涉及多种细菌和宿主依赖性毒素，这些毒素最近与冠状动脉疾病（CAD）风险增加有关，可能是通过激活急性期反应和促凝血止血因子。最近的研究表明，某些细胞因子如IL-6或TNFα的血浆水平升高与心血管疾病之间存在密切且强烈的相关性。HP感染会诱导血小板活化和聚集，这可能是HP感染与CAD之间关联的致病解释。本研究的目的是确定接受常规冠状动脉检查的患者中HP感染的血清流行率以及针对CagA的抗体，CagA是由最具毒性的HP菌株表达的一种抗原，可诱导增强的胃炎症反应。我们研究了76例CAD患者和81例冠状动脉循环无明显变化的健康对照患者。血管造影由两位独立的经验丰富的心脏病专家解读，他们对HP状态结果不知情。通过ELISA测量血清中抗HP和抗CagA IgG抗体的存在以及血浆白细胞介素-8（IL-8）水平。此外，还测量了所有研究患者的血浆C反应蛋白、纤维蛋白原、总胆固醇和血脂水平。在81.5%的病例和51%的对照中发现HP血清阳性，患病率差异具有统计学意义，HP患者的优势比为4.3。在47.3%的CAD患者中检测到CagA蛋白抗体，但在健康对照中仅为28%（OR = 2.3对OR = 10）。CAD患者的C反应蛋白、血浆纤维蛋白原和总胆固醇分别高于对照组。目前的数据表明CAD与HP感染之间存在显著联系。HP感染显著增加了CAD的风险，尤其是在同时考虑抗HP IgG和抗CagA IgG时。细胞毒性HP菌株的较高流行率可能通过在动脉壁中诱导持续的低度炎症反应并增强急性期反应物的合成来加剧动脉粥样硬化过程。
