Hoffmeister A, Rothenbacher D, Bode G, Persson K, März W, Nauck M A, Brenner H, Hombach V, Koenig W
Department of Internal Medicine II-Cardiology, University of Ulm, Ulm, Germany.
Arterioscler Thromb Vasc Biol. 2001 Mar;21(3):427-32. doi: 10.1161/01.atv.21.3.427.
Infectious agents may be involved in atherothrombogenesis. The potential pathogenic pathway, however, remains unclear. We investigated the association between various infectious agents and lipoproteins known to have an atherogenic effect. We recruited 470 healthy blood donors and 238 patients with angiographically proven coronary heart disease (CHD), aged 40 to 68 years. Seropositivity to Chlamydia pneumoniae (CP), chlamydial lipopolysaccharide, and cytomegalovirus (CMV) was determined; infection with Helicobacter pylori (HP) was assessed by using the [(13)C]urea breath test. In all subjects, total cholesterol, high density lipoprotein (HDL) cholesterol, lipoprotein(a), and various apolipoproteins (apos) were determined. In unadjusted analysis, mean HDL cholesterol concentration was significantly decreased in HP-positive healthy subjects (1.36 vs 1.44 mmol/L, P=0.006) compared with HP-negative subjects. The HDL cholesterol to total cholesterol ratio was significantly decreased in HP-positive (0.259 vs 0.276, P=0.01) and CP-seropositive (0.266 vs 0.280, P=0.04) healthy subjects compared with (sero)negatives. Mean apoAI levels were significantly lower in HP-positive healthy subjects (1.46 vs 1.51 g/L, P=0.03) and in CMV-positive healthy subjects (1.47 vs 1.52 g/L, P=0.01) compared with (sero)negative subjects. After multivariable adjustment by means of linear regression analysis, only the association between HP infection and decreased HDL cholesterol (P=0.002), decreased HDL cholesterol to total cholesterol ratio (P:=0.005), decreased apoAI (P=0.02), and increased apoB (P=0.02) persisted and remained significant. There was no independent association between other lipoproteins and serological markers of CP or CMV infection. Current infection with HP, but not seropositivity to CP or CMV, was associated with an atherogenic, modified lipid profile. These lipid alterations could explain, at least in part, the reported weak association between chronic HP infection and atherosclerotic diseases.
感染因子可能参与动脉粥样硬化血栓形成过程。然而，其潜在的致病途径仍不清楚。我们研究了各种感染因子与已知具有致动脉粥样硬化作用的脂蛋白之间的关联。我们招募了470名健康献血者和238名经血管造影证实患有冠心病（CHD）的患者，年龄在40至68岁之间。测定了肺炎衣原体（CP）、衣原体脂多糖和巨细胞病毒（CMV）的血清阳性率；采用[(13)C]尿素呼气试验评估幽门螺杆菌（HP）感染情况。在所有受试者中，测定了总胆固醇、高密度脂蛋白（HDL）胆固醇、脂蛋白(a)和各种载脂蛋白（apo）。在未经调整的分析中，与HP阴性的健康受试者相比，HP阳性的健康受试者的平均HDL胆固醇浓度显著降低（1.36对1.44 mmol/L，P = 0.006）。与（血清）阴性的健康受试者相比，HP阳性（0.259对0.276，P = 0.01）和CP血清阳性（0.266对0.280，P = 0.04）的健康受试者的HDL胆固醇与总胆固醇之比显著降低。与（血清）阴性的受试者相比，HP阳性的健康受试者（1.46对1.51 g/L，P = 0.03）和CMV阳性的健康受试者（1.47对1.52 g/L，P = 0.01）的平均apoAI水平显著较低。通过线性回归分析进行多变量调整后，只有HP感染与HDL胆固醇降低（P = 0.002）、HDL胆固醇与总胆固醇之比降低（P = 0.005）、apoAI降低（P = 0.02）和apoB升高（P = 0.02）之间的关联持续存在且仍具有统计学意义。CP或CMV感染的血清学标志物与其他脂蛋白之间没有独立关联。目前的HP感染，而非CP或CMV的血清阳性，与致动脉粥样硬化的、改变的血脂谱相关。这些血脂改变至少可以部分解释慢性HP感染与动脉粥样硬化疾病之间报道的微弱关联。
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