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目的总结系统性红斑狼疮(systemic lupus erythematosus,SLE)合并冠心病的临床特点,探讨其危险因素及发病机制。方法 2005年1月—2011年11月共收治SLE患者2 190例,选择其中合并冠心病患者38例为观察组;选择同期收治排除所有结缔组织疾病的单纯冠心病患者60例为对照组。比较两组患者的所有传统动脉粥样硬化危险因素,检测血生化指标和血清肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)水平,并进行超声心动图检查,记录左室舒张末期内径(leftventricularend-diastolicdiameter,LVDd)。结果血LP(a)、CRP水平观察组分别为(287.64±31.74)mg/L、(21.36±4.29)mmol/L,对照组分别为(211.28±26.57)mg/L、(14.57±4.93)mmol/L,;LVDd观察组(55.01±6.73)mm,对照组(46.49±9.31)mm;血清TNF-α水平观察组(30.31±14.03)pg/ml,对照组(28.75±15.46)pg/ml。两组比较差异均有统计学意义(均P<0.05)。TC、TG、LDL-C、HDL-C两组比较差异均无统计学意义(均P>0.05)。结论传统致动脉粥样硬化的高危因素不足以解释SLE早期发生冠心病,SLE合并冠心病可能具有其独特的高危因素,且炎症反应参与了其发生发展过程。
Objective To summarize the clinical features of systemic lupus erythematosus (SLE) complicated with coronary heart disease (CHD) and to explore its risk factors and pathogenesis. Methods From January 2005 to November 2011, a total of 2 190 SLE patients were enrolled and 38 patients with coronary heart disease were selected as the observation group. Sixty patients with simple coronary heart disease who excluded all connective tissue diseases were selected as the control group. All of the traditional risk factors of atherosclerosis were compared between the two groups. Blood biochemical parameters and serum tumor necrosis factor-α (TNF-α) levels were measured. Echocardiography was performed to check the left ventricular end-diastolic diameter leftventricularend-diastolicdiameter, LVDd). Results The blood levels of LP (a) and CRP in the observation group were (21.26 ± 4.29) mmol / L and (21.26 ± 4.27) mg / L and / L, the LVDd observation group (55.01 ± 6.73) mm, the control group (46.49 ± 9.31) mm; the serum TNF-α level observation group (30.31 ± 14.03) pg / ml and the control group (28.75 ± 15.46) pg / ml. The differences between the two groups were statistically significant (P <0.05). TC, TG, LDL-C and HDL-C had no significant difference between the two groups (all P> 0.05). Conclusion The traditional risk factors of atherosclerosis are not enough to explain the early occurrence of coronary heart disease in patients with SLE. SLE with coronary heart disease may have its own unique risk factors, and the inflammatory response is involved in its occurrence and development.