目的 探讨吸烟对稳定期COPD患者炎症反应和肺功能的影响。方法 选取2013年8月—2016年9月我院门诊收治的稳定期COPD患者70例为研究对象,其中吸烟35例(X1组)、不吸烟35例(X2组),另选取同期入院的不吸烟健康志愿者35例纳入健康组,采用酶联免疫吸附试验(ELISA)测定血清白介素-6(IL-6)、白细胞介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平,以肺功能检测仪测定三组一秒用力呼气容积(FEV1)、一秒用力呼气容积/用力肺活量比值(FEV1/FVC)、FEV1占预计值百分比(FEV1％),并采用自拟症状评分表及简明健康调查简表(SF-36)评价呼吸困难程度及生活质量。结果 X1组IL-6、IL-8及TNF-α依次为(135.27±1.24)pg/mL、(189.45±1.14)pg/mL、(39.39±1.14)pg/mL,明显高于X2组、健康组(P均<0.05);X1组FEV1(0.75±0.14)L、FEV1/FVC(3.65±1.87)％、FEV1％(3.45±0.12)％低于X2组、健康组(P均<0.05);X1组症状积分(10.17±1.02)分较X2组、健康对照组高(P<0.05),而其SF-36评分(54.27±1.46)分明显低于X2及健康组(P<0.05);X2组上述指标与健康组比较亦有统计学意义(P均<0.05)。结论 吸烟可明显增加稳定期COPD患者IL-6、IL-8、TNF-α等炎症因子水平,同时降低肺功能,临床应采取措施进行有效干预,防止患者病情恶化。

目的 探讨长期吸烟史对高危脑卒中患者口服阿司匹林二级预防效果的影响。方法 将2012年8月—2014年8月医院口服阿司匹林二级预防的高危脑卒中患者115例作为研究对象,根据有无吸烟史分为无吸烟史组(34例)和吸烟史组(81例),其中36例吸烟时间≥20 a(长期吸烟史组)、45例吸烟时间1～19 a(短期吸烟史组)。随访12个月,测定血小板颗粒膜蛋白(GMP-140)、D-二聚体(D-D)、纤维蛋白原(FIB)、组织型纤溶酶原激活物(t-PA)、血小板膜糖蛋白CD61、CD62p,记录1年阿司匹林抵抗和临床终点事件发生率。结果 长期吸烟史组治疗前后GMP-140、D-D、FIB、CD61、CD62p高于短期吸烟史组和无吸烟史组,t-PA低于短期吸烟史组和无吸烟史组,且短期吸烟史组和无吸烟史组组间比较,差异有统计学意义(P＜0.05);长期吸烟组阿司匹林抵抗发生率和临床终点事件发生率分别为33.33%、30.56%,高于无吸烟史组的8.82%、8.82%,差异有统计学意义(P＜0.05),其余组组间比较差异无统计学意义(P＞0.05)。结论 长期吸烟史会使脑卒中患者存在血栓前状态,增加阿司匹林抵抗和临床终点事件的发生几率。

Objective To explore effects of long-term smoking on secondary prevention for oral aspirin in high-risk stroke patients. Methods A total of 115 high-risk stroke patients who orally took aspirin for secondary prevention in our hospital from August 2012 to August 2014 were selected as the study subjects. According to smoking or not, they were divided into non smoking history group (34 cases) and smoking history group (81 cases). Among them, 36 cases whose smoking time was ≥ 20 years were included in the long-term smoking history group, and 45 cases whose smoking time was 1 to 19 years were included in the short-term smoking history group. The patients were followed up for 12 months. The platelet granule membrane protein (GMP-140), D-dimer (D-D), fibrinogen (FIB), tissue plasminogen activator (t-PA), platelet membrane glycoprotein CD61 and CD62p were determined. The incidence rates of 1-year aspirin resistance and clinical outcome events in the three groups were recorded. Results Before and after treatment, GMP-140, D-D, FIB, CD61 and CD62p in long-term smoking history group were higher than those in short-term smoking history group and non smoking history group while T-PA was lower, and there were significant differences between short-term smoking history group and non smoking history group (P<0.05). The incidence rates of aspirin resistance and clinical outcome events in long-term smoking history group (33.33%, 30.56%) were higher than those in non smoking history group (8.82%, 8.82%)(P<0.05), but there was no significant difference among other groups (P>0.05). Conclusion Long-term smoking history will cause prethrombotic state in stroke patients and increase the incidence rates of aspirin resistance and clinical outcome events.