[1]陈刘通,廖晨,涂洪波,等.吸烟及全身炎症反应与慢性阻塞性肺疾病患者中发生肺动脉高压的相关性研究[J].第三军医大学学报,2016,38(11):1293-1296.
 Chen Liutong,Liao Chen,Tu Hongbo,et al.Association of cigarette smoking and systemic inflammation with pulmonary hypertension in patients with chronic obstructive pulmonary disease[J].J Third Mil Med Univ,2016,38(11):1293-1296.
点击复制

吸烟及全身炎症反应与慢性阻塞性肺疾病患者中发生肺动脉高压的相关性研究(/HTML )
分享到:

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
38卷
期数:
2016年第11期
页码:
1293-1296
栏目:
临床医学
出版日期:
2016-06-15

文章信息/Info

Title:
Association of cigarette smoking and systemic inflammation with pulmonary hypertension in patients with chronic obstructive pulmonary disease
作者:
陈刘通廖晨涂洪波冯双双白莉
第三军医大学新桥医院全军呼吸内科研究所,全军呼吸病研究重点实验室
Author(s):
Chen Liutong Liao Chen Tu Hongbo Feng Shuangshuang Bai Li

Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China

关键词:
慢性阻塞性肺疾病肺动脉高压吸烟炎症反应
Keywords:
chronic obstructive pulmonary disease pulmonary hypertension cigarette smoking systemic inflammation
分类号:
R163; R544; R563.9
文献标志码:
A
摘要:

目的      研究吸烟、全身炎症反应与慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者中发生肺动脉高压(pulmonary hypertension,PH)之间的关系。      方法      连续收集我研究所2013年4月至2015年3月收治的111例COPD合并PH的住院患者作为病例组,匹配年龄、性别后以同期111例COPD未合并PH的住院患者作为对照组,记录患者年龄、性别、吸烟史等一般资料,采集患者入院24 h内血沉 (erythrocyte sedimentation rate, ESR)、白细胞(white blood cell, WBC)、中性粒细胞/淋巴细胞比例(neutral granular cell/lymphocyte ratio, NLR)、血清C-反应蛋白(C-reactive protein, CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、纤维蛋白原、降钙素原(procalcitonin, PCT)、动脉血气、胸部CT及心脏彩超等结果。      结果      COPD合并PH组的吸烟指数、CRP、IL-6及TNF-α均明显高于COPD未合并PH组(P<0.01),且与肺动脉收缩压呈正相关(r=0.271、0.181、0.270、0.208, P<0.05),多因素Logistic回归分析结果显示吸烟、CRP、IL-6及TNF-α是PH形成的独立危险因素(OR=6.185、6.740、3.434、2.700,P<0.05)。       结论      吸烟及血清中CRP、IL-6及TNF-α升高与肺动脉压力升高呈正相关,提示吸烟、机体炎症反应与COPD发生PH密切相关。

Abstract:

Objective      To investigate the relationship of smoking and systemic inflammatory response with pulmonary hypertension (PH) in the patients with chronic obstructive pulmonary disease (COPD).       Methods      A total of 111 COPD patients with PH admitted in our department from April 2013 to March 2015 were consecutively recruited in this study, and another 110 age- and sex-matched COPD patients without PH served as control group. The clinical data of these patients including age, sex, smoking history, erythrocyte sedimentation rate (ESR), white blood cell count (WBC), neutral granular cell/lymphocyte ratio (NLR), serum C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), fibrinogen, procalcitonin (PCT), arterial blood gas, chest CT and Doppler echocardiography results were recorded and compared between the 2 groups.       Results      Smoking index and serum levels of CRP, IL-6 and TNF-α were significantly higher in the COPD patients complicated with PH than those without PH, and were positively correlated with pulmonary arterial systolic pressure (r=0.271, 0.181,0.270,0.208, P<0.05). Multiple logistic regression analysis showed that smoking, CRP, IL-6 and TNF-α were independent risk factors for pulmonary hypertension (OR= 6.185, 6.740, 3.434, 2.700, P<0.05).       Conclusion      Elevated smoking index and higher serum levels of CRP, IL-6 and TNF-α are positively correlated with increase of PH in COPD patients. Our results suggest tobacco smoking and systemic inflammation are closely associated with the development of PH in COPD patients.

参考文献/References:

[1]Fabbri L, Pauwels R A, Hurd S S, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary updated 2003[J]. COPD, 2004, 1(1): 105-141. DOI: 10.1081/COPD-120030163
[2]蔡柏蔷. 慢性阻塞性肺疾病合并肺动脉高压诊治的新认识[J].中国实用内科杂志, 2010, 30(12): 1068-1071.
[3]中华医学会呼吸病学分会慢性阻塞性肺疾病学组. 慢性阻塞性肺疾病诊治指南(2013年修订版)[J].中华结核和呼吸杂志, 2013, 36(4): 255-264. DOI: 10.3760/cma.j.issn.1001-0939.2013.04.007
[4]张珍祥. 吸烟与慢性阻塞性肺疾病[J].中华结核和呼吸杂志, 2009, 32(10): 790-792. DOI: 10.3760/cma.j.issn.1001-0939.2009.10.030
[5]肖丹, 王辰. 防治慢性阻塞性肺疾病最重要的措施: 戒烟和防止被动吸烟[J].中华内科杂志, 2010, 49(5): 374-375.DOI: 10.3760/cma.j.issn.0578-1426.2010.05.003
[6]Barbera J A. Mechanisms of development of chronic obstructive pulmonary disease-associated pulmonary hypertension[J]. Pulm Circ, 2013, 3(1): 160-164. DOI: 10.4103/2045-8932.109949
[7]Galie N, Hoeper M M, Humbert M, et al. Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT) [J]. Eur Heart J. 2009, 30(20): 2493-2537. DOI: 10.1093/eurheartj/ehp297
[8]Zhang J, Lin X F, Bai C X. Comparison of clinical features between non-smokers with COPD and smokers with COPD: a retrospective observational study[J]. Int J Chron Obstruct Pulmon Dis, 2014, 9: 57-63. DOI: 10.2147/COPD.S52416
[9]Peinado V I, Pizarro S, Barbera J A. Pulmonary vascular involvement in COPD[J]. Chest, 2008, 134(4): 808-814. DOI: 10.1378/chest.08-0820
[10]Ferrer E, Peinado V I, Diez M, et al. Effects of cigarette smoke on endothelial function of pulmonary arteries in the guinea pig [J]. Respir Res, 2009, 10: 76. DOI: 10.1186/1465-9921-10-76
[11]Fabbri L M, Rabe K F. From COPD to chronic systemic inflammatory syndrome?[J]. Lancet, 2007, 370(9589): 797-799. DOI: 10.1016/S0140-6736(07)61383-X
[12]Wouters E F, Groenewegen K H, Dentener M A, et al. Systemic inflammation in chronic obstructive pulmonary disease: the role of exacerbations [J]. Proc Am Thorac Soc, 2007, 4(8): 626-634. DOI: 10.1513/pats.200706-071TH
[13]Joppa P, Petrasova D, Stancak B, et al. Systemic inflammation in patients with COPD and pulmonary hypertension[J]. Chest, 2006, 130(2): 326-333. DOI: 10.1378/chest.130.2.326
[14]Savale L, Tu L, Rideau D, et al. Impact of interleukin-6 on hypoxia-induced pulmonary hypertension and lung inflammation in mice[J]. Respir Res, 2009, 10: 6. DOI: 10.1186/1465-9921-10-6
[15]Crotty-Alexander L E, Shin S, Hwang J H. Inflammatory Diseases of the Lung Induced by Conventional Cigarette Smoke: A Review[J]. Chest, 2015, 148(5): 1307-1322. DOI: 10.1378/chest.15-0409
[16]Lee H, Park J R, Kim E J, et al. Cigarette smoke-mediated oxidative stress induces apoptosis via the MAPKs/STAT1 pathway in mouse lung fibroblasts[J]. Toxicol Lett, 2016, 240(1): 140-148. DOI: 10.1016/j.toxlet.2015.10.030
[17]涂洪波, 陈刘通, 孙丽, 等. 二甲双胍对尼古丁诱导肺动脉平滑肌细胞增殖的影响及机制研究[J].第三军医大学学报, 2015, 37(7): 623-628. DOI: 10.16016/j.1000-5404.201410118

相似文献/References:

[1]李永华,张志辉,冉擘力,等.经导管封堵对先天性心脏病伴肺动脉高压患者血浆脑钠素的影响及其药物干预研究[J].第三军医大学学报,2008,30(04):345.
 I Yong-hua,ZHANG Zhi-hui,RAN Bo-li,et al.Effects of Enalapril or Metoprolol on plasm brain natriuretice peptide in congenital heart disease combined with pulmonary artery hypertension after transcatheter closure[J].J Third Mil Med Univ,2008,30(11):345.
[2]唐旭东,肖颖彬,周建国,等.Survivin在先天性心脏病肺动脉高压发生机制中的作用[J].第三军医大学学报,2008,30(01):27.
 TANG Xu-dong,XIAO Ying-bin,ZHOU Jian-guo,et al.Role of survivin in pulmonary hypertension of congenital heart disease[J].J Third Mil Med Univ,2008,30(11):27.
[3]杨静,宋晓英,张羽,等.狼疮相关性肺动脉高压的临床研究[J].第三军医大学学报,2007,29(03):273.
[4]李志平,范士志,蒋耀光,等.风心病合并肺动脉高压体外循环后前列腺素E1抵抗现象的研究[J].第三军医大学学报,2007,29(09):792.
 LI Zhi-ping,FAN Shi-zhi,JIANG Yao-guang,et al.Resistance to prostaglandin E1 in postoperative early stage of valvular replacement in rheumatic heart disease patients[J].J Third Mil Med Univ,2007,29(11):792.
[5]刘铭,杨康,曾会昌,等.46例成人继发孔房间隔缺损合并肺动脉高压的外科治疗经验[J].第三军医大学学报,2005,27(24):2464.
[6]徐效龙,祁国荣,王黎明,等.12例覆膜支架治疗高原巨大动脉导管未闭伴重度肺动脉高压的近期疗效分析[J].第三军医大学学报,2013,35(06):579.
[7]罗锋,向小勇,赵兴吉.大鼠左全肺切除致右心室重塑的研究[J].第三军医大学学报,2010,32(15):1642.
 Luo Feng,Xiang Xiaoyong,Zhao Xingji.Right ventricular remodeling induced by left total pneumonectomy in rats[J].J Third Mil Med Univ,2010,32(11):1642.
[8]汪健春,钟前进,肖颖彬.bcl-2/bax表达在左向右分流型肺动脉高压肺血管重构中的作用[J].第三军医大学学报,2009,31(24):2425.
 WANG Jian-chun,ZHONG Qian-jin,XIAO Ying-bin.Role of bcl-2 and bax expressions in pulmonary vascular remodeling of PAH rats secondary to left-right shunt CHD[J].J Third Mil Med Univ,2009,31(11):2425.
[9]徐贤华,彭华生,胡猛,等.电压门控性钾通道亚型Kv2.1在低氧性肺动脉高压形成和恢复中的作用[J].第三军医大学学报,2009,31(21):2112.
 XU Xian-hua,PENG Hua-sheng,HU Meng,et al.Role of voltage-gated K+ channel Kv2.1 in development and regression of hypoxic pulmonary artery hypertension in rats[J].J Third Mil Med Univ,2009,31(11):2112.
[10]王关嵩,钱频,李琦,等.低氧肺动脉高压时血红素氧合酶基因表达状况的研究[J].第三军医大学学报,2009,31(15):1428.
 WANG Guan-song,QIAN Pin,LI Qi,et al.Expression of heme oxygenase in pulmonary arteries of rats with hypoxic pulmonary hypertension[J].J Third Mil Med Univ,2009,31(11):1428.

更新日期/Last Update: 2016-05-29