Tseĭmakh I Ia, Momot A P, Kostiuchenko G I, Mamaev A N, Filonova Iu A, Kornilova T A, Chuchalin A G
Ter Arkh. 2013;85(3):17-22.
To analyze the systemic manifestations of vascular endothelial damage, the activation of hemostatic and inflammatory responses in patients with an infectious inflammation-dependent exacerbation of chronic obstructive pulmonary disease (COPD).
The paper provides the data of examinations of 111 patients with the clinical signs of an infectious inflammation-dependent exacerbation of COPD who had 2 or 3 positive criteria elaborated by N. Anthonisen et al. (1987). The patients were divided into 2 phenotypically different subgroups: 1) 92 (82.9%) COPD patients without clinical manifestations of bronchoectasis; 2) 19 (17.1%) patients with COPD concurrent with documented bronchiectasis. The patient subgroups were matched for smoking status and the characteristics of COPD and respiratory failure. The investigators assessed the time course of changes in the serum level of endothelin-1 (ET-1), the aggregation function of platelets, and the plasma concentrations of D-dimers and homocysteine in patients with COPD compared to healthy, never smokers (n = 35) and smokers (n = 27).
An increase in the levels of the endothelial dysfunction markers ET-1 and homocysteine was found in patients with COPD, which was comparable with the changes in these indicators in the group of smokers. In both subgroups, the rise in plasma D-dimer levels was more pronounced in the patients with a COPD exacerbation than in the smokers. Its therapy with systemic and inhaled glucocorticosteroids reduced C-reactive protein and ET-1 levels in both patient subgroups and in D-dimers in subgroup 1. Elevated D-dimer levels remained when achieving remission, which points to the risk of thrombogenic and thromboembolic events in the patients with an infectious inflammation-dependent exacerbation of COPD and concomitant circulatory system diseases.
The patients with an infectious inflammation-dependent exacerbation of COPD are observed to have elevated peripheral blood markers of endothelial dysfunction and thrombinemia. These changes are pathogenetically caused by smoking or neutrophilic inflammation and associated with a higher risk of thrombogenic events.
分析慢性阻塞性肺疾病（COPD）感染性炎症依赖性加重患者血管内皮损伤的全身表现、止血和炎症反应的激活情况。
本文提供了111例具有COPD感染性炎症依赖性加重临床体征患者的检查数据，这些患者符合N. Anthonisen等人（1987年）制定的2项或3项阳性标准。患者被分为2个表型不同的亚组：1）92例（82.9%）无支气管扩张临床表现的COPD患者；2）19例（17.1%）合并有记录的支气管扩张的COPD患者。患者亚组在吸烟状况、COPD和呼吸衰竭特征方面相匹配。与健康的从不吸烟者（n = 35）和吸烟者（n = 27）相比，研究人员评估了COPD患者血清内皮素-1（ET-1）水平、血小板聚集功能以及D-二聚体和同型半胱氨酸血浆浓度的变化时间进程。
发现COPD患者内皮功能障碍标志物ET-1和同型半胱氨酸水平升高，这与吸烟组这些指标的变化相当。在两个亚组中，COPD加重患者血浆D-二聚体水平的升高比吸烟者更明显。用全身和吸入糖皮质激素治疗可降低两个患者亚组的C反应蛋白和ET-1水平，并降低亚组1中的D-二聚体水平。缓解时D-二聚体水平仍升高，这表明COPD感染性炎症依赖性加重且伴有循环系统疾病的患者存在血栓形成和血栓栓塞事件的风险。
观察到COPD感染性炎症依赖性加重患者外周血内皮功能障碍和凝血酶血症标志物升高。这些变化在发病机制上是由吸烟或中性粒细胞炎症引起的，并与血栓形成事件的较高风险相关。
