title: [Role of endothelial dysfunction, the interface between hemostatic and system inflammatory responses in the pathogenesis of an infectious inflammation-dependent exacerbation of chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  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).
  
  
  METHODS
  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).
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.forename: I Ia
authors.initials: IIa
authors.lastname: Tseĭmakh
authors.forename: A P
authors.initials: AP
authors.lastname: Momot
authors.forename: G I
authors.initials: GI
authors.lastname: Kostiuchenko
authors.forename: A N
authors.initials: AN
authors.lastname: Mamaev
authors.forename: Iu A
authors.initials: IuA
authors.lastname: Filonova
authors.forename: T A
authors.initials: TA
authors.lastname: Kornilova
authors.forename: A G
authors.initials: AG
authors.lastname: Chuchalin
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001987:Bronchiectasis / Q000097:blood / Q000503:physiopathology; D019332:Endothelin-1 / Q000097:blood; D004730:Endothelium, Vascular / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006487:Hemostasis / Q000502:physiology*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000382:microbiology / Q000503:physiopathology; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000209:etiology / Q000473:pathology; D012907:Smoking / Q000097:blood / Q000473:pathology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D019332:Endothelin-1; D006710:Homocysteine