[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].

AIM: 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). SUBJECTS AND 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. CONCLUSION: 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.

[Obstructive sleep apnea syndrome in patients with chronic obstructive pulmonary disorder].

Sleep obstructive apnea syndrome (SOAS) is a life-threatening respiratory disorder. Its combination with COPD further deteriorates respiratory distress and accelerates the development of pulmonary hypertension (crossover syndrome). Systemic inflammation with concomitant oxidative stress in patients with SOAS and COPD suggests their influence on the development of circulatory disorders. Night-time cyclic hypoxia in patients with SOAS triggers systemic inflammation, oxidative stress, and atherogenesis which accounts for the frequent complications more severe in combination of SOAS and COPD than in either of these diseases. Intermittent hypoxia in patients with SOAS is associated with hypoventilation resulting from COPD, deteriorates clinical conditions of the patients, and requires the choice of specific methods of respiratory support.

[Comparative analysis of various methods of determination of fibrinogen in the plasma]. / Sravnitel'nyi analiz razlichnykh metodov opredeleniia fibrinogena v plazme krovi.

Fibrinogen was measured in the plasma of normal subjects and patients with various hemostasis disorders by gravimetric methods with thromboplastin coagulation and coagulation with Echis multisquamatus snake venom. Coagulation was assessed using optic Coag-Mate HM (Netherlands) and roll Amelung KC4A (Germany) coagulometers during coagulation with thrombin after Klauss and with the above venom. The results were compared with those of fibrinogen measurements by radial immunodiffusion using Behring antifibrinogen serum. The data of all methods coincided if the initial levels of fibrinogen were normal, whereas in manifest hypo- or hyperfibrinogenemia Klauss' method was the most accurate and informative.

[Prevalence, diagnosis and clinical significance of thrombophilia caused by Va factor resistance to activated C protein]. / Rasprostranennost', diagnostika i klinicheskoe znachenie trombofilii, obuslovlennoi rezistentnost'iu faktora Va k aktivirovannomu proteinu C.

Examining 26 patients with early recurrent venous thrombophilias and ischemic attacks revealed that 6 cases had Va factor resistance to activated C protein. The latter suggests that thrombophilia associated with hereditary C- protein resistance is recorded in the Russian population, among the residents of West Siberia in particular.

[Significance of heparin elimination from plasma in the assessment of coagulogram and antithrombin III activity]. / Znachenie éliminatsii iz plazmy geparina dlia otsenki koagulogrammy i aktivnosti antitrombina III.

An original adsorbent for non-fractionated and low-molecular weight heparin (fraxiparin,Sanofi) has been developed and tried in experiments and in a clinical setting. Tests carried out in 58 patients with disseminated intravascular coagulation and thromboses treated with heparin demonstrated the possibility of obtaining objective data on the status of the blood clotting system. Heparin adsorption is particularly important in measurements of heparin III activity, for even low concentrations of heparin mask the defect of this anticoagulant.