UDC

616.24-002:612.115

Authors

Bedilo Natalya Vitalyevna
Postgraduate Student, Northern State Medical University;
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)
Vorobyevа Nadezhda Aleksandrovna
Northern State Medical University;
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)
Ismaylova Nadezhda Vladimirovna
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)
Veshchagina Natalya Albertovna
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)
Nasonov Ilya Yakovlevich
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)
Malugin Yury Yuryevich
City Clinical Hospital No. 1 named after E.E. Volosevich (Arkhangelsk, Russia)

Abstract

We studied markers of fibrinоlysis (D-dimer, PAI-1) in 61 patients with community-acquired pneumonia
(CAP) on the day of admission and upon discharge from hospital. 17 patients had a severe pneumonia,
6 people died. Both markers had increased values on the day of admission and were reduced by the
discharge but were still outside the normal range. D-dimer and PAI-1 depended on the severity of CAP and
extent of the inflammatory process. The risk of severe pneumonia increased if the level of D-dimer at the
onset of the disease exceeded 2.0 μg/mL (relative risk = 21.8, 95 % confidence interval: 3.09-154.8) and
PAI-1 activity exceeded 30 IU/L (relative risk = 2.05, 95 % confidence interval: 0.88-4.74). Radiographic
results were best reflected by the level of D-dimer measured prior to discharge of the patients.

Keywords

community-acquired pneumonia, hemostasis, D-dimer, plasminogen activator inhibitor-1 (PAI-1)

References

1. Bulygina N.V., Bedilo N.V. Nekotorye voprosy epidemiologii vnebol’nichnykh pnevmoniy v Arkhangel’ske [Some Issues of Community-Acquired Pneumonia Epidemiology in Arkhangelsk]. Adaptatsiya cheloveka na Severe:mediko-biologicheskie aspekty: materialy Vseros. molodezhnoy nauch.-prakt. konf. [Human Adaptation in the North: Medical and Biological Aspects: Proc. All-Russian Youth Theor. and Pract. Conf.]. Arkhangelsk, 2012, pp. 41–43. 
2. Vorob’eva N.A. DVS-sindrom – chto novogo v staroy probleme? [DIC: What’s New in the Old Issue?]. Arkhangelsk, 2006, p. 176. 
3. Chuchalin A.G. Sinopal’nikov A.I., Kozlov R.S., Tyurin I.E., Rachina S.A. Vnebol’nichnaya pnevmoniya u vzroslykh: prakticheskie rekomendatsii po diagnostike, lecheniyu i profilaktike [Community-Acquired Pneumonia in Adults: Guidelines for Diagnosis, Treatment and Prevention]. Moscow, 2010. 82 p. 
4. Beutler B., Rietschel E.T. Innate Immune Sensing and Its Roots: The Story of Endotoxin. Nat. Rev. Immunol., 2003, no. 3, pp. 169–176. 
5. Biemond B.J., Levi M., Ten Cate H., et al. Plasminogen Activator and Plasminogen Activator Inhibitor I Release During Experimental Endotoxaemia in Chimpanzees: Effect of Interventions in the Cytokine and Coagulation Cascades. Clin. Sci. (Lond.), 1995, no. 88, pp. 587–594. 
6. Chapman H.A. Plasminogen Activators, Integrins, and the Coordinated Regulation of Cell Adhesion and Migration. Curr. Opin. Cell Biol., 1997, no. 9, pp. 714–724. 
7. Idell S. Endothelium and Disordered Fibrin Turnover in the Injured Lung: Newly Recognized Pathways. Crit. Care Med., 2002, no. 30, pp. 274–280. 
8. Idell S., Koenig K.B., Fair D.S., Martin T.R., McLarty J., Maunder R.J. Serial Abnormalities of Fibrin Turnover in Evolving Adult Respiratory Distress Syndrome. Am. J. Physiol., 1991, vol. 261 (4 Pt 1), pp. L240– L248. 
9. Glas G.J., van der Sluijs K.F., Schultz M.J., Hofstra J.-J.H., et al. Bronchoalveolar Hemostasis in Lung Injury and Acute Respiratory Distress Syndrome. J. Thromb. Haemost., 2013, no. 11, pp. 17–25. 
10. Jesmin S., Gando S., Matsuda N., et al. Temporal Changes in Pulmonary Expression of Key Procoagulant Molecules in Rabbits with Endotoxin-Induced Acute Lung Injury: Elevated Expression Levels of Protease-Activated Receptors. Thromb. Haemost., 2004, no. 92, pp. 966–979. 
11. Kjøller L., Kanse S.M., Kirkegaard T., et al. Plasminogen Activator Inhibitor-1 Represses Integrin- and Vitronectin-Mediated Cell Migration Independently of Its Function as an Inhibitor of Plasminogen Activation. Exp. Cell Res., 1997, no. 232, pp. 420–429. 
12. Maris N.A., De Vos A.F., Bresser P., et al. Activation of Coagulation and Inhibition of Fibrinolysis in the Lung After Inhalation of Lipopolysaccharide by Healthy Volunteers. Thromb. Haemost., 2005, no. 93, pp. 1036–1040. 
13. Marshall B.C., Sageser D.S., Rao N.V., Emi M., Hoidal J.R. Alveolar Epithelial Cell Plasminogen Activator. Characterization and Regulation. J. Biol. Chem., 1990, no. 265, pp. 8198–8204. 
14. Prabhakaran P., Ware L.B., White K.E., Cross M.T., et al. Elevated Levels of Plasminogen Activator Inhibitor-1 in Pulmonary Edema Fluid Are Associated with Mortality in Acute Lung Injury. Am. J. Physiol. Lung Cell. Mol. Physiol., 2003, no. 285, pp. L20–L28. 
15. Querol-Ribelles J.M., Tenias J.M., Grau E. et al. Plasma D-dimer Levels Correlate with Outcomes in Patients with Community-Acquired Pneumonia. Chest, 2004, vol. 126, no. 4, pp. 1087–1092. 
16. Sawdey M.S., Loskutoff D.J. Regulation of Murine Type I Plasminogen Activator Inhibitor Gene Expression in Vivo. Tissue Specificity and Induction by Lipopolysaccaride, Tumor Necrosis Factor-α, and Transforming Growth Factor-β. J. Clin. Invest., 1991, no. 88(4), pp. 1346–1353. 
17. Shilon Y., Shitrit A.B., Rudensky B., et al. A Rapid Quantitative D-dimer Assay at Admission Correlates with the Severity of Community Acquired Pneumonia. Blood Coagul. Fibrinolysis, 2003, no. 14(8), pp. 745–748. 
18. Sitrin R.G., Pan P.M., Srikanth S., Todd R.F. Fibrinogen Activates NF-kappa B Transcription Factors in Mononuclear Phagocytes. J. Immunol., 1998, no. 161, pp. 1462–1470. 
19. van Till J.W., Levi M., Bresser P., Schultz M.J., Gouma D.J., Boermeester M.A. Early Procoagulant Shift in the Bronchoalveolar Compartment of Patients with Secondary Peritonitis. J. Infect. Dis., 2006, no. 194 (9), pp. 1331–1339.