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2015 | 124 | 1 | 46-48
Tytuł artykułu

Potential anti-inflammatory activity of low molecular weight heparin in patients with exacerbations of COPD – short report

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Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Introduction. Anti-inflammatory, separate from anti-thrombotic activity of low molecular weight heparin, is still not well documented. Aim. We estimated the influence of enoxaparin on serum levels of tumor necrosis factor alpha, as the pro-inflammatory cytokine, and interleukin-12, as the heparin-binding, anti-inflammatory cytokine, in patients with exacerbations of chronic obstructive pulmonary disease. Material and methods. Seventy-three consecutive patients (48 males, 25 females) aged 56-75 years without thromboembolic history, were enrolled into the study. They were randomized to group who received enoxaparin in one daily dose 40 mg, or to group who did not receive it. Patients receiving oral anti-coagulants were excluded from the study. Using ELISA approach, we evaluated serum levels of tumor necrosis factor-alpha and interleukin-12 at the following periods: before the first dose of enoxaparin, after 7 days of treatment and 14 days of treatment. Serum level of the C-reactive protein was evaluated simultaneously. Results. In enoxaparin recipients statistically significant (p<0.01) decreasing of TNF-alpha serum levels (from 168.33 pg/ml in admission, to 85.67 pg/ml in the end of study) to compare enoxaparine non-recipients, was observed. Interleukin-12 serum levels were significantly higher in enoxaparine recipients both after 7 days (67.46 pg/ml) and 14 days (89.32 pg/ml) of the study (p<0.05). C-reactive proteins serum levels were significantly higher in enoxaparine non-recipients than recipients (p<0.05) in all study period. Conclusions. Enoxaparin in daily dose 40 mg, significantly depressed serum levels of TNF-alpha and promote serum levels of interleukin-12. Enoxaparin administration may be beneficial for the patients with COPD exacerbation during the first 14 days of treatment
Wydawca

Rocznik
Tom
124
Numer
1
Strony
46-48
Opis fizyczny
Daty
wydano
2014-03-01
online
2014-04-23
Twórcy
  • Department of Pulmonology, Oncology and Allergology, Medical University of Lublin, Poland 8 Jaczewskiego Str., 20-950 Lublin, Poland tel : +48 81 742-44-31, +48 510-973-716, doctor_86@o2.pl
  • Department of Dermatology, Venerology and Paediatric Dermatology, Medical University of Lublin, Poland
  • Trainee doctor, extern; Independent NHS Clinical Hospital No. 4, Lublin, Poland
  • Department of Pulmonology, Oncology and Allergology, Medical University of Lublin, Poland
Bibliografia
  • 1. Sin DD, Anthonisen NR, Soriano JB, et al. Role of comorbidities. Eur Resp J. 2006;28(6):1245-57.[Crossref]
  • 2. Wedzicha JA, Donaldson GC. Exacerbations of chronic obstructive pulmonary disease. Respir Care. 2003;48(12):1204-13.[PubMed]
  • 3. Bathroorn E, Huib K, Postma D, et al. Airways inflammation and treatment during acute exacerbations of COPD. Int J Chron Obstruct Pulmon Dis. 2008;3(2):217-29.
  • 4. Hurst JR, Perera WR, Wilkinson TM, et al. Systemic and upper and lower airway inflammation at exacerbation of chronic obstructive pulmonary disease. Am J Resp Crit Care Med. 2006;173(1):71-8.
  • 5. Wounters EF. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005;2(1):26-33.[Crossref]
  • 6. Gan WQ, Man SF, Sethilselvan A, Sin DD. Association between chronic obstructive pulmonary disease ans systemic inflammation: a review ans meta-analysis. Thorax. 2004;59:574-80.
  • 7. Young E. The anti-inflammatory effects of heparin and related compounds. Thromb Res. 2008;122(6):743-52.[WoS]
  • 8. Tyrell DJ, Home AP, Holme R, et al. Heparin in inflammation: potential therapeutic applications beyond anticoagulation. Adv Pharmacol. 1999;46:151-208.
  • 9. Yoshida T, Tuder MR. Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease. Physiol Rev. 2007;87:1047-82.[WoS]
  • 10. Hasan M, Najjam S, Gorgon MY, et al. IL-12 is a heparin-binding cytokine. J Immunol. 1999;162:1064-70.
  • 11. World Medical Association Declaration of Helsinki Ethical Principles for Medical Research Involving Human Subjects. 59 WMA General Assembly, Seoul, October 2008.
  • 12. Global Initiative for Lung Disease, Bethesda. Global Obstructive Lung Disease 2008.
  • 13. Green D, Hirsh J, Heit J et al. Low-molecular-weight heparin: a critical analysis of clinical trials. Pharmacol Rev. 1994;46:89-109.
  • 14. Lianchun W, Jilian RB, Ajit V, Jeffrey DE. Heparin’s anti-inflammatory effects require glucosamine 6-0-desulphation and are mediated by blockade of L- and p-selections. J Clin Invest. 2002;110:127-36.
  • 15. Terranova VP, Difloria R, Lyall RM, et al. Human endothelial cells are chemotactic to endothelial cell growth factor and heparin. J Cell Biol. 1985;101:2330-4.
  • 16. Parish DR, Coom DR, Jacobsen KB, et al. Evidence that sulfated polysaccharides inhibit tumor metastasis by blocking tumor -cell- derived heparinases. Int J Cancer.1987;40:511-8.
  • 17. Brown RA, Leveb R, Jones NA Page CO. Effects of heparin and related molecules upon neutrophil aggregation and elastase release in vitro. Br J Pharmacol. 2003;139:845-53.
  • 18. Seemungal T, Harper-Owen R, Bhowmik A, et al. Respiratory viruses, symptoms and inflammatory markers in acute and stable chronic obstructive lung disease. Am J Respir Crit Care Med. 2001;164:1618-23.
  • 19. Van MX, Liu G, Wang Y, Thorlacius H. Protective effect of low molecular weight heparin on experimental colitis: role of neutrophil recruitment and TNF-alpha production. Inflamm Res. 2002;51:182-7.
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_pjph-2014-0010
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