Barış YILMAZ, Dilek KANMAZ, Yasemin TORAMAN, Sema ALTUN, Yasemin BAHAR, Esin YENTÜRK, Esin TUNCAY

Stabil kronik obstrüktif akciğer hastalarında inflamatuvar belirteçler; c-reaktif protein, fibrinojen ve lökosit

KOAH hastalarında stabil evrede inflamatuar proçesin devam edip etmediğini ve inflamatuar mediyatörlerin hava akımı kısıtlılığı ile ilişkisini araştırmayı amaçladık.Olgularımız, hastanemiz polikliniğine başvuran stabil KOAH tanısı almış 48 hastadan, kontrol grubu ise aktif sigara içicisi olmayan 21 sağlıklı gönüllüden seçildi. Her iki gurubun da yaş, boy, kilo, sigara kullanım süreleri sorgulandı, solunum fonksiyon testleri, hemogram, CRP ve fibrinojen değerlerine bakıldı. KOAH grubunda arter kan gazları, kontrol grubunda satürasyon değerleri tetkik edildi.Çalışmamızda, KOAH grubunun yaş ortalaması 60±9, kontrol grubunun ise 34±9 idi. KOAH grubundaki olgularda lökosit (p:0.00) ve CRP (p:0.02) düzeylerinin kontrol grubuna göre anlamlı derecede yüksek olduğu, ancak fibrinojen (p:0.149) düzeyinde gruplar arasında farklılık bulunmadığı tespit edildi. Stabil KOAH evreleri arasında, CRP (p:0.9) ve lökosit (p:0.7) düzeylerinde anlamlı farklılık tespit edilmedi. İleri evre KOAH olgularında fibrinojen ortalaması diğer evrelere göre yüksekti, ancak istatistiksel olarak anlamlı farklılık bulunmadı (p:0.228).Sonuç olarak stabil KOAH olgularında CRP ve lökosit gibi inflamatuvar belirteçlerin yüksek olduğu, stabil KOAH ve kontrol grubunun fibrinojen düzeyleri arasında ilişki olmasa da, fibrinojen ile FEV1 arasında ters orantılı ve anlamlı bir ilişki olduğu (p:0.047), ayrıca fibrinojenin yaşla paralel olarak arttığı sonucuna varıldı (p:0.013).

Inflammatory markers ın patıents wıth chronıc obstructıve lung dısease; c-reactıve proteın, fıbrınogen, leukocyte

In this study we aimed to investigate, if the inflammatory process is going on or not at stable phase of COPD patients and relation of inflammatory mediators with airflow obstruction. We selected our cases from our outpatient clinic patients among the ones diagnosed as stable COPD and healthy volunteers who weren’t active smokers. Both groups were classified for age, height, weight, smoking duration and checked for pulmonary function test, hemogram, CRP, fibrinojen levels respectively. We checked arterial blood gas in COPD group and saturation levels in control group. In our study, average age of patients in COPD and control groups were 60±9 and 34±9 respectively. We revealed that CRP (p:0.02) and leukocyte levels (p:0.00) at COPD patients were higher than control group and this was statistically significant. But there wasn’t any significant difference between two groups according to fibrinogen levels (p:0.149). There wasn’t a significant differencebetween CRP (p:0.9) and leukocyte (p:0.7) levels at stable COPD phases. Average of fibrinogen levels were higher at patients with severe disease than other phases but this wasn’t statisticallysignificant (p:0.228). In conclusion, we revealed that CRP and leukocyte levels were higher at stable COPD patients. Although there was not a relation between fibrinogen levels of stable COPD and control groups, there was an inversely proportional and significant relation between fibrinogen and FEV 1 (p:0.047). In addition we found that fibrinogen levels were increasing with age (p:0.013).

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1. Pauwels RA, Buist AS, Calverley PM, et al. Global strategy for the diagnosis, manage- ment, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO Global Iniative for chronic obstructive lung disease (GOLD) Workshop summary. Am J Respir Crit Care Med 2001; 163: 1256-76.
2. Gavin C. Donaldson, Terence A.R. Seemungal, Irem S. Airway and Systemic Inflammation and Decline in Lung Function in Patients with COPD. Chest 2005; 128(4): 1995-2004.
3. J.P. de Torres, E. Cordoba-Lanus, C.Lopez- Aguilar. C-reaktive protein levels and clinically important predictive outcomes in stable COPD patients. Eur Respir J 2006 Feb 2;published online ahead of print as doi: 10.1183/09031936.06.00109605.
4. Wu SJ, Chen P, Jiang XN, Liu ZG. C-reactive protein level and the correlation between lung function and CRP levels in patients with chronic obstructive pulmonary diseases. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2005; 30(4): 444-6.
5. Mannino DM, Ford ES, Redd SC. Obstructive and restrictive lung disease and markers of inflammation:data from the third National Health and Nutrition Examination. Am J Med 2003; 114: 758-62.
6. Gan Wq, Man SFP, Senthilselvan A, Sin DD. Association between chronic obstructive pulmonary di sease and systemic inflammation: a systematic rewiew and meta-analysis. Thorax 2004; 59: 574-80.
7. Wen Qi Gan, MD; S.F. Paul Man, MD, FCCP and Don D. Sin, MD, FCCP. The Interactions Between Cigarette Smoking and Reduced Lung Function on Systemic Inflamation. Chest 2005; 127: 558-64.
8. Sin Don D, Man SF. Why Are Patients With Chronic Obstructive Pulmonary Disease at Increased Risk of Cardiovascular Diseases ? Circulation 2003; 107: 1514-9.
9. Yasuda N, Gotoh K, Minatoguchi S, et al. An increase of soluble Fas, an inhibitor of apoptosis, associated with progression of COPD. Respir Med 1998; 92: 993-9.
10. Kelly M, Dentener MA, Creutzberg EC, et al. Patophysiology of COPD. Thorax 2002; 57: 563-4.
11. Pinto-Plata VM, Mullerova H, Toso JF, Feudjo-Tepie M, Soriano JB, Vessey RS, Celli BR. C-reactive protein in patients with COPD, control smokers and nonsmokers. Thorax 2006; 61(1): 23-8.
12. Nascetti S, Elosua R, Pena A, et al. Variables associated with fibrinojen in a population- based study: Interaction between smoking and age on fibrinojen concentration. European Journal of Epidemiology 2001; 17: 953-8.
13. Folsom AR. Epidemiology of fibrinogen. Eur Heart J 1995; 16(suppl A): 21-4.
14. De Maat MP, Pietersma A, Kofflard M, et al. Association of plasma fibrinogen levels with coronary artery disease, smoking and inflam- matory markers. Atherosclerosis 1996; 121: 185-91.
15. Davis MC. Oral contraceptive use and hemo- dynamic, lipid, and fibrinogen responses to smoking and stress in woman. Health Psychol 1999; 18: 122-30.
16. Fruzetti F, Ricci C, Fioretti P. Hemostasis profile in smoking and nonsmoking women taking low-dose oral contraceptives. Contraception 1994; 49: 579-92.
17. Dahl M, Tybjerg-Hansen A, Vestbo J, et al. Elevated Plasma Fibrinojen with Reduced Pulmonary Function and Increased Risk of Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med 2001; 164: 1008-11.
18. Hiroyasu I, Shimamoto T, Sato S. Passive Smoking and Plasma Fibrinojen Concentra- tions. Am J Epidemiol 1996;144: 1151-4.
19. Mennen LI, Balkau B, Charles MA, D’Hour A, et al. Gender differences in the relation between fibrinojen, tissue-type plasminojen activator antigen and markers of insulin resistance: effects of smoking: DESIR Study Group. Thromb Haemost 1999; 82: 1106- 11.
20. Eliasson M, Asplung K, Evrin PE, Lundbland D. Relationship of cigarette smoking and snuff dipping to plasma fibrinogen, fibrino- lytic variables and serum insulin: the Nort- hern Sweden MONICA Study. Atherosclerosis 1995; 113: 41-53.
21. Hunter KA, Garlick PJ, Broom L, et al. Effect of smoking and abstention from smoking on fibrinogen synthesis in humans. Clinical Science 2001; 100: 459-65.
22. Sinha S, Luben RN, Welch A, et al. Fibrinojen and cigarette smoking in men and women in the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population. European Journal of Cardiovascular Pre- vention and rehabilitation 2005; 12(2): 144- 50.
23. Arslan S, Y›ld›z F, Argun Bar›fl S ve ark. Stabil ve Ataktaki Kronik Obstrüktif Akci¤er Hastal›¤› Tan›l› Bireylerde Sistemik ‹nflamas- yon ve Komorbiditeler. Türk Toraks Derne¤i 14. y›ll›k kongresi sözlü bildiri. SS302.
24. Noguera A, Busquets X, Sauleda J, et al. Expression of adhesion molecules and G proteins in circulating neutrophils in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158: 1664-8.
25. Bartu Saryal S, Ac›can T. (eds) Epidemiyoloji ve risk faktörleri. In: Güncel Bilgiler Ifl›¤›nda KOAH, Bilimsel T›p Kitabevi, Ankara 2003; s:12-32.
26. In: Fishman AP, Elias JA, et al. Pathogenetic Processes. Fishman’s Pulmonary Disease and Disorders. 4. Ed, McGraw-Hill, 2008; 715-717.