Varis etiyopatogenezinde lökosit aktivasyonu ile apopitozisin ilişkisi

Öz

Amaç: Variköz venler alt ekstremite en sık görülen rahatsızlıklarıdır. Bu çalışmanın amacı, lökosit aktivasyonunun ven duvarındaki apoptozis ve variköz venlerin patogenezindeki etkisini araştırmaktır.

Gereç ve Yöntemler: Çalışmaya variköz venleriolan 46 hasta dahil edildi. Hastalara semptomları, komplikasyonları veya kozmetik sebeplerle  strippingle yüksek ligasyon, ve eksizyon yapıldı. Serum kaspaz-8 ve kaspaz-9 ölçümüleri ELİSA kullanılarak yapıldı.

Bulgular: Sağlıklı sefalik ven ile variköz safen ven gruplarının sonuçları  arasında istatistiksel olarak anlamlı bir fark tespit edildi (p=0.04 and p<0.0001). 

Sonuç: Variköz ven oluşumunun altındaki karmaşık patofizyoloji henüz yeterince açıklanamamıştır. Hem lökosit aktivasyonunun hemde apopitozisdeki bozulmanın variköz ven oluşumuna katkısı olduğunu düşünmekteyiz.

Anahtar Kelimeler

• venöz yetmezlik,lökosit aktivasyonu,kaspaz,apopitozis

The relationship between leukocyte activation and apoptosis in venous insufficiency etiopathogenesis

Öz

Aim: Varicose veins are the most common disorders of the lower extremities. The purpose of this study is to investigate the effect of leukocyte activation in the vein wall and apoptosis in the etiopathogenesis of varicose veins.

Material and Methods:Forty-six patients with varicose veins were included in the study. High ligation with stripping with or without additional individual ligation and excision was performed for symptoms, complications or cosmetic needs. ELISA was used to measure the serum concentration of caspase-8 and caspase-9.

Results: There was a statistically significant difference between the cephalic vein and saphenous vein groups (p=0.04 and p<0.0001 respectively).

Conclusion: As a conclusion, the complex pathophysiology underlying varicose veins has yet to be fully defined. It is suggested that both leukocyte activation and dysregulation of apoptosis are associated with susceptibility for varicose vein formation however this argument needs further research.

Anahtar Kelimeler

• Apoptosis,Venous Insufficiency,caspas,leukocyte

Kaynakça

1. 1. Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins. Ann Epidemiol 2005; 15: 175-84.
2. 2. Baker SR, Stacey MC, Jopp-McKay AG, Hoskin SE, Thompson PJ. Epidemiology of chronic venous ulcers. Br J Surg1991; 78: 864-67.
3. 3. Lurie F.: Venous haemodynamics: what we know and don't know. Phlebology 2009; 24: 3-7
4. 4. Criqui MH, Denenberg JO, Bergan J, Langer RD, Fronek A. Risk factors for chronic venous disease: the San Diego PopulationStudy. J Vasc Surg 2007; 46: 331-37.
5. 5. Scott TE, LaMorte WW, Gorin DR, Menzoian JO. Risk factors for chronic venous insufficiency: a dual case-control study. J Vasc Surg 1995; 22: 622-68.
6. 6. Chiesa R, Marone EM, Limoni C, Volonte M and Petrini O. Chronic venous disorders: correlationbetweenvisiblesigns, symptoms, and presence of functionaldisease. J Vasc Surg 2007; 46: 322-30.
7. 7. Stacey MC, Burnand KG, Lea Thomas M, Pattison M. Influence of phlebographic abnormalities on the natural history of venous ulceration. Br J Surg1991; 78: 868-71.
8. 8. Myers D, Wrobleski S, Londy F et al. New and effective treatment of experimentally induced venous thrombosis with anti- inflammatory rPSGL- Ig. Thromb Haemost 2002; 87: 374-82.

9. 9. Henke PK, Varga A, De S et al. Deep vein thrombosis resolution is modulated by monocyte CXCR2 mediated activity in a mouse model. Arterioscler Thromb Vasc Biol 2004; 24: 1130- 37.
10. 10. Oklu R, Habito R, Mayr M et al. Pathogenesis of varicose veins. J Vasc Interv Radiol. 2012; 23: 33-39.
11. 11. Ascher E, Jacob T, Hingorani A, Gunduz Y, Mazzariol F, Kallakuri S. Programmed cell death (Apoptosis) and its role in the pathogenesis of lower extremity varicose veins. Ann Vasc Surg 2000; 14: 24- 30.
12. 12. Yongbo X, Wei H, Lei W et al. Changes in levels of apoptosis in the walls of different segments of great saphenous varicose veins. Phlebology 2016; 31: 632-69.
13. 13. Castro-Ferreira R, Cardoso R, Leite-Moreira A, Mansilha A. The Role of Endothelial Dysfunction and Inflammation in Chronic Venous Disease. Ann Vasc Surg. 2018 ; 46: 380-93.
14. 14. Raffetto JD, Mannello F. Pathophysiology of chronic venous disease. Int Angiol 2014; 33: 212-21.
15. 15. Reed JC, Miyashita T, Takayama S et al. Bcl-2 family proteins: regulators of cell death involved in the pathogenesis of cancer and resistance to therapy. J Cell Biochem 1996; 60: 23-32.
16. 16. Fisher GH, Rosenberg FJ, Strauss SE et al. Dominant interfering fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell 1995; 81: 935-46.
17. 17. Saxena A, Mcmeekin JD, Thomson DJ. Expression of Bcl-x, Bcl-2, Bax and Bak in endarterectomy and atherectomy specimens. J Pathol 2002; 196: 335-42.
18. 18. Diaz JL, Oltersdorf T, Horne W et al. A common binding site mediates heterodimerization and homodimerization of Bcl-2 family members. J Biol Chem 1997; 272: 11350-55.
19. 19. Ducasse E, Giannakakis K, Speziale F et al. Association of Primary Varicose Veins with Dysregulated Vein Wall Apoptosis. Eur J Vasc Endovasc Surg 2008; 35: 224-29.
20. 20. Shiozaki EN, Shi Y. Caspases, IAPs and Smac/DIABLO: mechanisms from structural biology. Trends Biochem Sci 2004; 29: 486-94.
21. 21. Coleridge Smith PD, Thomas P, Scurr JH, Dormandy JA. Causes of venous ulceration: a new hypothesis. Br Med J (Clin Res Ed) 1988; 296: 1726-27.
22. 22. Castro-Ferreira R, Cardoso R, Leite-Moreira A, Mansilha A. The role of endothelial dysfunction and inflammation in chronic venous disease. Ann Vasc Surg 2018; 46: 380-93.
23. 23. Lim CS, Kiriakidis S, Paleolog EM, Davies AH. Increased activation of the hypoxia-inducible factor pathway in varicose veins. J Vasc Surg 2012; 55: 1427-39.
24. 24. Ascher E, Jacob T, Hingorani A, Tsemekhin B, Gunduz Y. Expression of molecular mediators of apoptosis and their role in the pathogenesis of lower-extremity varicose veins. J Vasc Surg 2001; 33: 1080-86.