Helikobakter Pilori Eradikasyonun Serum Paraoksonaz Enzim Aktivitesine Etkisi

Öz

Amaç: Helikobakter pilori (H. pilori) enfeksiyonu gastrointestinal ve ekstraintestinal hastalıklarla ilişkilidir. H. pilori bu hastalıklara spesifik virülans faktörleri yoluyla veya inflamasyon ve oksidasyonu arttırarak neden olur. HDL kolesterol ile ilişkili paraoksonaz-1 (PON-1) enzimi, HDL kolesterolün antioksidan ve antiaterojenik etkilerinden sorumludur. PON-1 seviyeleri bu nedenle kardiyovasküler hastalıklarla ilişkilidir. Bu çalışmada H. pilori eradikasyonu ve paraoksonaz aktivitesi arasındaki ilişkinin araştırılması amaçlanmıştır. Gereç ve Yöntem: Çalışma H. pilori eradikasyon tedavisi almış ve eradikasyon tedavisi kontrol edilmiş 126 yetişkin hastada prospektif olarak yapıldı. H. pilori 38 hastada (17 erkek, 21 kadın) pozitif, 88 hastada (43 erkek, 45 kadın ) negatifdi. Bulgular: H. pilori eradikasyon tedavisi sonrası paraoksonaz-1(PON-1) enzim seviyeleri; H. pilori negatif grupta 165,69 U/L ve H. pilori pozitif grupta 131,68 U/L olarak bulundu. Tedaviden sonra gruplar arasında paraoksonaz-1(PON-1) enzim seviyeleri açısından istatistiksel olarak anlamlı fark saptandı (p=0,02). Sonuç: H. pilori eradikasyon tedavisi sonrası paraoksonaz-1 (PON-1) enzim seviyelerinde artış, LDL oksidasyonunda azalmaya ve buna sekonder antiaterosklerotik etkiye neden olmaktadır.

Anahtar Kelimeler

• Helikobakter pilori,, Paraoksonaz,,Ateroskleroz

The Effect of Helicobacter Pylori Eradication on Paraoxonase Enzyme Activity

Öz

Purpose: Helicobacter pylori (H. pylori) infection is associated with gastrointestinal and extraintestinal diseases either directly via its special virulence factors or indirectly by increasing inflammation and oxidation. Paraoxonase-1 (PON–1) enzyme that is related to HDL cholesterol is responsible for the antioxidant and antiatherogenic effects of HDL cholesterol. PON–1 level is related to the risk of cardiovascular disease. We aimed to investigate the relation between H. pylori infection and PON-1 activity. Material -Method: We prospectively evaluated 126 adult patients in a tertiary reference hospital in Ankara, Turkey. After H. pylori eradication therapy and checking for treatment success, 38 H. pylori-positive (17 male, 21 female) and 88 H. pylori-negative (43 male, 45 female ) patients were included in this study. Results: PON–1 enzyme levels after H. pylori eradication therapy were 165,69U/L in H. pylori-negative and 131,68 U/L in H. pylori-positive groups. The difference in PON–1 enzyme levels after treatment in two groups was statistically significant (p=0,02). Conclusion: Increased PON–1 enzyme levels after H. pylori eradication therapy might play a role in the antiatherosclerotic effect by reducing LDL oxidation.

Anahtar Kelimeler

• Helicobacter pylori,Paraoxonase,Atherosclerosis

Kaynakça

1. Referans1. Xia HX, Keane CT, Chen J, et al. Transportation of Helicobacter pylori cultures by optimal systems. Journal of clinical microbiology. 1994; 32: 3075-7.
2. Referans2. Buck GE. Campylobacter pylori and gastroduodenal disease. Clinical microbiology reviews. 1990; 3: 1-12.
3. Referans3. Dooley CP CH, Fitzgibbons PL, Bauer M, Appleman MD, Perez GI, et al. Prevalance of Helicobacter Pylori Infection and Histologic Gastritis in Asymtomatic Persons. N Eng J Med 1989; 321: 1562-6.
4. Referans4. A. Ö. Helicobacter pylori 2006 “WGO-OMGE Practice Guideline” ve “Maastricht III Florence Consensus Report 2005”. Güncel Gastroenteroloji Dergisi. 2006; 10: 287-91.
5. Referans5. Howden CW. Clinical expressions of Helicobacter pylori infection. The American journal of medicine. 1996; 100: 27S-32S; discussion 32S-34S.
6. Referans6. Vaira D, Malfertheiner P, Megraud F, et al. Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. HpSA European study group. Lancet. 1999; 354: 30-3.
7. Referans7. Mackness B, Durrington PN, Abuashia B, et al. Low paraoxonase activity in type II diabetes mellitus complicated by retinopathy. Clinical science. 2000; 98: 355-63.
8. Referans8. Feingold KR, Memon RA, Moser AH, et al. Paraoxonase activity in the serum and hepatic mRNA levels decrease during the acute phase response. Atherosclerosis. 1998; 139: 307-15.

9. Referans9. Mackness MI, Harty D, Bhatnagar D, et al. Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus. Atherosclerosis. 1991; 86: 193-9.
10. Referans10. Sutherland WH, Walker RJ, de Jong SA, et al. Reduced postprandial serum paraoxonase activity after a meal rich in used cooking fat. Arteriosclerosis, thrombosis, and vascular biology. 1999; 19: 1340-7.
11. Referans11. Chandra M, Chandra N, Agrawal R, et al. The free radical system in ischemic heart disease. International journal of cardiology. 1994; 43: 121-5.
12. Referans12. Mackness B, Davies GK, Turkie W, et al. Paraoxonase status in coronary heart disease: are activity and concentration more important than genotype? Arteriosclerosis, thrombosis, and vascular biology. 2001; 21: 1451-7.
13. Referans13. Mackness B, Durrington P, McElduff P, et al. Low paraoxonase activity predicts coronary events in the Caerphilly Prospective Study. Circulation. 2003; 107: 2775-9.
14. Referans14. Shoji T, Nishizawa Y, Fukumoto M, et al. Inverse relationship between circulating oxidized low density lipoprotein (oxLDL) and anti-oxLDL antibody levels in healthy subjects. Atherosclerosis. 2000; 148: 171-7.
15. Referans15. Aviram M, Hardak E, Vaya J, et al. Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase-like activities. Circulation. 2000; 101: 2510-7.
16. Referans16. Aviram M, Rosenblat M, Bisgaier CL, et al. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest. 1998; 101: 1581-90.
17. Referans17. Mackness MI, Arrol S, Abbott C, et al. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis. 1993; 104: 129-35.
18. Referans18. Watson AD, Navab M, Hama SY, et al. Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized low density lipoprotein. J Clin Invest. 1995; 95: 774-82.
19. Referans19. Danesh J, Collins R, Peto R. Chronic infections and coronary heart disease: is there a link? Lancet. 1997; 350: 430-6.
20. Referans20. Mendall MA, Goggin PM, Molineaux N, et al. Relation of Helicobacter pylori infection and coronary heart disease. British heart journal. 1994; 71: 437-9.
21. Referans21. Kowalski M, Pawlik M, Konturek JW, et al. Helicobacter pylori infection in coronary artery disease. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society. 2006; 57 Suppl 3: 101-11.
22. Referans22. Thom DH, Grayston JT, Siscovick DS, et al. Association of prior infection with Chlamydia pneumoniae and angiographically demonstrated coronary artery disease. Jama. 1992; 268: 68-72.
23. Referans23. Saikku P, Leinonen M, Mattila K, et al. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet. 1988; 2: 983-6.
24. Referans24. Jackson LA, Campbell LA, Kuo CC, et al. Isolation of Chlamydia pneumoniae from a carotid endarterectomy specimen. The Journal of infectious diseases. 1997; 176: 292-5.
25. Referans25. Gunn M, Stephens JC, Thompson JR, et al. Significant association of cagA positive Helicobacter pylori strains with risk of premature myocardial infarction. Heart. 2000; 84: 267-71.
26. Referans26. Witztum JL, Steinberg D. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest. 1991; 88: 1785-92.
27. Referans27. Serdar Z, Aslan K, Dirican M, et al. Lipid and protein oxidation and antioxidant status in patients with angiographically proven coronary artery disease. Clin Biochem. 2006; 39: 794-803.
28. Referans28. Azarsiz E KM, Payzin S, Sözmen EY. PON1 activities and oxidative markers of LDL in patients with angiographically proven coronary artery disease. Int J Cardiol 2003; 91: 43-51.
29. Referans29. Graner M, James RW, Kahri J, et al. Association of paraoxonase-1 activity and concentration with angiographic severity and extent of coronary artery disease. Journal of the American College of Cardiology. 2006; 47: 2429-35.