Alterations in paraoxonase-1 levels and oxidative status with the eradication of Helicobacter pylori infection

Öz

Background and Aims: To compare the plasma paraoxonase-1 levels and oxidative stress markers in patients with different states of Helicobacter pylori infection. Materials and Methods: Patients with dyspeptic symptoms and referred for upper gastrointestinal system endoscopy were consequently included and grouped according to the presence of Helicobacter pylori infection. Helicobacter pylori was eradicated in patients with positive rapid urase test. Total antioxidant status, total oxidant status and oxidative stress index were calculated. Paraoxonase-1 levels and oxidative stress markers were compared between 3 groups and in treated patients before and after eradication. Results: One hundred eighty nine patients were included the study. In eighty two patients Helicobacter pylori were positive without the presence of duodenal ulcer, in 49 patients Helicobacter pylori were positive with the presence of duodenal ulcer and Helicobacter pylori were negative in 58 patients. In evaluation of paraoxonase-1 levels in women, there were not any statistically significant difference between groups but Helicobacter pylori negative patients had statistically significantly higher values than other 2 groups among men. Total antioxidant status levels were statistically significantly higher in both genders in Helicobacter pylori negative patients than other 2 groups. There were a statistically significant increase in total antioxidant status and paraoxonase-1 levels with the successful eradication of Helicobacter pylori infection. Conclusion: Plasma paraoxonase-1 and total antioxidant status were decreased while total oxidant status and oxidative stress index were increased in the patients with Helicobacter pylori infection. The differences were more prominent in males who are more prone to atherosclerotic diseases. Moreover, with the eradication of Helicobacter pylori infection, both paraoxonase-1 levels and total antioxidant status were increased significantly

Anahtar Kelimeler

• Helicobacter pylori
• oxidative status
• paraoxonase-1

Helicobacter pylori enfeksiyonunun eradike edilmesi ile paraoksonaz-1 düzeylerinde ve oksidatif durumdaki değişiklikler

Öz

Giriş ve Amaç: Helicobacter pylori enfeksiyonunun farklı kliniklerine sahip hastalarda plazma paraoksonaz-1 seviyelerini ve oksidatif stres belirteçlerini karşılaştırmak. Gereç ve Yöntem: Dispeptik semptomları olan ve üst gastrointestinal sistem endoskopisi için yönlendirilen hastalar çalışmaya dahil edildi ve Helicobacter pylori enfeksiyonu varlığına göre gruplandırıldı. Hızlı üreaz testi pozitif olan hastalarda Helicobacter pylori eredike edildi. Paraoksonaz-1 düzeyleri ve oksidatif stres belirteçleri, Helicobacter pylori pozitif olup duodenal ülseri olan ve olmayan grup ve Helicobacter pylori negatif olan gruplar arasında ve tedavi edilen hastalarda eradikasyon öncesi ve sonrasında karşılaştırıldı. Bulgular: Çalışmaya 189 hasta dahil edildi. 82 hastada duodenum ülseri olmadan Helicobacter pylori pozitif, 49 hastada duodenum ülseri varken Helicobacter pylori pozitif, 58 hastada Helicobacter pylori negatifti. Kadınlarda paraoksonaz-1 düzeyleri değerlendirildiğinde gruplar arasında istatistiksel olarak anlamlı bir fark bulunmazken, Helicobacter pylori negatif hastaların değerleri erkeklerde diğer 2 gruba göre istatistiksel olarak anlamlı derecede yüksekti. Helicobacter pylori negatif hastalarda total antioksidan kapasitesi düzeyleri her iki cinsiyette de diğer 2 gruba göre istatistiksel olarak anlamlı derecede yüksekti. Helicobacter pylori enfeksiyonunun başarılı bir şekilde ortadan kaldırılmasıyla total antioksidan kapasitesi ve paraoksonaz-1 düzeylerinde istatistiksel olarak anlamlı bir artış oldu. Sonuç: Helicobacter pylori enfeksiyonu olan hastalarda plazma paraoksonaz-1 ve total antioksidan kapasitesi azalırken total oksidatif durum ve oksidatif stres indeksi arttı. Aterosklerotik hastalıklara daha yatkın olan erkeklerde farklılıklar daha belirgindi. Ayrıca Helicobacter pylori enfeksiyonunun ortadan kaldırılmasıyla hem paraoksonaz-1 düzeyleri hem de total antioksidan kapasitesi önemli ölçüde arttı.

Anahtar Kelimeler

• Helicobacter pylori
• oksidatif durum
• paraoksonaz-1

Kaynakça

1. 1. Stolte M. Helicobacter pylori gastritis and gastric MALT-lymphoma. The Lancet. 1992;339(8795):745-6.
2. 2. Makola D, Peura DA, Crowe SE. Helicobacter pylori infection and related gastrointestinal diseases. J Clin Gastroenterol. 2007;41(6):548-58.
3. 3. Yanai A, Maeda S, Shibata W, et al. Activation of IκB kinase β and NF-κB is essential for Helicobacter pylori-induced chronic gastritis in Mongolian gerbils. Infect Immun. 2008;76(2):781-7.
4. 4. Salama NR, Hartung ML, Müller A. Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori. Nat Rev Microbiol. 2013;11(6):385-99.
5. 5. Vijayvergiya R, Vadivelu R. Role of Helicobacter pylori infection in pathogenesis of atherosclerosis. World J Cardiol. 2015;7(3):134-43.
6. 6. Hardbower DM, de Sablet T, Chaturvedi R, Wilson KT. Chronic inflammation and oxidative stress: the smoking gun for Helicobacter pylori-induced gastric cancer? Gut Microbes. 2013;4(6):475-81.
7. 7. Suzuki H, Hibi T. Oxidative stress in Helicobacter pylori assocaited gastroduodenal disease. J Clin Biochem Nutr. 2006;39(2):56-63.
8. 8. Mashimo M, Nishikawa M, Higuchi K, et al. Production of reactive oxygen species in peripheral blood is increased in individuals with Helicobacter pylori infection and decreased after its eradication. Helicobacter. 2006;11:266-71.

9. 9. Kang MR, Park KH, Oh SJ, et al. Cardiovascular protective effect of glabridin: Implications in LDL oxidation and inflammation. Int Immunopharmacol. 2015;29(2):914-8.
10. 10. Eren E, Yilmaz N, Aydin O. Functionally defective high-density lipoprotein and paraoxonase: a couple for endothelial dysfunction in atherosclerosis. Cholesterol. 2013;2013:792090.
11. 11. Eckerson HW, Wyte MC, La Du BN. The human serum paraoxonase/ arylesterase polymorphism. Am J Hum Genet. 1983;35:1126-38.
12. 12. O Erel. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem. 2004;37(2):112-9.
13. 13. O Erel. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38(12):1103-11.
14. 14. Ece A, Gürkan F, Celik F, et al. Paraoxonase, total antioxidant activity and peroxide levels in marasmic children: relationships with leptin. Clin Biochem. 2007;40:634-9.
15. 15. Altinda Ö, Karakoç M, Soran N, et al. Paraoxonase and arylesterase activities in patients with rheumatoid arthritis. Turk J Rheumatol. 2007;22:132-6.
16. 16. Aslan M, Nazligul Y, Horoz M, et al. Serum paraoxonase-1 activity in Helicobacter pylori infected subjects. Atherosclerosis. 2008;196(1):270-4.
17. 17. Akbas HS, Basyigit S, Suleymanlar I, et al. The assessment of carotid intima media thickness and serum paraoxonase-1 activity in Helicobacterpylori positive subjects. Lipids Health Dis. 2010;9:92.
18. 18. Mete R, Oran M, Alpsoy S, et al. Carotid intima-media thickness and serum paraoxonase-1 activity in patients with Helicobacter pylori. Eur Rev Med Pharmacol Sci. 2013;17(21):2884-9.
19. 19. Handa O, Naito Y, Yoshikawa T. Helicobacter pylori: a ROS-inducing bacterial species in the stomach. Inflamm Res 2010;59(12):997-1003.
20. 20. Kebapcilar L, Sari I, Renkal AH, et al. The influence of Helicobacter pylori eradication on leptin, soluble CD40 ligand, oxidative stress and body composition in patients with peptic ulcer disease. Intern Med. 2009;48(24):2055-9.
21. 21. Dulger AC, Aslan M, Nazligul Y, et al. Peripheral lymphocyte DNA damage and oxidative status after eradication therapy in patients infected with Helicobacter pylori. Pol Arch Med Wewn. 2011;121(12):428-32.
22. 22. Soundaravally R, Pukazhvandthen P, Zachariah B, Hamide A. Plasma ferritin and indices of oxidative stress in Helicobacter pylori infection among schoolchildren. J Pediatr Gastroenterol Nutr. 2013;56(5):519-22.
23. 23. Kumari S, Verma AK, Rungta S, et al. Serum prolidase activity, oxidant and antioxidant status in nonulcer dyspepsia and healthy volunteers. ISRN Biochem. 2013 Oct 29;2013:182601.
24. 24. Zhang J, Wang D, He S. Roles of antibody against oxygenized low density lipoprotein in atherosclerosis: recent advances. Int J Clin Exp Med. 2015;8(8):11922-9.
25. 25. Vijayvergiya R, Agarwal N, Bahl A, et al. Association of Chlamydia pneumoniae and Helicobacter pylori infection with angiographically demonstrated coronary artery disease. Int J Cardiol. 2006;107:428-9.
26. 26. Goyal P, Kalek SC, Chaudhry R, Chauhan S, Shah N. Association of common chronic infections with coronary artery disease in patients without any conventional risk factors. Indian J Med Res. 2007;125:129-36.
27. 27. Al-Nozha MM, Khalil MZ, Al-Mofleh IA, Al-Ghamdi AS. Lack of association of coronary artery disease with H.pylori infection. Saudi Med J. 2003;24:1370-3.
28. 28. Kanbay M, Gür G, Yücel M, Yilmaz U, Muderrisoglu H. Helicobacter pylori seroprevalence in patients with coronary artery disease. Dig Dis Sci. 2005;50:2071-4.
29. 29. Kowalski M. Helicobacter pylori (H. pylori) infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H. pylori specific DNA in human coronary atherosclerotic plaque. J Physiol Pharmacol. 2001;52(Suppl 1):3-31.
30. 30. Huang B, Chen Y, Xie Q, et al. CagA-positive Helicobacter pylori strains enhanced coronary atherosclerosis by increasing serum OxLDL and HsCRP in patients with coronary heart disease. Dig Dis Sci. 2011;56(1):109-14.
31. 31. Cremonini F, Gabrielli M, Gasbarrini G, Pola P, Gasbarrini A. The relationship between chronic H. pylori infection, CagA seropositivity and stroke: meta-analysis. Atherosclerosis. 2004;173:253-9.
32. 32. Chan FK, Leung WK. Peptic ulcer disease. Lancet. 2002;360:933-41.