Volkan GÖKBULUT, HAKAN DURSUN, Mustafa KAPLAN, ERKİN ÖZTAŞ

Ülseratif kolitli hastalarda paraoksanaz 1 ve arilesteraz seviyeleri ve bu parametrelerin hastalık aktivitesi ile ilişkileri

Giriş ve Amaç: Bu çalışmada ülseratif kolitli hastalarda serum paraoksonaz 1 ve arilesteraz düzeyleri ve bu parametrelerin hastalık aktivitesi ile ilişkileri araştırıldı. Gereç ve Yöntem: Çalışmaya 38 aktif dönemde ülseratif kolit hastası ve 38 sağlıklı kontrol grubu hastası dahil edildi. Çalışma grubu hastalarından hem aktif dönemde hem de remisyon sağlanınca paraoksonaz 1 ve arilesteraz enzim aktiviteleri çalışıldı. Paraoksonaz 1 ve arilesteraz enzim aktiviteleri aktif dönem, remisyon dönemi ve kontrol grubu arasında kıyaslandı. Bulgular: Çalışma grubu hastalarının yaş ortalaması 40.3±14.6 yıl (19-78) olup hastaların 20’si erkek (%52.6) ve 18’i kadın (%47.4) idi. Kontrol grubu hastalarının demografik özellikleri çalışma grubuna benzerdi. Aktif dönemdeki ülseratif kolit hastalarının ortalama serum paraoksonaz 1 değeri 65.8±15.0 U/L, ortalama serum arilesteraz değeri ise 151.0±236.6 U/mL olarak tespit edildi. Remisyon dönemindeki hastalarda ortalama serum paraoksonaz 1 değeri 82.4±58.4 U/L, ortalama serum arilesteraz değeri ise 94.1±134.6 U/ mL olarak tespit edildi. Kontrol grubundaki hastalarda ortalama serum paraoksonaz 1 değeri 131.7±63.5 U/L, ortalama serum arilesteraz değeri ise 287.3±295.6 U/mL olarak tespit edildi. Ülseratif kolitli hastalarda ortalama paraoksonaz 1 ve arilesteraz düzeyleri aktif ve remisyon dönemi arasında istatistiksel olarak anlamlı fark göstermedi (p>0.05). Aktif ve remisyon dönemindeki ülseratif kolitli hastalarda ortalama paraoksonaz 1 ve arilesteraz değerleri kontrol grubundaki sağlıklı bireylere göre istatistiksel olarak anlamlı şekilde düşük bulundu (p

Paraoxonase 1 and arylesterase levels in patients with ulcerative colitis and their relationship with disease activity

Background and Aims: In this study, we studied serum paraoxanase 1 and arylesterase levels in patients with ulcerative colitis and their relationship with disease activity. Material and Methods: Thirty-eight patients with active ulcerative colitis and 38 healthy controls were included in this study. Paraoxanase 1 and arylesterase enzyme activities in both active and remission phases were studied. Paraoxanase 1 and arylesterase enzyme activities in the active disease phase, the remission phase, and the control group were compared. Results: The mean patient age in the study group was 40.3±14.6 years (19-78); 20 patients were male (52.6%) and 18 were female (47.4%). The demographic characteristics of the patients in the control group were similar to those of the study group. The mean serum paraoxanase 1 level was 65.8±15.0 U/L, and the mean serum arylesterase level was 151.0±236.6 U/mL in patients in the active phase. The mean serum paraoxanase 1 level was 82.4±58.4 U/L, and the mean serum arylesterase level was 94.1±134.6 U/mL in patients in the remission phase. The mean serum paraoxanase 1 level was 131.7±63.5 U/L, and the mean serum arylesterase level was 287.3±295.6 U/mL in the control group. There was no statistically significant difference in mean paraoxanase 1 and arylesterase levels between patients in the active and remission phases (p > 0.05). The mean levels of paraoxanase 1 and arylesterase in patients in the active and remission phases were significantly lower than those in healthy controls (p < 0.05). Conclusion: In patients with ulcerative colitis, paraoxanase 1 and arylesterase enzyme activities were found to be significantly lower than those in the control group, but there was no relationship between disease activity and paraoxanase 1 and arylesterase enzyme activities.

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Çavuşoğlu H, İliçin G, Ünal S, Biberoğlu K, Süleymanlar G. İnflamatuar barsak hastalığı. İç Hastalıkları. 2. baskı. Ankara: Güneş Kitabevi, 2003:1577-90.
Tezel A. Etiopathogenesis of ulcerative colitis. Turkiye Klinikleri J Gastroenterohepatol-Special Topics 2009;2:7-12.
Fiocchi C. Future of IBD pathogenesis: How much work is left to do? Inflamm Bowel Dis 2008;14(Suppl 2):S145-7.
Friedman S, Blumberg RS. Inflammatory bowel disease. In; Braunwald E, Fauci AS, Kasper DL, et al. (eds). Harrison’s Principles of Internal Medicine. 16th ed. New York; McGraw-Hill. 2005;1776-89.
Draganov DI, Teiber JF, Speelman A, et al. Human paraoxonases (PON1, PON2, and PON3) are lactonases with overlapping and distinct substrate specificities. J Lipid Res 2005;46:1239-47.
Mackness B, Durrington PN, Mackness MI. Human serum paraoxonase. Gen Pharmacol 1998;31:329-36.
Costa LG, Vitalone A, Cole TB, Furlong CE. Modulation of paraoxonase (PON1) activity. Biochem Pharmacol 2005;69:541-50.
Mackness B, McElduff P, Mackness MI. The paraoxonase-2-310 polymorphism is associated with the presence of microvascular complications in diabetes mellitus. J Intern Med 2005;258:363-8.
Baum L, Ng HK, Woo KS, et al. Paraoxonase 1 gene Q192R polymorphism affects stroke and myocardial infarction risk. Clin Biochem 2006;39:191-5.
Suchocka Z, Swatowska J, Pachecka J, Suchocki P. RP-HPLC determination of paraoxonase activity in human blood serum. J Pharm Biomed Anal 200611;42:113-9.
Gokdemir MT, Karakilcik AZ, Gokdemir GS. Prognostic importance of paraoxonase, arylesterase and mean platelet volume efficiency in acute ischaemic stroke. J Pak Med Assoc 2017;67:1679-83.
Utanğaç MM, Yeni E, Savaş M, et al. Paraoxonase and arylesterase activity in bladder cancer. Turk J Urol 2017;43:147-51.
Kul A, Uzkeser H, Ozturk N. Paraoxonase and arylesterase levels in Behcet’s Disease and their relations with the disease activity. Biochem Genet 2017;55:335-44.
Trulove SC, Witts LJ. Cortisone in ulcerative colitis; preliminary report on a therapeutic trial. Br Med J 1954;2:375-8.
Isik A, Koca SS, Ustundag B, et al. Paraoxonase and arylesterase levels in rheumatoid arthritis. Clin Rheumatol 2007;26:342-8.
Kafadar AM, Ergen A, Zeybek U, et al. Paraoxonase 192 gene polymorphism and serum para¬oxonase activity in high grade gliomas and menegiomas. Cell Biochem Funct 2006;24:455-60.
Yıldırım A, Aslan Ş, Ocak T, Yıldırım S, Kara F, Şahin YN. Serum paraoxonase/arylesterase activities and malondialdehyde levels in trauma patients. Eurasian J Med 2007;39:85-8.
Akçay MN, Yilmaz I, Polat MF, Akçay G. Serum paraox¬onase levels in gastric cancer. Hepatogastroenterology 2003;50(Suppl 2):cclxxiii-cclxxv.
Akçay MN, Polat MF, Yilmaz I, Akçay G. Serum paraoxonase levels in pancreatic cancer. Hepatogastroenterology 2003;50(Suppl 2):ccxxv-ccxxvii.
Elkiran ET, Mar N, Aygen B, et al. Serum paraoxonase and arylesterase activities in patients with lung cancer in a Turkish population. BMC Cancer 2007;15:48.
Başkol G, Başkol M, Yurci A, et al. Serum paraoxonase 1 activity and malondialdehyde levels in patients with ulcerative colitis. Cell Biochem Funct 2006;24:283-6.
D’Inca R, Cardin R, Benazzato L, et al. Oxidative DNA damage in the mucosa of ulcerative colitis increases with disease duration and dysplasia. Inflamm Bowel Dis 2004;10:23-7.
Sturniolo GC, Mestriner C, Lecis PE, et al. Altered plasma and mucosal concentrations of trace elements and antioxidants in active ulcerative colitis. Scand J Gastroenterol 1998;33:644-9.
Ferretti G, Bacchetti T, Moroni C, et al. Copper-induced oxidative damageon astrocytes: protective effect exerted by human high density lipoproteins. Biochimica Biophysica Acta 2003;1635:48-54.
Rothem L, Hartman C, Dahan A, et al. Paraoxonases are associated with intestinal inflammatory diseases and intracellularly localized to the endoplasmic reticulum. Free Radic Biol Med 2007;43:730-9.
Boehm D, Krzystek-Korpacka M, Neubauer K, et al. Paraoxonase-1status in Crohn’s disease and ulcerative colitis. Inflamm Bowel Dis 2009;15:93-9.
Aviram M, Rosenblat M. Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development. Free Radic Biol Med 2004;37:1304-16.
Mackness B, Durrington P, McElduff P, et al. Low paraoxonase activity predicts coronaryevents in the Caerphilly Prospective Study. Circulation 2003;107:2775-9.
Nakamura M, Saito H, Kasanuki J, et al. Cytokine production in patients with inflammatory bowel disease. Gut 1992;33:933-7.
Olson AD, Ayass M, Chensue S. Tumor necrosis factor and IL-1 beta expression in pediatric patients with inflammatory bowel disease. J Pediatr Gastroenterol Nutr 1993;16:241-6.
Funakoshi K, Sugimura K, Sasakawa T, et al. Study of cytokines in ulcerative colitis. J Gastroenterol 1995;30(Suppl 8):61-3.
Kumon Y, Nakauchi Y, Suehiro T, et al. Proinflammatory cytokines but not acute phase serum amyloid A or C-reactive protein, downregulate paraoxonase 1 (PON1) expression by Hep G2 cells. Amyloid 2002;9:160-4.
Van Lenten BJ, Hama SY, de Beer FC, et al. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest 1995;96:2758-67.