Journals / Çocuk Dergisi / 2006 / Cilt: 6 - Sayı: 2

Oxidant and antioxidant system evaluation in children with juvenile rheumatoid arthritis, receiving non-steroidal antiinflammatory drugs

Nonsteroid antiinflamatuvar ilaç kullanan jüvenil romatoid artritli hastalarda oksidan ve antioksidan sistemlerinin değerlendirilmesi

Pages
128–133
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The reason of this decrease OFR in these children may chronically used NSAID which blocked siklooxygenase enzyme.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background: Juvenile rheumatoid arthritis (JRA) is the most commonly diagnosed rheumatic disease in children which has exceedingly complex etiology.
📊
Key Findings & Data:Oxidative free radicals (OFR) production at inflammation sites contributes to tissue damage and may also play a significant role in the pathogenesis of JRA.
💡
Conclusion & Impact:The reason of this decrease OFR in these children may chronically used NSAID which blocked siklooxygenase enzyme.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Anti-enflamatuvar ajanlar · steroid olmayan · Antioksidanlar

Abstract

Background: Juvenile rheumatoid arthritis (JRA) is the most commonly diagnosed rheumatic disease in children which has exceedingly complex etiology. Oxidative free radicals (OFR) production at inflammation sites contributes to tissue damage and may also play a significant role in the pathogenesis of JRA. The aim of this study was to measure OFR indirectly by using biochemical assays in JRA children, receiving only non-steroidal anti-inflammatory drugs (NSAID). Material and Methods: Twenty JRA children, receiving NSAID and 20 healthy controls were included for the study. Superoksit dismutase (SOD), glutatyon peroxidase (GPx), malondialdehyde (MDA), vitamin E, total sulphidril (T-SH) and erythrocyte dephormability assays were measured. Results: SOD activity was not found to be different between patients and controls. Serum GPx, MDA, T-SH concentrations and erythrocyte dephormability index in patients were significantly lower than in healthy controls (p<0.01), whereas, plasma vitamin E concentrations of patients were found to be higher than those in controls (p<0.01). Discussion: This study showed that OFR did not increase, even slightly decrease in JRA children, receiving NSAID. The reason of this decrease OFR in these children may chronically used NSAID which blocked siklooxygenase enzyme.

Özet

Giriş: Jüvenil romatoid artrit (JRA) çocukluk çağının en sık görülen, etyolojisi oldukça karmaşık olan romatolojik hastalığıdır. İnflamasyondaki doku hasarına katkıda bulunan serbest oksijen radikalleri (SOD) JRA etyopatogenezinde de önemli rol oynayabilir. Bu çalışmanın amacı non-steroidal antiinflamatuar ilaç (NSAİİ) tedavisi alan JRA’lı çocuklarda, SOD’u indirekt olarak gösteren biyokimyasal parametrelerin değerlendirilmesidir. Yöntem ve Gereçler: Çalışma JRA nedeniyle sadece NSAİİ alan 20 hasta ile aynı yaş grubundaki 20 sağlıklı çocukta yapılmıştır. Hasta ve kontrol grubunda süperoksit dismutaz (SOD), glutatyon peroksidaz (GPx), malondialdehit (MDA), Vitamin E, total sulfidril (T-SH) ve eritrosit deformabilitesi ölçülmüştür. Sonuçlar: Ortalama SOD aktivitesi, gruplar arasında istatistiksel olarak anlamlı bir fark göstermedi (p>0.05). Ortalama GSH, MDA, T-SH ve eritrosit deformibilitesi düzeyleri JRA’lı hastalarda daha düşük idi ve aradaki fark istatistiksel olarak anlamlı bulundu (p<0.01). Ortalama E vitamini düzeyi JRA’lı hastalarda daha yüksekti ve aradaki fark istatistiksel olarak anlamlı bulundu (p<0.01). Tartışma: Bu çalışma JRA’lı NSAİİ kullanan hastalarda SOR artışı olmadığı, hatta kontrol grubuna oranla baskılanmış olduğunu göstermektedir. Bu baskılanmanın nedeni tüm hastaların siklooksijenazı inhibe ederek SOR yapımını azaltan kronik NSAİİ kullanmaları olabilir.

🔖

Cite This Article

PUNAR, Ş. J., ÖMEROĞLU, E. R., ÖNER, N., NİŞLİ, K., AYDIN, Z., TELCİ, A. (2006). Oxidant and antioxidant system evaluation in children with juvenile rheumatoid arthritis, receiving non-steroidal antiinflammatory drugs. Çocuk Dergisi, Cilt: 6 - Sayı: 2, 128–133. https://ajindex.com/articles/213500

References (15)

  1. Cassidy TJ, Patty RE. Juvenile rheumatoid arthritis. In: Textbook of Pediatric Rheumatology. Third ed. Philadelphia: WB Saunders, 1995: 133-23. 2.Jones OY, Spencer CH, Bowyer SL, Dent PB, Gottlieb BS, Rabinovich CE. A multicenter case-control study on predictive factors distinguishing childhood leukemia from juvenile rheumatoid arthritis. Pediatrics 2000
  2. Hsu CT, Lin YT, Yang YH, Chiang BL. Factors affecting clinical and therapeutic outcomes of patients with juvenile rheumatoid arthritis. Scand J Rheumatol 2004
  3. Schneider R, Passo MH. Juvenile rheumatoid arthritis. Rheum Dis Clin North Am 2002
  4. Ramos VA, Ramos PA, Dominguez MC. Role of oxidative stress in the maintenance of inflamation in patients with juvenile rheumatoid arthritis. J Pediatr (Rio J) 2000
  5. Araujo V, Arnal C, Boronat M, Ruiz E, Dominguez C. Oxidant-antioxidant imbalance in blood of children with juvenile rheumatoid arthritis. Biofactors 1998
  6. Southorn PA, Powis G. Free radicals medicine II: Involvement in human disease. Mayo Clin Proc 1988
  7. Lunec J, Halloran SP, White AG, et al. Free radical oxidation (peroxidation) products in serum and sinovial fluid in rheumatoid artritis. J Rheumatol 1981
  8. Southorn PA, Powis G. Free radicals in medicine I: Chemical nature and biologic reactions. Mayo Clin Proc 1988
  9. Greenwald A. Oxygen radicals, inflammations and arthritis: Pathophysiological considerations and implications for treatment. Semin Arthritis Rheum 1991
  10. Halliwell B. Oxygen radicals, nitric oxide and human infla-matory joint disease. Ann Rheum Dis 1995
  11. Halliwell B, Gutteridge JMC. Oxygen toxicity, oxygen radicals, transitional metals and disease. Biochem J 1984
  12. Kehrer JP. Free radicals as mediators of tissue injury and disease. Crit Rev Toxicol 1993
  13. Igari T, Kaneda H, Horiuchi S, et al. A remarkable increase of superoxide dismutase activity in sinovial fluid of patients with rheumatoid arthritis. Clin Orthopaedics 1982
  14. Marklund SL, Bjelle A, Elmqvist LG. Superoxide dismutase isoenzymes of the sinovial fluid in the rheumatoid arthritis and reactive arthritis. Ann Rheum Dis 1986
  15. Sklowska M, Gromadzinska J, Biernacka M, et al. Vitamin E, thiobarbituric acid reactive substance concentrations and superoxide dismutase activity in the blood of children with juvenile rheumatoid arthritis. Clin Exp Rheumatol 19