Journals / Turkish Journal of Rheumatology(.)Archives of Rheumatology / 2012 / Cilt: 27 - Sayı: 3

Çinlilerde Plazma Homosistein Düzeyleri ve Metilentetrahidrofolat Redüktaz C677T Gen Polimorfizminin Ankilozan Spondilit ile İlişkisi

The Relationship of Plasma Homocysteine Levels and the Methylenetetrahydrofolate Reductase C677T Gene Polymorphism to Ankylosing Spondylitis in a Chinese Population

Pages
174–178
DOI
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Conclusion: Our study result showed that the plasma Hcy levels were significantly increased in patients with AS, and the MTHFR T/T genotype mutation was an important influential mechanism which precipitated hyperhomocysteinemia and might be related to AS

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Objective & Hypothesis:The aim of this study was to investigate the relationship of both the plasma homocysteine (Hcy) level and N5,N10-methylenetetrahydrofolate reductase (MTFHR) gene polymorphism with ankylosing spondylitis (AS).
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Key Findings & Data:Patients and methods: Two hundred Chinese patients with AS and 120 healthy controls were included.
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Conclusion & Impact:Conclusion: Our study result showed that the plasma Hcy levels were significantly increased in patients with AS, and the MTHFR T/T genotype mutation was an important influential mechanism which precipitated hyperhomocysteinemia and might be related to AS
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

The aim of this study was to investigate the relationship of both the plasma homocysteine (Hcy) level and N5,N10-methylenetetrahydrofolate reductase (MTFHR) gene polymorphism with ankylosing spondylitis (AS). Patients and methods: Two hundred Chinese patients with AS and 120 healthy controls were included. The plasma Hcy level was examined by enzyme-linked immunosorbent assay (ELISA), while the MTHFR gene polymorphism was analyzed by the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: The two groups were examined according to age, and no statistically significant differences were found. The plasma Hcy level in the AS group was significantly higher than the control group (t=24.402, p=0.000). The ratio of the T/T genotype mutation was different in the AS group and the control group (X2=9.874, p=0.002) There was no marked difference in the frequencies of the MTHFR C/C, or C/T genotype between the two groups. The plasma Hcy level of the T/T genotype was significantly higher than that of the C/T or C/C genotype in the AS group (q=6.496, p<0.01; q=12.088, p<0.01). Conclusion: Our study result showed that the plasma Hcy levels were significantly increased in patients with AS, and the MTHFR T/T genotype mutation was an important influential mechanism which precipitated hyperhomocysteinemia and might be related to AS

Özet

Bu çalışmada hem plazma homosistein düzeyi (Hcy) hem de N5,N10-metilentetrahidrofolat redüktaz (MTFHR) gen polimorfizminin ankilozan spondilit (AS) ile olan ilişkisi değerlendirildi.Hastalar ve yöntemler: Çalışmaya 200 Çinli AS hastası ve 120 sağlıklı kontrol dahil edildi. Plazma Hcy düzeyi enzim bağlı immünosorbent assay (ELISA) ile muayene edildi, MTHFR gen polimorfizmi ise polimeraz zincir reaksiyonu (PCR) ve restriksiyon fragment uzunluk polimorfizmi (RFLP) ile analiz edildi.Bulgular: İki grup da yaşa göre değerlendirildi ve gruplar arasında istatistiksel açıdan anlamlı bir farka rastlanmadı. AS grubunda plazma Hcy düzeyi, kontrol grubuna kıyasla anlamlı düzeyde daha yüksekti (t=24.402, p=0.000). T/T genotip mutasyon oranı, AS grubunda ve kontrol grubunda farklıydı (X2=9.874, p=0.002). İki grup arasında MTHFR C/C, C/T genotip sıklığı açısından belirgin bir fark yoktu. AS grubunda T/T genotipin plazma Hcy düzeyi, C/T veya C/C genotipine kıyasla, anlamlı düzeyde daha yüksekti (q=6.496, p<0.01; q=12.088, p<0.01).Sonuç: Çalışma bulguları, plazma Hcy düzeylerinin AS hastalarında anlamlı düzeyde arttığını ve hiperhomosisteinemiye zemin hazırlayan ve AS ile ilişkili olabilen MTHFR T/T genotip mutasyonu açısından önemli bir etki mekanizması olduğunu gösterdi

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Cite This Article

MAO, N., CHEN, J., PENG, W., CHEN, L., XIE, X. (2012). Çinlilerde Plazma Homosistein Düzeyleri ve Metilentetrahidrofolat Redüktaz C677T Gen Polimorfizminin Ankilozan Spondilit ile İlişkisi. Turkish Journal of Rheumatology(.)Archives of Rheumatology, Cilt: 27 - Sayı: 3, 174–178. https://ajindex.com/articles/375964

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References (9)

  1. Lazzerini PE, Capecchi PL, Selvi E, Lorenzini S, Bisogno S, Galeazzi M, et al. Hyperhomocysteinemia, inflammation and autoimmunity. Autoimmun Rev 2007;6:503-9.
  2. Liu CC, Ou TT, Wu CC, Li RN, Lin YC, Lin CH, et al. Global DNA methylation, DNMT1, and MBD2 in patients with systemic lupus erythematosus. Lupus 2011;20:131-6.
  3. David R, Mellissa M. Epigenetics and human disease: translating basic biology 11 into clinical applications. CMAJ, 2006;1:341-8. Vayá A, Santaolaria M, Micó L, Calvo J, Oropesa R, Villa P, et al. Thrombotic events in systemic lupus erythematosus. Its association with acquired and inherited thrombophilic defects. Clin Hemorheol Microcirc 2008;40:79-87.
  4. Kartal Durmazlar SP, Akgul A, Eskioglu F. Homocysteine may involve in the pathogenesis of Behcet's disease by inducing inflammation. Mediators Inflamm 2008;2008:407972. Kutilek S, Nemec V, Bockayova E. Elevated serum homocysteine levels in paediatric patients with primary Raynaud's phenomenon. Rev Bras Reumatol 2012;52:128- 30. [Abstract] Xu XY, Zhou WH, Xiao CS, Li XF, Wang LY. A clinical study of hyperhomocysteinemia in rheumatological diseases. Zhonghua Nei Ke Za Zhi 2005;44:111-4. [Abstract] Başkan BM, Sivas F, Aktekin LA, Doğan YP, Ozoran K, Bodur H. Serum homocysteine level in patients with ankylosing spondylitis. Rheumatol Int 2009;29:1435-9.
  5. Gonzalez-Lopez L, Sanchez-Hernandez JD, Aguilar- Chavez EA, Cota-Sanchez AR, Lopez-Olivo MA, Villa- Manzano AI, et al. Hyperhomocysteinemia in ankylosing spondylitis: prevalence and association with clinical variables. Rheumatol Int 2008;28:1223-8.
  6. Capkin E, Karkucak M, Akyüz A, Alver A, Turkyilmaz AK, Zengin E. The relationship between plasma homocysteine level and different treatment modalities in patients with ankylosing spondylitis. Rheumatol Int 2011. [Epub ahead of print] Wei JC, Jan MS, Yu CT, Huang YC, Yang CC, Tsou HK, et al. Plasma homocysteine status in patients with ankylosing spondylitis. Clin Rheumatol 2007;26:739-42.
  7. Schroecksnadel K, Frick B, Wirleitner B, Winkler C, Schennach H, Fuchs D. Moderate hyperhomocysteinemia and immune activation. Curr Pharm Biotechnol 2004;5:107-18.
  8. Holm PI, Hustad S, Ueland PM, Vollset SE, Grotmol T, Schneede J. Modulation of the homocysteine-betaine relationship by methylenetetrahydrofolate reductase 677 C->t genotypes and B-vitamin status in a large- scale epidemiological study. J Clin Endocrinol Metab 2007;92:1535-41.
  9. Koubaa N, Hammami S, Nakbi A, Ben Hamda K, Mah