Association between serum uric acid and inflammation markers in ankylosing spondylitis patients treated with tumor necrosis factor-α or nonsteroidal anti-inflammatory drugs

Objectives: Uric acid has an important role in the production of various inflammatory cytokines such as tumor necrosis factor-α (TNF-α). Although serum uric acid levels in various rheumatic diseases have been performed the relationships between serum uric acid levels with inflammatory markers and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores in ankylosing spondylitis patients treated with anti-TNF-α and nonsteroid anti-inflammatory drugs (NSAIDs) have not been described yet. The aim of this study was to compare the relationships between serum uric acid levels, inflammatory markers and BASDAI scores in ankylosing spondylitis patients treated anti-TNF-α and NSAIDs. Methods: A total of 132 ankylosing spondylitis patients fulfilling the 1984 Modified New York Criteria who had serum uric acid, erythrocyte sedimentation rate and C-reactive protein levels in medical records were included in this retrospective cross-sectional study. Patients were divided in two groups (anti-TNF-α and NSAIDs). Their files were examined in detail. Later demographic and laboratory features were recorded to the research form. Results: Serum uric acid levels were significantly lower in the anti-TNF-α group (mean: 4.9 mg/dL, range: 4.10-5.45 mg/dL) than in the NSAIDs group (mean: 5.20 mg/dL, range 4.70-5.90 mg/dL) (p = 0.021). Also, positive correlations were found between C-reactive protein (p = 0.003) and BASDAI (p = 0.009) with serum uric acid. Conclusions: According to this  study, we can consider that serum uric acid level could be used as an inflammatory laboratory marker, such as C-reactive protein in ankylosing spondylitis patients. However, we believe that more studies are needed about this research. 

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  • [1] Reveille JD, Weisman MH. The epidemiology of back pain, axial spondyloarthritis and HLA-B27 in the United States. Am J Med Sci 2013;345:431-6.
  • [2] Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med 2005;143: 499-516.
  • [3] Kanellis J, Watanabe S, Li JH, Kang DH, Li P, Nakagawa T, et al. Uric acid stimulate monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2. Hypertension 2003;41:1287-93.
  • [4] Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension 2003;41:1183-90.
  • [5] Oeckinghaus A, Ghosh S. The NF-kappaB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol 2009;1:a000034.
  • [6] Choe JY, Kim SK. Association between serum uric acid and inflammation in rheumatoid arthritis: perspective on lowering serum uric acid of leflunomide. Clin Chim Acta 2015;438:29-34.
  • [7] Sheikh M, Movassaghi S, Khaledi M, Moghaddassi M. Hyperuricemia in systemic lupus erythematosus: is it associated with the neuropsychiatric manifestations of the disease? Rev Bras Reumatol Engl Ed 2016;56:471-77.
  • [8] Prasad PV, Bikku B, Kaviarasan PK, Senthilnathan A. A clinical study of psoriatic arthropathy. Indian J Dermatol Venereol Leprol 2007;73:166-70.
  • [9] Kwon HH, Kwon IH, Choi JW, Youn JI. Cross-sectional study on the correlation of serum uric acid with disease severity in Korean patients with psoriasis. Clin Exp Dermatol 2011;36:473-8.
  • [10] Gisondi P, Targher G, Cagalli A, Girolomoni G. Hyperuricemia in patients with chronic plaque psoriasis. J Am Acad Dermatol 2014;70:127-30.
  • [11] Li X, Miao X, Wang H, Wang Y, Li F, Yang Q, et al. Association of serum uric acid levels in psoriasis: a systematic review and meta-analysis. Medicine (Baltimore) 2016;95:e3676.
  • [12] Kanellis J, Kang DH. Uric acid as a mediator of endothelial dysfunction, inflammation, and vascular disease. Semin Nephrol 2005;25:39-42.
  • [13] Isha VK, Lal JH. C-reactive protein and uric Acid levels in patients with psoriasis. Ind J Clin Biochem 2011;26:309-11.
  • [14] Lyngdoh T, Marques-Vidal P, Paccaud F, Preisig M, Waeber G, Bochud M, et al. Elevated serum uric acid is associated with high circulating inflammatory cytokines in the population-based Colaus study. PLoS One 2011;6:e19901.
  • [15] Jiménez Balderas FJ, Robles EJ, Juan L, Badui E, Arellano H, Espinosa Said L, et al. Purine metabolism in ankylosing spondylitis: clinical study. Arch Invest Med (Mex) 1989;20:163-70.
  • [16] Van Leeuwen AM, Bladh ML. Davis's Comprehensive Handbook of Laboratory and Diagnostic Tests with Nursing Implications. 6th ed. Philadelphia, PA: PA. Davis Company, 2015., p.329.
  • [17] Nashel DJ, Petrone DL, Ulmer CC, Sliwinski AJ. C-reactive protein: a marker for disease activity in ankylosing spondylitis and Reiter's syndrome. J Rheumatol 1986;13:364-7.
  • [18] Benhamou M, Gossec L, Dougados M. Clinical relevance of C-reactive protein in ankylosing spondylitis and evaluation of the NSAIDs/coxibs' treatment effect on C-reactive protein. Rheumatology (Oxford) 2010;49:536-41.
  • [19] Siebuhr AS, Bay-Jensen AC, Karsdal MA, Lories RJ, de Vlam K. CRP and a biomarker of type I collagen degradation, C1M, can differentiate anti inflammatory treatment response in ankylosing spondylitis. Biomark Med 2016;10:197-208.