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Abstract

Background. Rugerio et al 2006 reported that there were a positive correlation between the level of hyperuricemia and the level of IL-1β, IL-6, and TNF-α pro infl ammatory cytokines value. On the other hand, Choi et al reported a negative correlation between hyperuricemia and the level of pro infl ammatory cytokine in the late phase of hyperuricemia.

Methods. Venous blood samples were collected and stored at a temperature of - 80oC from in- and outpatients with hyperuricemia with age of more than 17
years old at Dr. Kariadi Hospital, Semarang. The level of uric acids (mg/dl) were examined with enzymatic colorimetric technique (Roche Diagnostics) whereas
the levels of IL-1β, IL-6, and TNF-α pro infl ammatory cytokines (pg/ml) were examined with enzyme linked immunosorbent assay (ELISA) technique using ultra
sensitive commercial kit (Human ultra sensitive, Biosource International Inc Europe), and ELX 800, 2002 machine. The normality of the data was tested with
One-Sample Kolmogorov-Smirnov technique and the correlation was tested with Spearman correlation (data with abnormal distribution) or Pearson correlation (data
with normal distribution).

Results. There was a weak positive correlation between the level of hyperuricemia and the level of IL-1 β cytokine in Spearman correlation test with r value = 0.246 and p value > 0.05 in Spearman correlation test. On the other hand, there was a weak negative correlation between the level of hyperuricemia and the level of TNF-α cytokine with r value = - 0.096 and p value > 0.05. There was also weak negative correlation between the level of hyperuricemia and the level of IL-6 cytokine with r value = - 0.072 and p value > 0.05 in Pearson correlation test.

Conclusion. There was a weak positive correlation but not sifnificant between the level of hyperuricemia and the level of IL-1β.

Article Details

How to Cite
Hadi, S., Sudarsono, D., & Suntoko, B. (2018). Hyperuricemia and Pro Inflammatory Cytokine (IL-1β, IL-6, and TNF-α). Indonesian Journal of Rheumatology, 1(2). https://doi.org/10.37275/ijr.v2i1.21

References

  1. Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern
  2. Med 2005;143:499-516.
  3. Ruggerio C, Cherubini A, Ble A, Bos AJG, Maggio M, Dixit VD, et al. Uric acid and infl ammatory markers. European Heart Journal 2006; 27: 1174-81.
  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. Dalbeth N, Haskard DO. Mechanisms of infl ammation in gout. Rheumatology 2005; 44(9): 1090-6.
  6. Chen CJ, Shi Y, Hearn A, Fitzgerald K, Golenbock D, Reed G, et
  7. al. MyD88-dependent IL-1 receptor signaling is essential for gouty
  8. infl ammation stimulated by monosodium urate crystals. J Clin Invest
  9. ;116(8):2262-71.
  10. Brockopp DY, Hastings-Tolsma M, Tolsma-Hastings MT. Fundamentals
  11. of nursing research. Trans Asih Y, Maryunani A. Jakarta: EGC; 1995. p. 181-97.
  12. Johnson AG. Statistics. San Diego: Harcourt Brace Jovanovich; 1988.
  13. p. 352-60.
  14. Terketaub R. Update on crystal induced arthritis and hyperuricemia.
  15. Proceeding of the American College of Rheumatology 71st Annual
  16. Meeting; 2007. p. 1 – 6.