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The Inflammatory Process in the Mechanism of Decreased Serum Uric Acid Concentrations During Acute Gouty Arthritis

WAKO URANO, HISASHI YAMANAKA, HIROSHI TSUTANI, HIROSHI NAKAJIMA, YUKO MATSUDA, ATSUO TANIGUCHI, MASAKO HARA, and NAOYUKI KAMATANI

ABSTRACT.

Objective. To clarify the mechanism of decreased serum uric acid (SUA) concentrations during acute gouty arthritis.

Methods. Data from patients with acute gouty arthritis during and after an attack were investigated retrospectively. Other investigations, including changes in urinary excretion and biochemical markers, were performed prospectively.

Results. SUA was significantly lower in the acute phase (7.5 ± 1.4 mg/dl) than in the intercritical phase (8.5 ± 0.9 mg/dl) (p < 0.0001). During the acute gout phase, a normal SUA level was found in 20 of 41 patients (49%). C-reactive protein (CRP) during acute attacks was significantly correlated with plasma interleukin 6 (IL-6) and cortisol (r = 0.645, p < 0.005; r = 0.460, p < 0.05). Percentage change in SUA at onset of attack correlated with CRP and IL-6 (r = 0.762, p < 0.0001; r = 0.630, p < 0.005), as well as with increased urinary excretion of uric acid, estimated by percentage change in fractional excretion of uric acid (FEua) during attack (r = 0.447, p < 0.05). Further, change in FEua was correlated with plasma cortisol levels during the acute attack (r = 0.534, p < 0.05).

Conclusion. Decrease in SUA during acute gouty arthritis is associated with increased urinary excretion of uric acid; an inflammatory process may play a role in the mechanism. (J Rheumatol 2002;29:1950-3)

Key Indexing Terms:

GOUTY ARTHRITIS
INTERLEUKIN 6
C-REACTIVE PROTEIN
CORTISOL
URIC ACID
URICOSURIC


From the Institute of Rheumatology, Tokyo Women's Medical University, Tokyo, and First Department of Internal Medicine, Fukui Medical University, Fukui, Japan.

W. Urano, MD, Research Associate; H. Yamanaka, MD, PhD, Associate Professor, Institute of Rheumatology, Tokyo Women's Medical University; H. Tsutani, MD, PhD, First Department of Internal Medicine, Fukui Medical University; H. Nakajima, MD, Research Associate; Y. Matsuda, MD, PhD, Research Associate; A. Taniguchi, MD, PhD, Assistant Professor; M. Hara, MD, PhD, Professor; N. Kamatani, MD, PhD, Director and Professor, Institute of Rheumatology, Tokyo Women's Medical University.

Address reprint requests to Dr. W. Urano, Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku-ku, Tokyo 162-0054, Japan. E-mail: wako@ior.twmu.ac.jp

Submitted August 7, 2001; revision accepted February 15, 2002.




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