The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis

被引:18
作者
Urano, W
Yamanaka, H
Tsutani, H
Nakajima, H
Matsuda, Y
Taniguchi, A
Hara, M
Kamatani, N
机构
[1] Tokyo Womens Med Univ, Inst Rheumatol, Shinjuku Ku, Tokyo 1620054, Japan
[2] Fukui Med Univ, Dept Internal Med 1, Fukui, Japan
关键词
gouty arthritis; interleukin; 6; C-reactive protein; cortisol; uric acid; uricosuric;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
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.
引用
收藏
页码:1950 / 1953
页数:4
相关论文
共 27 条
[1]
COMPARISON OF PARENTERAL ADRENOCORTICOTROPIC HORMONE WITH ORAL INDOMETHACIN IN THE TREATMENT OF ACUTE GOUT [J].
AXELROD, D ;
PRESTON, S .
ARTHRITIS AND RHEUMATISM, 1988, 31 (06) :803-805
[2]
BROZIK M, 1992, J RHEUMATOL, V19, P63
[3]
Campion E W, 1987, Am J Med, V82, P421, DOI 10.1016/0002-9343(87)90441-4
[4]
AUGMENTED EXPRESSION OF INTERLEUKIN-6 AND INTERLEUKIN-1 GENES IN THE MESANGIUM OF IGM MESANGIAL NEPHROPATHY [J].
CHEN, WP ;
LIN, CY .
NEPHRON, 1994, 68 (01) :10-19
[5]
Desgeorges A, 1997, J RHEUMATOL, V24, P1510
[6]
Cytokine activation of the HPA axis [J].
Dunn, AJ .
NEUROIMMUNOMODULATION: PERSPECTIVES AT THE NEW MILLENNIUM, 2000, 917 :608-617
[7]
EDWARDS NL, 1997, PRIMER RHEUMATIC DIS, P234
[8]
INFLAMMATORY MICROCRYSTALS STIMULATE INTERLEUKIN-6 PRODUCTION AND SECRETION BY HUMAN-MONOCYTES AND SYNOVIOCYTES [J].
GUERNE, PA ;
TERKELTAUB, R ;
ZURAW, B ;
LOTZ, M .
ARTHRITIS AND RHEUMATISM, 1989, 32 (11) :1443-1452
[9]
INTERLEUKIN-6 AND THE ACUTE PHASE RESPONSE [J].
HEINRICH, PC ;
CASTELL, JV ;
ANDUS, T .
BIOCHEMICAL JOURNAL, 1990, 265 (03) :621-636
[10]
INTERLEUKIN-6 IN SYNOVIAL-FLUID AND SERUM OF PATIENTS WITH RHEUMATOID-ARTHRITIS AND OTHER INFLAMMATORY ARTHRITIDES [J].
HOUSSIAU, FA ;
DEVOGELAER, JP ;
VANDAMME, J ;
DEDEUXCHAISNES, CN ;
VANSNICK, J .
ARTHRITIS AND RHEUMATISM, 1988, 31 (06) :784-788