title: The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis.
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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: The Institute of Rheumatology, Tokyo Women's Medical University, Japan. wako@ior.twmu.ac.jp
authors.forename: Wako
authors.initials: W
authors.lastname: Urano
authors.forename: Hisashi
authors.initials: H
authors.lastname: Yamanaka
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsutani
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakajima
authors.forename: Yuko
authors.initials: Y
authors.lastname: Matsuda
authors.forename: Atsuo
authors.initials: A
authors.lastname: Taniguchi
authors.forename: Masako
authors.initials: M
authors.lastname: Hara
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Kamatani
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015210:Arthritis, Gouty / Q000097:blood* / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D018836:Inflammation Mediators / Q000032:analysis*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011336:Probability; D011379:Prognosis; D012189:Retrospective Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D014527:Uric Acid / Q000097:blood / Q000378:metabolism*
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D014527:Uric Acid; D002097:C-Reactive Protein; D006854:Hydrocortisone