TY - JOUR
T1 - Uric acid-lowering treatment with benzbromarone in patients with heart failure a double-blind placebo-controlled crossover preliminary study
AU - Ogino, Kazuhide
AU - Kato, Masahiko
AU - Furuse, Yoshiyuki
AU - Kinugasa, Yoshiharu
AU - Ishida, Katsunori
AU - Osaki, Shuichi
AU - Kinugawa, Toru
AU - Igawa, Osamu
AU - Hisatome, Ichiro
AU - Shigemasa, Chiaki
AU - Anker, Stefan D.
AU - Doehner, Wolfram
PY - 2010/1
Y1 - 2010/1
N2 - Background-Hyperuricemia is common in chronic heart failure (CHF), and it is a strong independent marker of prognosis. Upregulated xanthine oxidase (XO) activity and impaired renal excretion have been shown to account for increased serum uric acid (UA) levels in CHF. Therapeutic interventions with allopurinol to reduce UA levels by XO inhibition have been shown to be beneficial. Discussions are ongoing whether UA itself is actively involved or it is a mere marker of upregulated XO activity within CHF pathophysiology. Therefore, the aim of this study was to test the effect of lowering UA by uricosuric treatment without XO inhibition on hemodynamic and metabolic characteristics of CHF. Impaired renal excretion of UA was taken into account. Methods and Results-Serum UA (SUA), urinary UA (uUA) excretion, and renal clearance test for UA (Cl UA) were measured in 82 patients with CHF. SUA was significantly increased compared with controls of similar age (control, 5.45 ±0.70 mg/dL; New York Heart Association I, 6.48±1.70 mg/dL; New York Heart Association II, 7.34±1.94 mg/dL; New York Heart Association III, 7.61 ±2.11 mg/dL; PUA. On multivariate analysis, insulin, brain natriuretic peptide (P
AB - Background-Hyperuricemia is common in chronic heart failure (CHF), and it is a strong independent marker of prognosis. Upregulated xanthine oxidase (XO) activity and impaired renal excretion have been shown to account for increased serum uric acid (UA) levels in CHF. Therapeutic interventions with allopurinol to reduce UA levels by XO inhibition have been shown to be beneficial. Discussions are ongoing whether UA itself is actively involved or it is a mere marker of upregulated XO activity within CHF pathophysiology. Therefore, the aim of this study was to test the effect of lowering UA by uricosuric treatment without XO inhibition on hemodynamic and metabolic characteristics of CHF. Impaired renal excretion of UA was taken into account. Methods and Results-Serum UA (SUA), urinary UA (uUA) excretion, and renal clearance test for UA (Cl UA) were measured in 82 patients with CHF. SUA was significantly increased compared with controls of similar age (control, 5.45 ±0.70 mg/dL; New York Heart Association I, 6.48±1.70 mg/dL; New York Heart Association II, 7.34±1.94 mg/dL; New York Heart Association III, 7.61 ±2.11 mg/dL; PUA. On multivariate analysis, insulin, brain natriuretic peptide (P
KW - Benzbromarone
KW - Chronic heart failure
KW - Insulin sensitivity
KW - Uric acid
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U2 - 10.1161/CIRCHEARTFAILURE.109.868604
DO - 10.1161/CIRCHEARTFAILURE.109.868604
M3 - Article
C2 - 19933411
AN - SCOPUS:76549098607
VL - 3
SP - 73
EP - 81
JO - Circulation: Heart Failure
JF - Circulation: Heart Failure
SN - 1941-3297
IS - 1
ER -