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Background: Non-rheumatologists are often not aware that the serum urate (SU) may be normal during acute episodes of gout. Even rheumatologists may consider it unusual. It has been suggested that SU is often normal during acute gout 1,2.
Objectives: To study the frequency of normal SU levels during an acute gouty attack in the largest studies of acute gout treatment to date.
Methods: Data collected at days 2, 5, and 8 from 2 randomized, active-comparator-controlled clinical trials to assess the efficacy of etoricoxib or indomethacin for 7 days in acute gout 3,4 were used to assess SU levels during acute attacks. Efficacy was similar with both agents so both groups were combined for analysis. Analyses were performed overall and among subgroups (concurrent allopurinol use, gender, race, monoarticular or polyarticular attack, number and frequency of prior gout attacks). A change of 1 mg/dL in SU was considered a meaningful increase or decrease.
Results: A total of 339 patients were enrolled in the 2 studies. Mean (SD) age was 50.5 (13.0). A SU ≤ 8 mg/dl was observed in 32% (n=102) of patients; (49% (n=27) of patients on allopurinol vs. 29% (n=82) of those not on allopurinol (p<0.0001). A SU ≤ 6mg/dl was observed in 11% (n=32) of patients; 29% (n=16) of patients on allopurinol vs. 11% (n=32) of those not on allopurinol. At baseline mean SU was 7.6 vs. 8.5 mg/dL (p=0.076) in allopurinol users vs. non-users, respectively. On day 8 (following treatment) mean SU was 7.4 vs. 8.7 mg/dL (p<0.001), respectively. At baseline, significant differences (p<0.05) in SU values were observed according to frequency of prior gouty attacks per year (1-3 vs. >4 per year; mean SU 8.3 vs. 9.4 mg/dl respectively) but not according to other baseline characteristics. At day 8, significant differences (p<0.05) in SU values were observed) according to the frequency of prior gouty attacks per year (8.6 vs. 9.6 mg/dl, respectively) and according to attack type (monoarticular vs. or polyarticular; mean SU 8.4 vs. 9.0 mg/dl, respectively). Patients on chronic allopurinol treatment were more likely to have lower SU at baseline (p<0.001) during the acute attack. Patients with >4 gouty attacks per year and polyarticular attacks were found to have higher SU during attacks p<0.05).
Conclusion: In the largest studies of acute gouty arthritis to date, 49% of patients had SU ≤8mg/dl and 11% of patients had a SU ≤ 6mg/dl during their acute attack. Attacks still occurred despite SU levels being below 6.8mg/dl, the saturation level for urate. This may be attributed to persistence of tophi and an increased body uric acid pool. Additional studies are needed to further understand the correlation between SU and the body uric acid pool as well as the relationship to timing of changes during acute gout.
References: 1 J Rheumatol 1997;24:2265 2 J Rheumatol 2002;29:1950 3 Arthritis Rheum 2004;50:5986 4 BMJ 2002;324:1488
Objectives: To study the frequency of normal SU levels during an acute gouty attack in the largest studies of acute gout treatment to date.
Methods: Data collected at days 2, 5, and 8 from 2 randomized, active-comparator-controlled clinical trials to assess the efficacy of etoricoxib or indomethacin for 7 days in acute gout 3,4 were used to assess SU levels during acute attacks. Efficacy was similar with both agents so both groups were combined for analysis. Analyses were performed overall and among subgroups (concurrent allopurinol use, gender, race, monoarticular or polyarticular attack, number and frequency of prior gout attacks). A change of 1 mg/dL in SU was considered a meaningful increase or decrease.
Results: A total of 339 patients were enrolled in the 2 studies. Mean (SD) age was 50.5 (13.0). A SU ≤ 8 mg/dl was observed in 32% (n=102) of patients; (49% (n=27) of patients on allopurinol vs. 29% (n=82) of those not on allopurinol (p<0.0001). A SU ≤ 6mg/dl was observed in 11% (n=32) of patients; 29% (n=16) of patients on allopurinol vs. 11% (n=32) of those not on allopurinol. At baseline mean SU was 7.6 vs. 8.5 mg/dL (p=0.076) in allopurinol users vs. non-users, respectively. On day 8 (following treatment) mean SU was 7.4 vs. 8.7 mg/dL (p<0.001), respectively. At baseline, significant differences (p<0.05) in SU values were observed according to frequency of prior gouty attacks per year (1-3 vs. >4 per year; mean SU 8.3 vs. 9.4 mg/dl respectively) but not according to other baseline characteristics. At day 8, significant differences (p<0.05) in SU values were observed) according to the frequency of prior gouty attacks per year (8.6 vs. 9.6 mg/dl, respectively) and according to attack type (monoarticular vs. or polyarticular; mean SU 8.4 vs. 9.0 mg/dl, respectively). Patients on chronic allopurinol treatment were more likely to have lower SU at baseline (p<0.001) during the acute attack. Patients with >4 gouty attacks per year and polyarticular attacks were found to have higher SU during attacks p<0.05).
Conclusion: In the largest studies of acute gouty arthritis to date, 49% of patients had SU ≤8mg/dl and 11% of patients had a SU ≤ 6mg/dl during their acute attack. Attacks still occurred despite SU levels being below 6.8mg/dl, the saturation level for urate. This may be attributed to persistence of tophi and an increased body uric acid pool. Additional studies are needed to further understand the correlation between SU and the body uric acid pool as well as the relationship to timing of changes during acute gout.
References: 1 J Rheumatol 1997;24:2265 2 J Rheumatol 2002;29:1950 3 Arthritis Rheum 2004;50:5986 4 BMJ 2002;324:1488
N. Schlesinger, None; J.M. Norquist, Merck, 1; J.A. Boice, Merck, 1; D.J. Watson, Merck, 1.