Effects of Conventional Uric Acid–Lowering Therapy on Monosodium Urate Crystal Deposits

Abstract

Objective Few studies have systematically and quantitatively addressed the impact of urate‐lowering therapy on monosodium urate (MSU) deposits. This study was undertaken to analyze the effect of lifestyle measures and conventional urate‐lowering therapy on MSU deposits in patients with gout. Methods In this prospective study, subjects with gout according to the American College of Rheumatology/European League Against Rheumatism classification criteria and presence of MSU deposits seen on dual‐energy computed tomography (DECT) scans received either lifestyle intervention or conventional urate‐lowering therapy for a mean period of 18 months before a follow‐up DECT scan. Detected MSU deposits were quantified by volumetric measurement and validated by semiquantitative scoring, and baseline and follow‐up measurements were compared. Results Baseline and follow‐up DECT scans were available for all 83 subjects. Six subjects discontinued treatment, and 77 subjects underwent a lifestyle intervention (n = 24) or were treated with allopurinol (n = 29), febuxostat (n = 22), or benzbromarone (n = 2) over the entire observation period. The mean serum uric acid (UA) level decreased from 7.2 to 5.8 mg/dl in the overall population. In patients who discontinued treatment, no change in MSU deposits or serum UA levels was observed. The burden of MSU deposits significantly decreased in patients undergoing lifestyle intervention (MSU volume P = 0.007; MSU score P = 0.001), and in patients treated with allopurinol (MSU volume and score P < 0.001) or febuxostat (MSU volume P < 0.001; MSU score P = 0.001). No significant decline in MSU deposits was noted in patients who discontinued treatment. Conclusion These data show that lifestyle intervention and xanthine oxidase inhibitors significantly decrease the MSU deposit burden. Hence, conventional gout therapy not only lowers serum UA levels, but also reduces pathologic MSU deposits.

Volumetric reduction and dissolution prediction of monosodium urate crystal during urate-lowering therapy – a study using dual-energy computed tomography

“…At the upper therapeutic range of SU up to 0.43 mmol/l (7.2 mg/dl), some degree of dissolution is still possible within a reasonable time frame. This is consistent with the finding that tophi could be partly resolved on DECT over 22 ± 11 months through lifestyle change alone when SU was brought down to an average of 6.7 ± 1.7 mg/dl [30]. However, complete dissolution is impractical if SU > 0.36 mmol (6 mg/dl).…”

Why Hyperuricemia Does Not Necessarily Induce Gout?

“…The traditional treatment for gout attack has been well established for improvement of quality of life, although treatment with ULT alone may not be optimal for patients [90]. The current recommendation is additionally to employ anti-inflammatory therapy [91] and to reduce pathologic MSU deposition [92]. Commencing ULT alone during an acute gout attack could have neither significant efficacy on localized pain, recurrent flares, or adverse effects [48] nor been associated with the risk of gout flare [93], or able to ameliorate gout associated diabetes incidence or reverse beta-cell apoptosis with significance [94] or improvement of kidney function [95].…”

High serum uric acid concentration is a risk factor for radiographic spondyloarthritis: a cross-sectional study

“…In the past, reports already con rmed that high serum uric acid increased the burden of monosodium urate (MSU) deposits. [20,21] Previous studies reported that MSU deposits would lead to structural damage in corresponding organs where the MSU deposits were found. A nephrological research found that high SUA led to uric acid super saturated in the urine, and supersaturation in the urine increased monosodium urate (MSU) deposits in the kidney formed uric acid stones.…”