OR WAIT null SECS
Differences among baseline clinical and laboratory characteristics between cases and controls were observed in those with a presence of subcutaneous tophi and higher serum urate levels.
Baseline findings demonstrated that monosodium urate (MSU) crystals, as well as subclinical inflammation, may independently predict gout flares over 12 months. Data from the study “Ultrasonography in the Prediction of Gout Flares: A 12-Month Prospective Observational Study,” was recently presented at the European Alliance of Associations for Rheumatology (EULAR) 2022 conference.
“Gout flares are a distinctive feature of gout,” investigators stated. “Although imaging techniques, such as ultrasonography (US), can visualize MSU crystals and synovial inflammation and estimate their burden, the role of imaging in predicting gout flares has not been fully investigated.”
Patients with gout currently receiving urate-lowering therapy (ULT) for 6 or more months were included in the 12-month prospective, observational, single-center study. Patients with at least 1 self-reported gout flare during the follow-up period were considered “cases,” while those who did not flare were placed in the “control” group in a nested case-control analysis. Patients received an examination, using standardized US scanning protocol, at baseline. This included assessments of the knees, ankles, elbows, wrists, 1st metatarsophalangeal joints, and 2nd metacarpophalangeal joints. Clinical exams were performed every 6 months, during which patients reported gout flares using an internationally validated definition.
MSU deposits, including aggregates, double contour (DC) sign and tophi, as well as inflammation, using the Power Doppler (PD) signal, were determined according to the 2015 Outcome Measure in Rheumatology definitions and summated scores were calculated. Multivariate logistic regression and a multivariate zero-inflated Poisson regression analysis were used to determine any link between baseline findings and gout flares over 12 months. Covariates, such as age, gender, the presence of subcutaneous tophi, current serum urate >360 μmol/l, disease duration, an increased dose of ULT during the study, and flare prophylaxis were tested separately.
Of the 81 patients with gout initially enrolled, 71 completed the study. No differences among baseline clinical and laboratory characteristics of cases and controls were observed except for the presence of subcutaneous tophi (23.3% vs 4.9%, respectively; P=0.02) and higher serum urate (SU) levels (360.8 vs 301.4 μmol/l mol/L, respectively; P=0.01). During the study, 42.3% (n=30) of participants experienced 1 or more gout flares over 12 months, with a median of 2.0 flares.
Those with flares had a greater baseline US burden of MSU deposits (2.0±1.8 vs 0.5±0.9, P=0.01 for DC sign; 2.6±2.0 vs 1.6±1.6, P=0.03 for aggregates; and 2.1±2.3 vs 0.8±1.0, P=0.01 for tophi). These patients also had greater subclinical inflammation (3.73±3.53 vs 0.82±1.44, P<0.01).
The Multivariate logistic regression analyses also indicated that the baseline extent of MSU deposits and subclinical inflammation, as estimated by US, was significantly linked to gout flares over 12 months. While aggregate scores were not significantly significant (adjusted odds ratio [aOR]: 1.40, 95%CI: 0.94-2.10; P=0.10), DC sign score (aOR: 2.20, 95%CI: 1.22-4.34; P=0.01), PD score (aOR: 1.63, 95%CI: 1.12-2.40; P=0.01), and tophi score (aOR: 2.16, 95%CI: 1.12-4.18; P=0.02) predicted potential gout flares. The multivariate Poisson regression models reported similar results regarding DC score (adjusted incidence rate ratio [aIRR]: 1.39, 95%CI: 1.18-1.64, P<0.01), tophi score (aIRR: 1.30, 95%CI: 1.17-1.45, P<0.01), PD score (aIRR: 1.29, 95%CI: 1.19-1.40, P<0.01), and aggregates score (aIRR: 1.13, 95%CI: 1.00-1.29, P=0.05).