摘要
Background Hyperuricemia is closely associated with cardiovascular disease (CVD). However, it has not been definitively established whether this association is independent of traditional cardiovascular risk factors in gout patients. Objectives To clarify the incidence of subclinical atherosclerosis and associated factors in gouty arthritis patients by ultrasonography. Methods We conducted this cross-sectional study to investigate the frequency and clinical factors correlated with carotid changes in patients with gout by ultrasonography. Results 200 consecutive patients with gout were recruited. Carotid ultrasound was performed in all patients in First hospital of Peking University from 2014 to 2020, finding atheroma plaques in 33.0% patients. None of these patients received urate-lowering drugs. On univariate analysis, the pattern was significantly associated with age, estimated gout duration, clinical tophi, double contour sign at the scanned joint and decreased estimated glomerular filtration rate; While arterial hypertension, hyperuricemia were not associated with carotid plaques. On multivariable analysis, the atheroma plaques were associated with estimated disease duration, clinical tophi, double contour sign and decreased estimated glomerular filtration rate. Thus, carotid plaque was frequently demonstrated in gout patients with tophaceous gout and associated with features of tubulointerstitial nephritis. This finding reveals the hypothesis of crystal-led inflammation and comorbidities relates to gout associated cardiovascular disease, predominantly seen in high uric acid burden patients, which could be an important treatment target for gout therapy. Conclusion Ultrasonography can detect crystal deposits in joints and connective tissues. We investigated the frequency and clinical correlates of plaques in carotid by ultrasound in consecutive gout patients. The pattern was significantly associated with age, estimated gout duration, clinical tophi, double contour sign and decreased estimated glomerular filtration rate. References [1]Dehlin M, Jacobsson L, Roddy E. Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors. Nat Rev Rheumatol 2020;16:380–90. [2]Andrés M, Quintanilla M-A, Sivera F, Sánchez-Payá J, Pascual E, Vela P, et al. Silent Monosodium Urate Crystal Deposits Are Associated With Severe Coronary Calcification in Asymptomatic Hyperuricemia: An Exploratory Study. Arthritis Rheumatol 2016;68:1531–9. [3]Andrés M, Bernal JA, Sivera F, Quilis N, Carmona L, Vela P, et al. Cardiovascular risk of patients with gout seen at rheumatology clinics following a structured assessment. Ann Rheum Dis 2017;76:1263–8. [4]Richette P, Perez-Ruiz F, Doherty M, Jansen TL, Nuki G, Pascual E, et al. Improving cardiovascular and renal outcomes in gout: what should we target? Nat Rev Rheumatol 2014;10:654–61. [5]Neogi T, Jansen TLTA, Dalbeth N, Fransen J, Schumacher HR, Berendsen D, et al. 2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann. Rheum. Dis. 2015;74:1789–98. Disclosure of Interests None declared