I. Calabuig (1), A. Martínez-Sanchis (1), M. Andrés (1,2).
Affiliation(s):
1. Sección de Reumatología, Hospital General Universitario de Alicante-Isabial, Alicante.
2. Universidad Miguel Hernández, Alicante, Spain.
Background/purpose: Carotid subclinical atherosclerosis is prevalent in patients with gout, although poorly predicted by cardiovascular risk assessment tools. Gout itself is deemed to contribute to its development. However, a previous report did not show an association between clinical characteristics of gout and the presence of subclinical atherosclerosis [Ann Rheum Dis. 76:1263]. This study aimed to explore the association between sonographic signs of urate crystal deposits and carotid atherosclerosis.
Methods: Consecutive new patients with crystal-proven gout attended in a tertiary Rheumatology unit were eligible for the study. It included musculoskeletal and carotid ultrasound assessment, performed by a trained sonographer blinded to clinical data. Patients were examined during intercritical periods; flare prophylaxis with low-dose colchicine or other agents was permitted, but patients under urate-lowering treatment were excluded. The musculoskeletal scans evaluated wrists, 2nd MCPs and 1st MTPs joints, and triceps and patellar tendons, for the presence of signs suggestive of urate crystal deposits (double contour, hyperechoic aggregates, and tophi), following OMERACT definitions. Also, local Power-Doppler (PD) signal was registered and graded as 0 to 3. The sum of locations showing crystal deposits or positive PD signal (≥1) was estimated in order to assess crystal and inflammatory burden, respectively. Carotid arteries were scanned for increased intima-media thickness (IMT) and presence of atheroma plaques, according to Mannheim consensus. The association analysis was done by logistic regression estimating odds ratios (OR), considering increased IMT or atheroma plaques as the independent variable.
Results: Eighty-eight new patients with gout were enrolled, mean aged 62.0 years (SD 14.5), 89.8% males. Mean gout duration was 5.9 years (SD 9.0), clinical tophi were observed in 16.1% of patients and mean serum urate level at diagnosis was 8.4 mg/dl (SD 1.5). All participants showed at least one sonographic sign of crystal deposits at the examined locations, with a mean sum of 9.4 (SD 4.0). Regarding individual signs, their mean (SD) sum was as follows: 4.6 (2.1) for tophi, 3.9 (2.8) for aggregates and 0.9 (1.0) for double contour. The mean sum of locations with positive PD signal was 1.1 (SD 1.0). Regarding carotid scans, increased IMT was seen in 26 patients (30.6%) and atheroma plaques in 51 (58.0%). Positive PD signal was significantly associated with the presence of atheroma plaques (OR 1.7, 95%CI 1.1-2.8; p=0.028). Tophi showed a trend with both increased IMT (OR 1.2, 95%CI 1.0-1.6; p=0.091) and atheroma plaques (OR 1.2, 95%CI 1.0-1.5; p=0.068), while no association was seen for other sonographic signs.
Conclusion: Sonographic deposits were consistently observed in new patients with gout. Crystal and inflammatory load, here shown as tophi and positive PD signal, seem associated with carotid atherosclerosis. This new finding may contribute to understanding the complex relationship between gout and atherosclerosis.