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Urate crystal deposition is associated with inflammatory markers and carotid artery pathology in patients with intercritical gout: results from the NOR-Gout study
BACKGROUND: Gout is of unknown reason associated with cardiovascular disease. Ultrasound is sensitive for detecting crystal deposition and plasma calprotectin is a sensitive inflammatory marker. This study explores the associations between crystal deposition, inflammation and carotid artery patholog...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310249/ https://www.ncbi.nlm.nih.gov/pubmed/35863863 http://dx.doi.org/10.1136/rmdopen-2022-002348 |
Sumario: | BACKGROUND: Gout is of unknown reason associated with cardiovascular disease. Ultrasound is sensitive for detecting crystal deposition and plasma calprotectin is a sensitive inflammatory marker. This study explores the associations between crystal deposition, inflammation and carotid artery pathology. METHOD: A cross-sectional analysis of baseline assessments from the NOR-Gout study was undertaken. Crystal deposition was assessed by ultrasound (double contour, tophi, aggregates) and dual-energy CT (DECT) and laboratory assessments included plasma calprotectin. The carotid arteries were bilaterally examined for carotid intima–media thickness (cIMT) and presence of plaques. Spearman correlations, Mann-Whitney tests and linear regression analyses were used to explore associations between crystal deposition, inflammatory markers, and carotid pathology. RESULTS: 202 patients with intercritical gout (95.5% men, mean (SD) age 56.5 (13.8) years, disease duration 7.9 (7.7) years) were included. Calprotectin was correlated with all scores of crystal deposition by ultrasound (r=0.26–0.32, p<0.001) and DECT (r=0.15, p<0.05). cIMT was correlated with sum score aggregates (r=0.18–0.22, p<0.05). Patients with large tophi had higher levels of calprotectin as well as more frequent carotid plaque (p<0.05). CONCLUSIONS: Study findings point towards crystal deposition contributing to subclinical inflammation with subsequent vascular implications. However, future longitudinal studies are needed to confirm such causal relationships. |
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