Lifestyle factors predict gout outcomes: Results from the NOR-Gout longitudinal 2-year treat-to-target study.

OBJECTIVE: Gout is associated with lifestyle, body mass index (BMI) and comorbidities, including dyslipidaemia. We studied how in actively treated patients, anthropometric measures and lipid levels changed over 2 years and whether they predicted gout outcomes. METHODS: Patients with a recent gout flare and elevated serum urate (sUA) received gout education and treat-to-target urate-lowering therapy over 1 year. Anthropometric measures with BMI, waist circumference (WC) and waist-height ratio (WHR) as well as lipid levels were measured yearly over 2 years. We examined whether baseline anthropometric measures and lipid levels were related to flares and to achieving the sUA target. RESULTS: At baseline, patients (n=211) were with mean age of 56.4 years and 95% were male. Over 2 years, anthropometric measures were largely unchanged while cholesterol and low-density lipoprotein cholesterol (LDL-C) were reduced at year 1. Anthropometric measures were associated with presence of tophi. Higher baseline WC (OR: 0.96 per cm, 95% CI: 0.93 to 0.99) decreased and high level of high-density lipoprotein cholesterol (OR: 5.1 per mmol/L, 95% CI: 1.2 to 22.1) increased the chance of sUA target achievement at year 2. High LDL-C (OR: 1.8 per mmol/L, 95% CI: 1.2 to 2.6) predicted the chance of having a gout flare during year 2. CONCLUSION: In actively treated patients with gout, anthropometric measures were largely unchanged over 2 years and lipid levels were reduced. High WC and lipid levels predicted unfavourable gout outcomes after 2 years.

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 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.