Hyperuricemia is the most important risk factor for the development of gout; however, not all patients with hyperuricemia develop gout, and patients experiencing a gout attack are not necessarily found to have hyperuricemia. We hypothesized that the interactions between serum uric acid (sUA) and other potential metabolic comorbidities increase the risk of gout development.
A prospective study was conducted to link baseline metabolic profiles from the MJ Health Screening Center to gout outcomes extracted from the Taiwan National Health Insurance database. A Cox proportional hazards model was used to assess the metabolic risks for incident gout stratified by hyperuricemia status (sUA level >7 mg/dl or not).
During a mean followup period of 6.45 years (261,500 person-years), 1,189 patients with clinical gout (899 men, 202 women ages >50 years, and 88 women ages ≤50 years) were identified among the 40,513 examinees. The multivariate adjusted hazard ratios (HRs) of hyperuricemia for gouty arthritis were 5.80 (95% confidence interval [95% CI] 4.93–6.81) in men and 4.37 (95% CI 3.38–5.66) in women. Hypertriglyceridemia (triglyceride level >150 mg/dl) was found as an independent risk factor, with HRs of 1.38 (95% CI 1.18–1.60) in men with hyperuricemia and 1.40 (95% CI 1.02–1.92) in men without hyperuricemia. General obesity (body mass index >27 kg/m2) was independently associated with gout in older women, with HRs of 1.72 (95% CI 1.15–2.56) in women with hyperuricemia and 2.19 (95% CI 1.47–3.26) in women without hyperuricemia.
General obesity in women and hypertriglyceridemia in men may potentiate an sUA effect for gout development. Further investigation is needed.