OBJECTIVE: 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. METHODS: 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). RESULTS: 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/m(2) ) 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. CONCLUSION: General obesity in women and hypertriglyceridemia in men may potentiate an sUA effect for gout development. Further investigation is needed.
OBJECTIVE: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. METHODS: 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). RESULTS: 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/m(2) ) 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. CONCLUSION: General obesity in women and hypertriglyceridemia in men may potentiate an sUA effect for gout development. Further investigation is needed.
Authors: U Kiltz; R Alten; M Fleck; K Krüger; B Manger; U Müller-Ladner; H Nüßlein; M Reuss-Borst; A Schwarting; H Schulze-Koops; A Tausche; J Braun Journal: Z Rheumatol Date: 2016-08 Impact factor: 1.372