OBJECTIVE: Sleep apnea is associated with hyperuricemia owing to hypoxia-induced nucleotide turnover. We undertook this study to assess the relationship between incident sleep apnea and the risk of incident gout. METHODS: Using data from The Health Improvement Network in the UK, we identified individuals with a first-ever physician diagnosis of sleep apnea. For each patient with sleep apnea, up to 5 individuals without sleep apnea were matched by sex, age, birth year, and body mass index (within ±0.5 kg/m(2) ). We estimated the incidence rates of gout and examined the relationship between sleep apnea and the risk of incident gout using a Cox proportional hazards model, adjusting for potential confounders. In addition, we assessed the rate difference in gout due to sleep apnea using an additive hazard model. RESULTS: Among 9,865 patients with newly diagnosed sleep apnea and 43,598 matched individuals without sleep apnea, we identified 270 incident cases of gout over 1 year of followup, resulting in incidence rates of 8.4 per 1,000 person-years and 4.8 per 1,000 person-years, respectively. The crude and multivariable rate ratios of incident gout in patients with sleep apnea were 1.7 (95% confidence interval [95% CI] 1.3, 2.2) and 1.5 (95% CI 1.1, 2.1), respectively. The corresponding rate differences between patients with sleep apnea and the comparison cohort were 3.6 (95% CI 1.6, 5.6) and 2.8 (95% CI 0.7, 4.9) per 1,000 person-years. The effect of sleep apnea persisted across subgroups. CONCLUSION: This general population-based study indicates that sleep apnea is independently associated with an increased risk of incident gout. Future research should examine the potential benefits of correcting sleep apnea-induced hypoxia on the risk of hyperuricemia and gout flares.
OBJECTIVE:Sleep apnea is associated with hyperuricemia owing to hypoxia-induced nucleotide turnover. We undertook this study to assess the relationship between incident sleep apnea and the risk of incident gout. METHODS: Using data from The Health Improvement Network in the UK, we identified individuals with a first-ever physician diagnosis of sleep apnea. For each patient with sleep apnea, up to 5 individuals without sleep apnea were matched by sex, age, birth year, and body mass index (within ±0.5 kg/m(2) ). We estimated the incidence rates of gout and examined the relationship between sleep apnea and the risk of incident gout using a Cox proportional hazards model, adjusting for potential confounders. In addition, we assessed the rate difference in gout due to sleep apnea using an additive hazard model. RESULTS: Among 9,865 patients with newly diagnosed sleep apnea and 43,598 matched individuals without sleep apnea, we identified 270 incident cases of gout over 1 year of followup, resulting in incidence rates of 8.4 per 1,000 person-years and 4.8 per 1,000 person-years, respectively. The crude and multivariable rate ratios of incident gout in patients with sleep apnea were 1.7 (95% confidence interval [95% CI] 1.3, 2.2) and 1.5 (95% CI 1.1, 2.1), respectively. The corresponding rate differences between patients with sleep apnea and the comparison cohort were 3.6 (95% CI 1.6, 5.6) and 2.8 (95% CI 0.7, 4.9) per 1,000 person-years. The effect of sleep apnea persisted across subgroups. CONCLUSION: This general population-based study indicates that sleep apnea is independently associated with an increased risk of incident gout. Future research should examine the potential benefits of correcting sleep apnea-induced hypoxia on the risk of hyperuricemia and gout flares.
Authors: Rachel Murdoch; Michael J Barry; Hyon K Choi; Daniel Hernandez; Brianne Johnsen; Manuel Labrador; Susan Reid; Jasvinder A Singh; Robert Terkeltaub; Janitzia Vázquez Mellado; Nicola Dalbeth Journal: RMD Open Date: 2021-04
Authors: Caroline van Durme; Bart Spaetgens; Johanna Driessen; Johannes Nielen; Manuel Sastry; Annelies Boonen; Frank de Vries Journal: Arthritis Res Ther Date: 2020-04-25 Impact factor: 5.156