The cumulation of uric acid (UA) results in elevated levels of serum UA (SUA), otherwise known as hyperuricemia. When SUA becomes insoluble in the blood, monosodium urate (MSU) crystals are subsequently formed and deposit in and around the joints. Gout, an inflammatory arthritis, presents as immune responses in reaction to the deposition of MSU crystals. Gout has been linked with comorbidities such as hypertension, coronary artery disease (CAD), chronic kidney disease (CKD), obesity, and type 2 diabetes.
Characterized by recurrent bouts of upper airway obstruction during sleep, obstructive sleep apnea (OSA) is a severe sleep disorder the leads to intermittent hypoxia. Oxidative stress and chronic inflammation as a result of gout symptoms are major pathogenic factors of OSA. In addition, several observational epidemiological studies have reported that patients with OSA have higher levels of SUA.
Published in Seminars in Arthritis and Rheumatism, researchers conducted a series of observational studies reporting on the close associations of OSA with SUA levels and gout. Utilizing bidirectional univariable and multivariate Mendelian randomization (MR) based on publicly available genome-wide association studies, researchers investigated whether OSA is causally related to SUA levels, gout and vice versa. They also evaluated the independent causal effect of OSA on SUA and gout after adjusting for factors such as BMI type 2 diabetes, CAD, and CKD.
The univariable MR method showed that genetically predicted OSA liability was significantly associated with increased levels of SUA and risk of gout. The results of multivariate Mendelian randomization suggested that while OSA retained its significant association with increased SUA levels, the significant association between OSA and gout was nonexistent after adjusting for body mass index and type 2 diabetes. However, researchers noted that there was “no causal effect of OSA on SUA levels and gout was found in the reverse direction.”