Sleep apnea raises the risk of gout, according to a new study.
Using a large database of patients in the United Kingdom, researchers found that the likelihood of getting a gout diagnosis is 70 percent higher in patients previously diagnosed with sleep apnea compared with patients without a sleep apnea diagnosis.
In an interview with Rheumatology Network, Yuqing Zhang, professor of medicine and public health at the Boston University School of Medicine, said gout and sleep apnea are similar in nature.
"Sleep apnea patients share a lot of characteristics with gout patients, so they're at high risk of getting gout. Plus, sleep apnea causes a uric acid increase," he said.
The new research finds that the risk of gout increases with sleep apnea even when controlling for body mass — meaning the link is likely not simply the result of shared risk factors, but has to do with the consequences of nighttime hypoxia. The findings raise the possibility that by treating the hypoxia associated with sleep apnea, doctors could reduce gout attacks, Zhang said.
The study matched patients diagnosed with sleep apnea by sex, age, gender, birth year and body mass with patients without sleep apnea, and then compared the rate at which each group was diagnosed with gout at a one-year follow up. (None of the patients had a gout diagnosis at the time of inclusion.) They found that the rate of gout among the sleep apnea patients was 8.4 per 1,000 person-years versus 4.8 per 1,000 person-years among the patients without sleep apnea.
The crude rate ratio for gout among patients with sleep apnea was 1.7 (95 percent CI 1.3, 2.2), Zhang and his colleagues reported in the December issue of the journal Arthritis and Rheumatology, and the multivariable rate ratio was 1.5 (95 percent CI, 1.1, 2.1). The crude rate difference between patients with sleep apnea and those without in a later diagnosis of gout was 3.6 (95 percent CI, 1.6, 5.6) per 1,000 person-years, they reported, and the adjusted rate difference between patients with sleep apnea and those without was 2.8 (95 percent CI, 0.7, 4.9) per 1,000 person-years.
Previous work had suggested a link between sleep apnea and gout, Zhang said. Several studies have found that sleep apnea is linked to hyperuricemia and that sleep apnea is particularly common in gout patients. A 2015 study also revealed that gout attacks happen 2.4 times more often at night than during the day, with sleep apnea as a possible driver.
The mechanism linking hypoxia in sleep to gout is not entirely clear, but studies have found that hypoxia enhances nucleotide turnover, generating purines that metabolize to uric acid. There is also evidence that hypoxia alters the uric acid and creatine ratio in the urine, and that treating sleep apnea changes this ratio in favor of reduced uric acid, Zhang said.
To uncover the link between sleep and gout, Zhang and his team used The Health Improvement Network database from the U.K., which tracks medical records from more than 10.2 million patients. This allowed the researchers to match each patient with sleep apnea with between one and five patients who were very similar to them in age, gender and body mass index. The result was a dataset 9,865 members strong on patients with sleep apnea and a comparison group of 43, 598 patients without sleep apnea. Matching the groups on body mass index helped to control for the effect of excess weight on both gout and on sleep apnea.
By one year later, 76 patients in the sleep apnea group and 194 in the non-apnea group had developed gout, the researchers found. In general, gout is on the increase in both the United States and the United Kingdom. One 2011 study found that the prevalence of gout in the U.S. had increased over the previous two decades and now stands at 3.9 percent, likely a result of increased obesity. The question now is whether treating sleep apnea can reduce this burden of gout.
"A future study is looking at whether treatment of sleep apnea can reduce gout attacks," Zhang said. "One stone, two birds."