Abstract

Hyperuricemia is known to be a necessary and causal condition for gout, but much more prevalent than gout. Medicine has standardized treatments for gout, but has no such determination for asymptomatic hyperuricemia. Nevertheless, people with hyperuricemia, gouty or not, too often continue to be at risk for shortened lifespans from life-threatening comorbidities, all of which are known to be consequences of obstructive sleep apnea (OSA), which is shown herein to cause most hyperuricemia. This review also presents the wide variety of OSA consequences, many of which are irreversible and life-threatening, as the rationale for treating all hyperuricemia (gouty and asymptomatic) by diagnostic testing and effective treatment for OSA as soon as hyperuricemia is detected. It advocates frequent ultrasonic screening for aggregated urate crystals. Multiple epidemiological studies have found OSA to be significantly more prevalent in those people with gout diagnosed with OSA than it is in those never diagnosed with it. A clinical study shows an even higher prevalence of OSA in people with gout. The pathophysiology of hypoxia from OSA explains how it would lead to both the overproduction and the underexcretion of uric acid, leading to hyperuricemia and the precipitation of monosodium urate crystals which cause a gout flare. Resolving OSA has been shown to prevent or even reverse life-threatening diseases that are recognized comorbidities of hyperuricemia and gout, and can prevent further gout flares. In order to extend the length and quality of life of people with gout or hyperuricemia, when either first manifests a patient sleep study is recommended, followed by effective OSA treatment as warranted.

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