COMMENTARY

Sleep Apnea as a Cause of Gout Flares

Burton Abrams

Disclosures

January 05, 2009

To the Editor:

The immune system's response to precipitation of monosodium urate (MSU) crystals from serum uric acid into a joint is well established as a cause of the severe pain and inflammation of gout. Sleep apnea leading to the precipitation of MSU explains why so many gout flares begin while the gout sufferer is asleep.

Pulmonology journal literature[1,2] describes 2 mechanisms by which the hypoxemia of sleep apnea leads to MSU precipitation. First, the cellular reaction to the hypoxemia initiates a catabolic process in which adenosine triphosphate decomposition undergoes a chain of chemical transitions that culminate irreversibly in the generation of excess uric acid that is fed into the blood. Because the transition to uric acid is irreversible, with each apneic episode more and more uric acid accumulates in the blood -- faster than the kidneys can dispose of it. The second gout-producing mechanism from the hypoxemia is hypercapnia and acidosis, which increases the likelihood of MSU precipitation.

Other pulmonology journal literature has confirmed that hyperuricemia is a result of sleep apnea.[3,4,5]

About 30% of patients with sleep apnea and gout are not overweight. Screening patients with gout for sleep apnea is an important tool for treating their gout, even if they are not overweight. Using their gout as an indicator leading to diagnosis and treatment, if warranted, of the sleep apnea not only may prevent further gout flares, but more importantly will greatly lower their risks for the very serious -- even life-threatening -- cardiovascular, neurologic, and metabolic consequences of sleep apnea.

The lifestyle focus for treating gout needs to consider not only how the patient eats or drinks, but also how the patient sleeps.

Burton Abrams
burtabrams@hotmail.com

 


 

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