Sleep apnea and gout

Burton Abrams

Like Dr Tandeter,1 I am recovering from sleep apnea. Unlike him, however, I am not and never was overweight. In retrospect, I can deduce that my sleep apnea developed about 20 years ago, when I was 46 years old. The reason I can make that deduction is that was when I first experienced the severe pain of an overnight attack of gout. It was an unforgettable experience.

I recognized the connection between gout and sleep apnea about 15 years later when my sleep apnea was finally diagnosed and resolved—and my frequent bouts of gout ended permanently. Physiologic support for my observation comes from pulmonology journal literature dating back more than 20 years, which describes 2 physiologic mechanisms by which hypoxemia from sleep apnea can lead to gout flares. First, it causes hyperuricemia from cell catabolism, which culminates irreversibly in cellular generation of excess uric acid. Second, it causes hypercapnia and acidosis, which make the precipitation of uric acid from the blood as monosodium urate more likely.

Gout was not the only comorbidity that receded after my sleep apnea was resolved, although its recession was the most immediate. The other comorbidities were diabetes and atrial fibrillation. The atrial fibrillation had led to a transient ischemic attack, after which my sleep apnea was finally diagnosed.

As with Dr Tandeter, during my 15-year period with sleep apnea my wife noticed my loud snoring. At the end of that period, she realized that the breathing stoppages that she had also witnessed while I slept were a telltale sign of sleep apnea. But I never recalled experiencing excessive daytime sleepiness, which is why I never suspected sleep apnea. My recollection notwithstanding, I realize now that I am more fully awake during waking hours than I was when experiencing sleep apnea.

I don’t use continuous positive airway pressure to prevent recurrence of my sleep apnea. Position therapy works for me—I never sleep lying on my back. After 18 months of sleeping with props to ensure that I didn’t roll over onto my back, I am now trained to sleep that way always. How do I know that it works? I know from sleeping that way one night in a sleep lab, from my own measurements at home using a tape-printout pulse oximeter, and from the fact that I am gout-free.

My experience, along with that of Dr Tandeter, demonstrates how important it is for family physicians to screen all of their adult patients for sleep apnea, regardless of their body types, without waiting for some life-threatening development to prompt that screening. My personal physician has been screening all of his gout patients. He has reported to me that a large majority of those patients have subsequently been diagnosed with sleep apnea, even though neither he nor they previously suspected that result.

Sleep apnea is known to be very common, to have long-term, life-threatening consequences, and to be woefully underdiagnosed. It is important for family physicians to practise preventive medicine to achieve proper diagnosis and effective treatment before serious, irreversible consequences are incurred.