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JCR: Journal of Clinical Rheumatology:
doi: 10.1097/RHU.0b013e3181ef724d
Letters to the Editor

Gout as an Early Warning of Concomitant Sleep Apnea

Abrams, Burton MS

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Member of the Board of Directors, American Sleep Apnea Association, Washington, DC

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To the Editor:

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

Obstructive sleep apnea (OSA) is defined as airway obstruction resulting in episodic lack of breathing during sleep that is complete (apnea) or almost complete (hypopnea) for at least 10 seconds at a time with occurrence averaging at least 5 times per hour during the sleep period. The average occurrence of apneas or hypopneas per hour during the sleep period is termed the apnea hypopnea index.

The strongest evidence for gout resulting from concomitant sleep apnea is physiological, and it is supported by epidemiological evidence and comorbidities known to be common to both gout and OSA.

The pulmonology literature1,2 described 2 mechanisms by which the hypoxemia of sleep apnea can lead to MSU precipitation. First, the cellular reaction is to initiate a catabolic process in which adenosine triphosphate decomposition undergoes a chain of chemical transitions, which culminates irreversibly in the generation of excess uric acid that is fed into the blood. Because the transition to uric acid is irreversible, additional uric acid would be fed into the blood with each apneic episode, perhaps faster than its renal excretion rate. The second gout-producing mechanism from the hypoxemia is hypercapnia and acidosis, which increases the likelihood of MSU precipitation. If the concentration of uric acid flares is high enough, a gout flare might result before the individual has awakened.

The prevalence of gout in more than 60,000 patients with OSA, randomly selected from hospital records, was reported to be 2%.3 A meta-analysis of gout in the US adult general population4 estimates that the prevalence is 0.84%. Thus, gout in the United States is estimated to be 2.4 times as prevalent in those with OSA compared with the general population.

Both gout and OSA are known to be more prevalent in men than in women. The prevalence of both conditions in women increases significantly after menopause.5,6

The most easily recognized common comorbidity is excess body weight. The relative risk of incident gout in men shows a strong monotonic increase with body weight.7 Other studies8 show similar results for OSA, with each 1% increase or decrease in body weight respectively associated with a 3% increase or decrease in apnea hypopnea index.

Long-term unresolved OSA is known to have very serious cardiovascular, metabolic, and neurologic consequences, which can diminish the length and quality of life,3,9 and causes diseases such as hypertension, atherosclerosis, myocardial infarction, heart arrhythmias, and diabetes. Many of these diseases have been recognized as comorbidities associated with gout.10 Those associations could in part be due to the consequences of concomitant OSA.

Prospective studies are needed to determine several issues in the connection of gout with OSA. First, the prevalence of OSA in gout patients needs to be determined, using sleep laboratory polysomnography for the most reliable OSA diagnosis. Second, the degree of gout mitigation as a function of OSA treatment compliance needs to be determined.

Third, the frequency of flares in untreated gout that will allow reliable diagnosis of concomitant OSA needs to be determined.

Because the physiological connection indicates that a gout flare might be an immediate result of OSA, while life-threatening consequences of OSA generally develop over the long-term, gout can be considered to be an early warning of concomitant OSA. As such, routine screening of gout patients for OSA may be an important step to reduce gout patient risk for developing the serious comorbidities of OSA.

Burton Abrams, MS

Member of the Board of Directors

American Sleep Apnea Association

Washington, DC

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1. Grum CM. Cells in crisis: cellular bioenergenics and inadequate oxygenation in the intensive care unit. Chest. 1992;102:329–330.

2. Hasday JD, Grum CM. Nocturnal increase of urinary uric acid: creatine ratio: a biological correlate of sleep-associated hypoxemia. Am Rev Respir Dis. 1987;135:534–538.

3. Huang QR, Qin Z, Zhang S, et al. Clinical patterns of obstructive sleep apnea and its comorbid conditions: a data mining approach. J Clin Sleep Med. 2008;4:543–550.

4. Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. 1998;41:778–799.

5. Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Eng J Med. 1993;328:1230–1235.

6. Luk AJ, Simkin PA. Epidemiology of hyperuricemia and gout. Am J Manag Care. 2005;11:S435–S442.

7. Choi HK, Atkinson K, Karlson EW, et al. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study. Arch Intern Med. 2005;165:742–748.

8. Young T, Peppard PE, Taheri S. Excess weight and sleep-disordered breathing. J Appl Physiology. 2005;99:1592–1599.

9. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165:1217–1239.

10. Gabriel SE, Michaud K. Epidemiological studies in incidence, prevalence, mortality, and comorbidity of the rheumatic diseases. Arthritis Res Ther. 2009;11:229.

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This article has been cited 1 time(s).

Obstructive sleep apnoea in relation to rheumatic disease
Taylor-Gjevre, RM; Nair, BV; Gjevre, JA
Rheumatology, 52(1): 15-21.
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