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Inflammation of the upper airway, which has been recently observed in patients with Obstructive Sleep Apnea or OSA (see Glossary), may represent a complication of the disease which could add to the process of airway obstruction via congestion and swelling. The authors aimed to approach this issue in a first step involving a simple, noninvasive measure of upper airway inflammation: levels of exhaled pentane and nitric oxide, two nonspecific markers of inflammation. They studied 20 patients with moderate to severe OSA, as indicated by apnea/hypopnea indices or AHI (see Glossary) averaging 48 with a Standard Deviation or SD (see Glossary) of 7. These were compared with 8 healthy control subjects with an average AHI of 1 (SD=1). Patients with OSA had significantly lower arterial oxygen saturation lows at night (average=79%, SD=3%) than controls (ave=95%, SD=3%). They were also significantly heavier than controls as measured by the Body Mass Index or BMI (see Glossary), the patients averaging 41 kg/m2 (SD=2) vs. 27 (SD=1) for controls. The patients were slightly but nonsignificantly older than controls (42 yrs SD=2 vs. 33 yrs SD=3). Sex distribution was similar: 12/20 males among the OSA patients, 5/8 males among the controls. All subjects denied any history of repiratory diseases, rhinitis, sinusitis, smoking cigarettes within 3 months prior to the study, or currently taking any anti-inflammatory medications. All subjects underwent standard overnight polysomnography (see Glossary). In addition, four samples of exhaled air were collected from each subject shortly before sleep and immediately after awakening in the morning, and analyzed for pentane content and nitrous oxide levels. Separate samples were obtained by exhalation through the mouth and through the nose. The authors found that OSA patients had both oral and nasal levels of both pentane and nitrous oxide higher in the morning after sleep than in the evening before sleep. Among the controls, there was no difference between morning and evening samples of pentane, but an increased level of oral (not nasal) nitrous oxide in the morning. No pentane was detectable in the room air before or after sleep, but higher level of nitrous oxide were found in the room air after sleep than before. The authors considered their data to suggest the presence of upper airway inflammation after sleep in patients with moderate-severe OSA. Elevated pentane levels result from membrane fatty acids being oxidized; pentane is readily excreted by the lung. It is elevated in conditions such as cystic fibrosis and smoking, and during acute asthmatic attacks. Exhaled nitrous oxide levels are also elevated in conditions like asthma. The difference in the oral nitrous oxide levels (which were lower in patients than in controls both before and after sleep) may be related to the fact that oral nitrous oxide is lower in smokers than in nonsmokers, because of damage to airway lining cells that produce nitrous oxide, while higher nasal nitrous oxide is contributed by undamaged paranasal sinus cells. The authors cautioned that the higher room air levels of nitrous oxide in the morning could affect the results, though this was not found to be the case in two other studies of asthma. They noted that previous researchers have found other signs of upper airway inflammation, increased after sleep, in OSA patients. They considered it important to do further research to assess whether CPAP treatment will alter this picture.

Though the chemistry involved may be obscure to many--including myself!--the point is simple: this study adds more data to accumulating evidence that obstructive sleep apnea is associated with inflammation of the tissues (most probably, the lining) of the upper airway. I would guess this to be due to the trauma of repeated closure, spasm, and pressure changes in the airway, although other factors might include lack of oxygen and obesity. The importance of this inflammation probably lies in its contribution, via congestion and inflammation, to the obstructive process itself. I would certainly be interested to see whether CPAP reverses this--as I would expect--but I would be still more interested to know whether this inflammatory process progresses as the night's sleep progressses. In other words, is it significantly worse at the morning's wakening than halfway through the night? Are naps long enough to induce this process? The answers to these questions might have some bearing on the increase of obstructive events later in the night--typically associated with the increase in REM activity (see Glossary) at that time. Could the process not only cause increased obstruction but also irritation that could itself fragment sleep? Could it contribute to a preference for napping over longer sleep periods? Obviously, these questions are merely speculative. What is important is to realize that here we seem to have found another complication of sleep apnea which in turn contributes to the obstructive process, something else to consider along with many other factors coming to light--such as nasal congestion from allergies, sleep fragmentation from other stimuli, etc.

WHAT DO YOU THINK ABOUT THIS ARTICLE AND MY COMMENTS? CAN YOU RELATE THIS MATERIAL TO ANY PERSONAL EXPERIENCES?

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