Another Tool for a Common Problem . . .

Abstract & Commentary

Synopsis: Intranasal fluticasone helps sleep-disordered breathing in patients with allergic rhinitis.

Source: Kiely JL, et al. Thorax. 2004;59:50-55.

Kiely and colleagues studied a total of 23 patients with allergic rhinitis. There were 19 men and 4 women, and their mean age was 46 years. All of them were snorers. Using a definition for sleep apnea of an Apnea plus Hypopnea Index (AHI) >10 events/hr, 13 of these patients were classified with obstructive sleep apnea syndrome (OSAS). These 13 had a mean AHI of 30.3 and a mean lowest Sa02 78%. 10 of these patients were classified as "nonapneic snorers" (mean AHI, 5; mean lowest Sa02, 86%). Patients were treated with in a randomized, double blind, placebo controlled design, with each treatment lasting 4 weeks. They all had polysomnography (with snoring measured by a nasion microphone), and nasal airflow resistance measured at enrollment, then at the end of each study period. They kept daily diaries of alertness, sleep quality, snoring intensity and nasal congestion throughout the study.

The apneics were sleepier (mean Epworth score, 12 vs < 9) and heavier (Body Mass Index, 29.8 vs 25.6 Kg/m2) than the nonapneic snorers. The overall AHI was markedly reduced (from 20 to 11.9 event/hr) on fluticas one, compared with placebo, and for the apneic group it was 23.3 vs 30.3 on active drug vs placebo. Of note, the mean AHI was cut in half for the nonapneic snorers (from 5 to 2/7 events/h). Oxygen saturation was not significantly different between phases of the study, nor was snoring intensity. Measures of objective sleep quality were generally no different between active drug and placebo, except for in increase in Slow Wave Sleep of borderline significance on placebo, but subjective alertness and symptoms of rhinitis were improved on fluticasone compared with placebo. Nasal airflow resistance was lower during active treatment. Kiely et al modestly conclude, ". . . the data indicate that intranasal corticosteroids are likely to have a limited clinical role in the management of OSAS, since most patients continued to have significant OSAS on treatment."

Comment by Barbara A. Phillips, MD, MSPH

Would that ENT surgeons were so modest!! Frankly, the results here are very similar to those reported by most studies of upper airway surgery as treatment for sleep apnea, except that Kiely et al actually measured and reported AHI and objective sleep structure on placebo and treatment, lost no one to follow-up, had a larger "n" than is typically reported in surgical studies, and didn’t over state their findings.1 If you haven’t read the surgical literature lately, take a peek. Often, the "n" is 10-20 patients. Many are lost to follow-up. PSG data pre and post are rarely reported, and if they are, the patient is considered a "success" if the AHI is cut in half (which, as the authors of the current study point out, often leaves them with significant sleep-disordered breathing). Worse, instead of reporting PSG findings, surgical endpoints of "success" are often the Epworth Sleepiness Scale and some measures of snoring.

Yet patients with sleep-disordered breathing go to surgery every day. We encourage it, and their insurers pay for it. Why is this? Because CPAP, albeit very effective, is cumbersome, ongoing, unsexy treatment. Because surgeons tend to be very effective in marketing and in persuading insurers to pay. Because patients want a quick fix.

But it’s important to know that there actually is a fair amount of literature suggesting that nasal steroids can be useful for patients with nasal rhinitis and sleep-disordered breathing.2-5 And in the current study, Kiely et al used a fairly steep definition of sleep apnea; they required an AHI of 10 events or more to meet that definition. Many sleep clinicians and insurers in the United States define sleep apnea as an AHI of 5 events or more with symptoms. If we look at the group of non-apneic snorers reported here, it’s interesting to note that their mean AHI fell from 5 to 2.7 events/hr on active treatment. Surgeons would call this a cure!!

Where does this leave us? I think it gives us one more tool in our armamentarium of treatment options for mild sleep-disordered breathing. Because of varying definitions of apneas, hypopneas, and sleep apnea itself, we still don’t have a good handle on what the sequellae or prevalence of pathologic sleep-disordered breathing are. But we do know that those with milder disease tolerate CPAP less well, and we are often stuck, not knowing how best to help them. (Of course it would help if they lost weight—how often does that happen?). I personally have "cured" patients with mild sleep-disordered breathing and snoring with nasal steroids. And I think, in the long run, we are serving our patients better to write a prescription for a nasal steroid or to send them to the dentist than to send them to the surgeon if they can’t or won’t wear CPAP and have mild disease. 

Dr. Phillips, Professor of Medicine, University of Kentucky; Director, Sleep Disorders Center, Samaritan Hospital, Lexington, KY, is Associate Editor of Internal Medicine Alert.


1. Sher AE. Sleep Med Rev. 2002;6:195-212.

2. Hughes K, et al. Allergy. 2003; 58:380-385.

3. Craig TJ, et al. Allergy Asthma Proc. 2003;24:53-58.

4. Kakumanu S, et al. Am J Respir Med. 2002;1:195-200.

5. Brouillette R, et al. J Pediatr. 2001;138:38-44.