Young children with cystic fibrosis at risk for obstructive sleep apnea

This article discusses how young patients with cystic fibrosis, a chronic lung disease, are at increased risk for obstructive sleep apnea.

Urinary Leukotrienes and Pediatric Obstructive Sleep Apnea

Pediatric obstructive sleep apnea (OSA) is on the rise, especially as our children struggle more with obesity. Kids that have enlarged tonsils and/or adenoids are also at risk for OSA. Some researchers believe inflammation plays a role in OSA as well. There is a study in the Sleep Journal about leukotrienes, which are markers of inflammation. The study included 282 children aged 2 to 12 years old who snored regularly at least 4 nights per week. All of the children had sleep studies to check for OSA. On the morning after the sleep study, the researchers measured a specific leukotriene, aka LTE4, in their urine.

The results showed that the more severe the OSA (defined as mild, moderate, or severe), the higher the LTE4 levels. Also, urinary LTE4 levels were higher in the children with OSA that were overweight versus normal weight children with OSA. Finally, there was an association between enlarged adenoids / tonsils and OSA, but only for normal weight children.

The researchers theorized that the broken up sleep and low oxygen levels caused by OSA was linked with the elevated LTE4 levels - and this marker of inflammation was elevated even in mild OSA. However, they were unable to determine if the elevated LTE4 levels come before or after the children developed OSA. The researchers speculated that perhaps medications that block leukotrienes could be used in the management of pediatric OSA, such as in normal weight patients with milder cases.

Nasal Steroid Sprays and Pediatric Obstructive Sleep Apnea

Medscape has a review of a study in the June issue of the Archives of Otolaryngology - Head & Neck Surgery about how nasal steroid sprays may improve obstructive sleep apnea (OSA) in children.

Researchers compared the amount of an inflammatory cytokine called interleukin-6 (IL-6) in adenoids removed from children who were treated with a nasal steroid spray to controls who did not receive any nasal spray. The results showed that the adenoid cells released less IL-6 in those children who received the nasal steroid spray. The authors think that reducing IL-6 levels could reduce inflammation in the nasopharynx, which could improve nasal airflow, and consequently improve OSA.

These results are exciting because it could mean that treating nasal airway inflammation with a nasal spray might be an alternative to surgery in treating mild OSA in children.