Urine Concentrations of Cysteinyl Leukotrienes in Children with Obstructive Sleep-Disordered Breathing.

Urinary cysteinyl leukotriene E4 level and therapeutic response to montelukast in children with mild obstructive sleep apnea

“…17 This finding supported the findings of in vivo studies which found a positive relationship between urinary LT level and OSA severity. 5,6 Basing upon the findings of the association among LTs, adenotonsillar tissue proliferation and OSA, antileukotrienes such as montelukast have been increasingly used as an alternative treatment in children who have non-severe OSA. Several studies demonstrated a favorable effect of montelukast in decreasing adenotonsillar size and OSA severity.…”

“…Previous studies demonstrated the abundant expressions of leukotrienes (LTs) and their receptors in adenotonsillar tissues and the positive correlation between urinary cysteinyl leukotrienes (cysLTs) levels and OSA severity in children who had OSA. [2][3][4][5][6] These findings lead to the therapeutic use of leukotriene receptor antagonist such as montelukast in children who have mild OSA secondary to ATH. Several studies reported the significant benefits of montelukast in alleviating OSA severity in this particular population.…”

Expression of Leukotriene Biosynthetic Enzymes in Tonsillar Tissue of Children With Obstructive Sleep Apnea

“…7 This physiologic phenomenon might be exaggerated in certain subgroups of susceptible children such as those with increased urinary excretion of CysLTs or a history of wheezing requiring treatment with inhaled medications. 3,23 During the first 8 years of life, pharyngeal lymphoid tissue (adenoid and palatine tonsils) restricts the upper airway lumen in a variable degree in most children. 2 Thereafter, adenotonsillar tissue overgrowth resolves in nonsnorers but persists in children with snoring.…”

“…1 In children with snoring, adenotonsillar hypertrophy occurs during preschool years and persists beyond the eighth birthday, 2 and cysteinyl leukotrienes (CysLTs) have been implicated in its pathogenesis. [3][4][5] More specifically, tonsillar T and small B lymphocytes express CysLT receptors and the addition of leukotriene D 4 to tonsillar cell culture induces a proliferative response. 6,7 Administration of montelukast, an inhibitor of type 1 CysLT receptors, to children with mild OSA is accompanied by reduction in the size of adenoids and a decrease in the severity of intermittent upper airway obstruction during sleep.…”

Focus on prevention and treatment of obstructive sleep disordered breathing in childhood

“…A familiar predisposition to adenotonsillar hypertrophy and OSAS has been described and it may be attributed to the enhanced expression of leukotriene biosynthetic enzymes in tonsillar tissue and the increased production of cysteinyl leukotrienes which augment the proliferation rate of tonsillar lymphocytes [23][24][25]. Hence, we propose that early recognition of children at risk of adenotonsillar hypertrophy and SDB (e.g.…”