Urine levels of catecholamines in Greek children with obstructive sleep‐disordered breathing

Abstract

Summary. Introduction: Adults with obstructive sleep apnea have increased sympathetic activity. It was hypothesized that in children with symptoms of obstructive sleep-disordered breathing (SDB), morning urine levels of catecholamines correlate with severity of nocturnal hypoxemia. Methods: Children with snoring referred for polysomnography and controls without snoring were recruited. Morning urine norepinephrine, epinephrine, normetanephrine, and metanephrine levels were measured (ng/mg urine creatinine). Results: Twelve children (age 5.2 AE 2.3 years) with severe hypoxemia (oxygen saturation of hemoglobin-SpO 2 nadir 86%), 20 subjects (age 6.1 AE 2.1 years) with moderate hypoxemia (SpO 2 nadir 90% and >86%), 22 children (age 6.6 AE 1.5 years) with mild nocturnal hypoxemia (SpO 2 nadir >90%), and 10 controls (age 7.1 AE 2.8 years) were studied. Children with severe hypoxemia had significantly higher log-transformed norepinephrine levels (1.63 AE 0.29) compared to those with moderate hypoxemia (1.43 AE 0.22; P < 0.05) or compared to controls (1.39 AE 0.31; P < 0.05). In subjects with SDB, log-transformed oxygen desaturation of hemoglobin index or SpO 2 nadir predicted log-transformed norepinephrine levels after adjustment by age, gender and body mass index (r 2 ¼ 0.24; and r 2 ¼ 0.24, respectively; P < 0.01). Conclusions: Severity of nocturnal hypoxemia in children with intermittent upper airway obstruction during sleep correlates with morning urine levels of norepinephrine suggesting increased sympathetic tone.

Urinary Neurotransmitters Are Selectively Altered in Children With Obstructive Sleep Apnea and Predict Cognitive Morbidity

“…[5][6][7]25 However, the present study further indicates that the changes in urinary-catecholamine levels indeed occur during sleep, since urinary levels in the evening prior to the sleep study were similar between children with OSA and control subjects (data not shown). Thus, the recurrent hypoxemic events and the episodic arousals that characterize sleep in patients with OSA likely enhance sympathetic tonic outfl ow, and result in increased recovery of catecholamines in the urine.…”

“…[5][6][7] Considering the physiologic importance of neurotransmitters as signaling molecules in the nervous system and the potential alterations that may develop in the context of OSA, assessment of urinary neurotransmitters offers unique opportunities because of their stability, sensitivity, and particularly to the noninvasiveness of this approach. 8 The development of multiplexed techniques that enable simultaneous assessment of several neurotransmitters in biologic fl uids in general, and in urine in particular, provided us with the opportunity to explore the hypothesis that pediatric OSA would be associated with a unique pattern of alterations in urinary neurotransmitters, which may refl ect underlying cognitive defi cits.…”

Sleep clinical record: an aid to rapid and accurate diagnosis of paediatric sleep disordered breathing

“…The main consequence of repetitive apnoeas and hypopnoeas during sleep is intermittent hypoxia, which is a potent trigger of oxidative stress and inflammation [18][19][20][21][22]. Other mechanisms through which OSA may cause complications include increased sympathetic activity [23,24], increased serum cortisol [25], hypoxia-induced hormonal changes, arousal from sleep and secondary sleep debt [26][27][28]. Although audio-video taping and overnight pulse-oximetry may be used as first-line investigations, their quality varies considerably and they require strong parental motivation [29,30].…”

Effects of obstructive sleep apnea severity on serum lipid levels in Greek children with snoring

“…Clinically apparent cardiovascular morbidity is uncommon during childhood and there are no long-term cohort investigations exploring whether pediatric OSA predisposes to coronary artery disease, heart failure, and stroke in adult life. Nevertheless, a few pediatric reports have associated intermittent upper airway obstruction during sleep with pathophysiologic mechanisms implicated in the pathogenesis of cardiovascular disease such as sympathetic nervous system activation, systemic inflammation, endothelial dysfunction, and metabolic abnormalities [4][5][6][7][8][9][10].…”