Morning levels of C-reactive protein in children with obstructive sleep-disordered breathing
ABSTRACT Obstructive sleep-disordered breathing is associated with cardiovascular disease in adults, and elevated C-reactive protein (CRP) has been proposed as a link between the two disorders. We hypothesized that children with sleep-disordered breathing have higher CRP values than do control subjects. CRP was measured in 39 children (mean age +/- SD: 6.9 +/- 3.2 years) without snoring (controls) and in 102 children (6.2 +/- 2.2 years) with habitual snoring who underwent polysomnography. No significant differences were found in mean CRP values between control subjects (0.12 +/- 0.16 mg/dl; n = 39) and snorers with an apnea-hypopnea index of less than 1 episode/hour (0.15 +/- 0.26; n = 18), snorers with an index of 1 or more and less than 5 (0.15 +/- 0.26; n = 54), and snorers with an index of 5 or more (0.22 +/- 0.43; n = 30; p > 0.05). There was no correlation between CRP or log-transformed CRP values and apnea-hypopnea index, respiratory movement/arousal index, Sa(O(2)) nadir, oxygen desaturation (>/= 4%) of hemoglobin index, or percentage of sleep time with saturation less than 95% (p > 0.05). Thus, findings of higher CRP values in adults with sleep-disordered breathing and correlations of these values with polysomnography indices were not confirmed in children.
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- "In addition to increased Mediators of Inflammation oxidative stress, activation and propagation of inflammatory pathways in the context of immune dysregulation have been implicated in the deleterious consequences of OSA  , with the cumulative evidence strongly supporting the concept that pediatric OSA is a chronic, low grade inflammatory condition      . In this context, it is now recognized that OSA causes, albeit not always, systemic elevation in the levels of inflammatory mediators, such as CRP, TNFí µí»¼, IL-6, and INF-í µí»¾       , and the concomitant reduction of anti-inflammatory substances, such as IL-10, thereby tilting the balance toward a heightened proinflammatory state . Similarly, obesity has long been recognized as an indolent and persistent inflammatory condition in which the sustained activity of such processes promotes the occurrence of insulin resistance and vascular dysfunction     . "
ABSTRACT: Introduction. Obesity and obstructive sleep apnea syndrome (OSA) are common coexisting conditions associated with a chronic low-grade inflammatory state underlying some of the cognitive, metabolic, and cardiovascular morbidities. Aim. To examine the levels of inflammatory markers in obese community-dwelling children with OSA, as compared to no-OSA, and their association with clinical and polysomnographic (PSG) variables. Methods. In this cross-sectional, prospective multicenter study, healthy obese Spanish children (ages 4–15 years) were randomly selected and underwent nocturnal PSG followed by a morning fasting blood draw. Plasma samples were assayed for multiple inflammatory markers. Results. 204 children were enrolled in the study; 75 had OSA, defined by an obstructive respiratory disturbance index (RDI) of 3 events/hour total sleep time (TST). BMI, gender, and age were similar in OSA and no-OSA children. Monocyte chemoattractant protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1) levels were significantly higher in OSA children, with interleukin-6 concentrations being higher in moderate-severe OSA (i.e., AHI > 5/hrTST; , while MCP-1 levels were associated with more prolonged nocturnal hypercapnia . Conclusion. IL-6, MCP-1, and PAI-1 are altered in the context of OSA among community-based obese children further reinforcing the proinflammatory effects of sleep disorders such as OSA. This trial is registered with ClinicalTrials.gov NCT01322763.Mediators of Inflammation 06/2014; 2014. DOI:10.1155/2014/605280 · 3.24 Impact Factor
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- "In a series of recent studies, plasma concentrations of C-reactive protein were elevated in a severitydependent fashion among children and adolescents with OSA, even after correction for body-mass index (Tauman et al., 2004; Larkin et al., 2005; Kheirandish-Gozal et al., 2006). Only one study by Kaditis et al. (2005) failed to identify these relationships in a study of Greek children. Therefore, it is highly probable that OSA will elicit a variable, yet significant systemic inflammatory response, which in turn may initiate and propagate atherogenetic mechanisms. "
ABSTRACT: Pediatric sleep disordered breathing has emerged in the last few decades as a highly prevalent condition by virtue of its major morbidities encompassing the central nervous, cardiovascular, and metabolic systems. In this context, improved understanding of the pathophysiological mechanisms underlying the cellular and organ injury and repair mechanisms, and the variance of the phenotype at any level of disease severity is all the more critical if appropriate personalized therapies are to be developed in the future. In this paper, the current evidence and hypothetical framework pointing to the endothelium as a primary cellular target for many of the morbidities of pediatric sleep apnea is reviewed, and particular emphasis on the recruitment of the endothelial cell lineage will be explored. It is hoped that this perspective will foster both expansion and acceleration of discovery efforts aiming to ultimately prevent the potentially lifelong consequences of sleep apnea during childhood.Frontiers in Neurology 06/2012; 3:92. DOI:10.3389/fneur.2012.00092
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- "While it may be assumed that IL-6 plays a similar role in developing children as in adults, little research has been conducted. Another serum inflammation marker, C-reactive protein, has been shown to be elevated in children with sleep disordered breathing who reported sleepiness and neurobehavioral complaints (Tauman et al., 2004), yet this increase was not found in a separate study of children with sleep-disordered breathing (Kaditis et al., 2005). Other inflammatory markers, interferon-c and IL-8, appear to be elevated among children with mild obstructive sleep apnea, when compared with controls (Tam et al., 2006). "
ABSTRACT: We explored relations between children's sleep and levels of salivary interleukin-6 (IL-6). Children were healthy boys (n = 28) and girls (n = 36) who ranged in age between 8 and 9 years. Through actigraphy, the amount and quality of children's sleep was examined objectively in their homes for 1 week. Children also rated their Morningness/Eveningness predisposition and subjective sleepiness, and parents reported on their children's Sleep Disordered Breathing and Sleepiness. Children provided saliva samples before and after a series of cognitive/social tasks (an intelligence test, listening to a marital argument, and performing a star-tracing task), which were later assayed for IL-6. Children with higher salivary IL-6 levels reported increased Eveningness predispositions and their parents reported higher levels of Sleep Disordered Breathing. Furthermore, lower levels of sleepiness, longer sleep amount, and better quality sleep in children were each predictive of increased IL-6 reactivity from pre- to post-task conditions. The findings illustrate (for the first time to our knowledge) that sleep disruptions in otherwise healthy and normally developing children may be associated with individual differences in levels of IL-6 in saliva.Journal of Sleep Research 07/2007; 16(2):188-97. DOI:10.1111/j.1365-2869.2007.00593.x · 2.95 Impact Factor