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

Alexopoulos, Emmanouel Ι.; Gletsou, Eleftheria; Kostadima, Eleni; Kaditis, Dimitrios G.; Zakynthinos, Εpameinondas; Gourgoulianis, Konstantinos; Kaditis, Athanasios G.

doi:10.1007/s11325-010-0410-z

Cited by 28 publications

(24 citation statements)

References 33 publications

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“…OSA-associated nocturnal hypoxaemia in children independently predicted MetS and glucose intolerance [377][378][379], and prevalence of MetS increased with increasing severity of OSA [380][381][382], together with markers of inflammation [382], arterial alterations [383], and excessive daytime sleepiness [382,384]. In non-obese children, the HDL cholesterol level was recently found to be inversely correlated with OSA severity [385]. Conversely, other studies have suggested that IR in children with OSA is associated with obesity rather than OSA [386][387][388].…”

Section: Obesity and Osa In Childrenmentioning

confidence: 99%

Adipose tissue in obesity and obstructive sleep apnoea

Bonsignore¹,

McNicholas²,

Montserrat³

et al. 2011

Eur Respir J

116

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A European Respiratory Society research seminar on ''Metabolic alterations in obstructive sleep apnoea (OSA)'' was jointly organised in October 2009 together with two EU COST actions (Cardiovascular risk in the obstructive sleep apnoea syndrome, action B26, and Adipose tissue and the metabolic syndrome, action BM0602) in order to discuss the interactions between obesity and OSA.Such interactions can be particularly significant in the pathogenesis of metabolic abnormalities and in increased cardiovascular risk in OSA patients. However, studying the respective role of OSA and obesity is difficult in patients, making it necessary to refer to animal models or in vitro systems. Since most OSA patients are obese, their management requires a multidisciplinary approach.This review summarises some aspects of the pathophysiology and treatment of obesity, and the possible effects of sleep loss on metabolism. OSA-associated metabolic dysfunction (insulin resistance, liver dysfunction and atherogenic dyslipidaemia) is discussed from the perspective of both obesity and OSA in adults and children.Finally, the effects of treatment for obesity or OSA, or both, on cardio-metabolic variables are summarised. Further interdisciplinary research is needed in order to develop new comprehensive treatment approaches aimed at reducing sleep disordered breathing, obesity and cardiovascular risk.

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Section: Obesity and Osa In Childrenmentioning

confidence: 99%

Adipose tissue in obesity and obstructive sleep apnoea

Bonsignore¹,

McNicholas²,

Montserrat³

et al. 2011

Eur Respir J

116

View full text Add to dashboard Cite

show abstract

“…11,48,[73][74][75][76][77][78] In this context, increases in low-density lipoprotein and reciprocal decreases in high-density lipoprotein have been inconsistently identified among lean children with OSAS but are more likely to occur in obese children with OSAS. [79][80][81] Similarly, evidence of OSAS-associated reductions in systemic insulin sensitivity is now abundantly documented across multiple studies by several groups all over the world. Again, it is worth emphasizing that not all children are affected, and that only a subset of children with OSAS will display such metabolic perturbations.…”

Section: Metabolic Morbidity Markers Of Osasmentioning

confidence: 98%

Pediatric OSA Syndrome Morbidity Biomarkers

Kheirandish‐Gozal

Gozal

2017

Chest

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Since initial reports 40 years ago on pediatric OSA syndrome (OSAS) as a distinct and prevalent clinical entity, substantial advances have occurred in the delineation of diagnostic and treatment approaches. However, despite emerging and compelling evidence that OSAS increases the risk for cognitive, cardiovascular, and metabolic end-organ morbidities, routine assessment of such morbidities is seldom conducted in clinical practice. One of the major reasons for such discrepancies resides in the relatively labor-intensive and onerous steps that would be required to detect the presence of any of such morbidities, further adding to the already elevated cost of diagnosing the disorder. To circumvent these obstacles, the search for biomarker signatures of pediatric OSA and its cognitive and cardiometabolic consequences was launched, and considerable progress has occurred since then. Here, we review the current evidence for the presence of morbidity-related biomarkers among children with OSAS, and explore future opportunities in this promising arena.CHEST 2017; 151(2):500-506

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“…Normal body weight Unchanged triglycerides, total cholesterol and LDL, and decreased HDL in OSA [40] Overweight/obese DE LA EVA et al [24] LI et al [32] CANAPARI et al [20] FLINT et al [39] Increased triglycerides, and unchanged total cholesterol, HDL and LDL in OSA [20] Increased triglycerides, and unchanged total cholesterol and HDL in OSA [39] Wide range of body weights VERHULST et al [25] TAUMAN et al…”

Section: ] Paediatric Age (3-18 Years)mentioning

confidence: 99%

“…Unfortunately, the picture is far from being clear. Some studies did not find any relationship between OSA and lipids [19,28], while the results of other studies were discordant about which aspects of lipid metabolism may be affected by OSA, irrespective of age and obesity state of the children [20,25,27,29,34,35,39,40].…”

Section: ] Paediatric Age (3-18 Years)mentioning

confidence: 99%

The puzzle of metabolic effects of obstructive sleep apnoea in children

Marrone

Bonsignore

2016

Eur Respir J

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@ERSpublicationsIn obese children with obstructive sleep apnoea insulin resistance is common while lipids do not show a clear pattern http://ow.ly/XNR9sIn adults, obstructive sleep apnoea (OSA) is often associated with metabolic alterations. Although obesity is a major culprit [1], large epidemiological studies have reported a metabolic risk associated with OSA that is independent of obesity. In particular, meta-analyses have shown that effective treatment of OSA by continuous positive airway pressure (CPAP) improves glycaemic control in both diabetic [2] and nondiabetic patients [3].Intermittent hypoxia is an important mechanism by which OSA affects metabolism, as supported by experimental observations showing that intermittent hypoxia negatively interferes with both glucose and lipid metabolism [4,5]. Altered sleep structure, as often found in OSA, may also play an important role. In adult humans, experimental sleep fragmentation [6] and deprivation of slow wave sleep (SWS) [7] decreased insulin sensitivity. In healthy adolescents, two studies found that insulin sensitivity was negatively correlated to stage 1 non-rapid eye movement (non-REM) sleep, and positively to SWS duration [8,9]. Furthermore, in another population of healthy adolescents, partial sleep deprivation, with preserved SWS and a reduced amount of REM sleep, was followed by an increase in insulin resistance [10]. A correlation between short sleep duration and insulin resistance has also been found with actigraphic studies both in adolescents [11,12] and in younger children [13].Paediatric OSA shows major differences compared with the adult disease [14]. First, the number of respiratory events and the degree of nocturnal hypoxaemia are usually lower in children than in adults. Second, sleep duration is physiologically longer in children than in adults and respiratory events, although possibly causing some sleep fragmentation, are associated with a sleep structure that appears to be better preserved than in adults. Third, duration of disease and exposure to additional risk factors for several complications is limited in children, as opposed to the decades of exposure to sleep disordered breathing (SDB) and risk factors typical of adult patients. Therefore, differences between adults and children with OSA could explain a different impact on metabolism. The picture is even more complex if we consider that paediatric disease has two main phenotypes: one typical of lean children with adenotonsillar hypertrophy, which usually occurs at a younger age and has a similar prevalence in both sexes; and one typical of obese children that is more similar to adult OSA and usually appears in adolescence, more often in males [15]. Onset of puberty is an additional factor known to affect metabolism in children, increasing insulin resistance at least in males [16]. The impact of all these variables, and the small sample size of several paediatric studies, probably contribute to the difficulties in clear interpretation of the apparently conflicting data available i...

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

Abstract: HDL cholesterol levels are inversely related to severity of OSA in non-obese children with snoring.

Cited by 28 publications

References 33 publications

Adipose tissue in obesity and obstructive sleep apnoea

Adipose tissue in obesity and obstructive sleep apnoea

Pediatric OSA Syndrome Morbidity Biomarkers

The puzzle of metabolic effects of obstructive sleep apnoea in children

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