Effects of nondipping pattern on systemic inflammation in obstructive sleep apnea

Ulaşlı, Sevinç Sarınç; Sarıaydın, Muzaffer; Günay, Ersin; Halici, Bilal; Çeli̇k, Sefa; Koyuncu, Tülay; Ulu, Sena; Ünlü, Mehmet

doi:10.1007/s11325-015-1135-9

Cited by 21 publications

(17 citation statements)

References 25 publications

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“…Although the levels of IL-10 have been investigated in OSAS [4,[27][28][29][30][31][32], promoter polymorphisms of IL-10 gene have not been studied before. We found that IL-10-1082 GA, AA, GA-AA, −819 CT-TT, and −592 CA, AA, CA-AA genotypes increased the risk for developing OSAS as well as the severity of OSAS.…”

Section: Discussionmentioning

confidence: 99%

Association of Interleukin-10 gene promoter polymorphisms with obstructive sleep apnea

Özdaş

Özdaş²,

Acar

et al. 2015

Sleep Breath

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Section: Discussionmentioning

confidence: 99%

Association of Interleukin-10 gene promoter polymorphisms with obstructive sleep apnea

Özdaş

Özdaş²,

Acar

et al. 2015

Sleep Breath

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“…Recent findings of higher circulating levels of the inflammatory factor interleukin-2 in OSA patients with a nondipping blood pressure profile also support a role for inflammation in the development of nondipping blood pressure [30].…”

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confidence: 84%

Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms

2017

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Obstructive sleep apnoea (OSA) is highly prevalent, with recent general population studies indicating that up to 50% of males and 23% of females have moderate or severe sleep disordered breathing (SDB) based on an apnoea-hypopnoea index (AHI) of >15 events·h -1 [1, 2]. OSA is recognised as an independent risk factor for systemic hypertension [3] and a nondipping nocturnal blood pressure profile is particularly likely in patients with OSA [4], even in the absence of significant hypertension. Furthermore, hypertension is increasingly recognised as an important predictor of prevalent OSA and appears to be more predictive than excessive day-time sleepiness in some settings [5]. However, recent evidence also indicates that only moderate-severe OSA (AHI >20 events·h -1 ) constitutes a significant independent risk for hypertension [2] and cluster analysis of sleep clinic populations indicates that particular population subtypes are especially associated with hypertension [6].These recent reports regarding the very high general prevalence of SDB and factors that influence the relationship with hypertension prompt a reassessment of the clinical relevance regarding the association between OSA and hypertension, especially nocturnal hypertension, and the underlying mechanisms that may contribute to the development of a nondipping nocturnal blood pressure profile in OSA patients. This topic is important in the context of the recent SAVE (Sleep Apnea Cardiovascular Endpoints) trial report [7] involving 2717 patients with established cardiovascular disease and moderate or severe OSA associated with minimal sleepiness who were randomised to best usual care with or without added continuous positive airway pressure (CPAP) therapy and followed for up to 7 years. CPAP therapy was not associated with any improvement in cardiac or cerebrovascular outcome, although data on secondary and other end-points in the report indicated a small but significant reduction in diastolic blood pressure. This finding is particularly relevant in the context that the average compliance with CPAP was only 3.3 h and a recent meta-analysis indicates that beneficial effects of CPAP on blood pressure in OSA patients with minimal sleepiness are largely confined to patients using CPAP for >4 h per night [8].

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“…Increase in pro-inflammatory cytokines have been reported in both adult OSA (CRP [19,20], TNF-α, IL-6 [21], and IL-10) and pediatric OSA patients (HS-CRP) [10,11]. In this study, we investigated cytokines in children with both OSA and enlarged adenoids or tonsils and focused on their changes before and after T&A.…”

Section: Discussionmentioning

confidence: 99%

“…Similar to our previous finding [11], children with both diagnoses had higher cytokine levels than normal controls (Table 1). Although improvement is always noted, T&A cannot cure all children with OSA [19][20][21][22]. Some children kept having abnormal AHI and cytokine levels after T&A, and the intermittent hypoxia during sleep could still lead to chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Factors: Nonobese Pediatric Obstructive Sleep Apnea and Adenotonsillectomy

Huang

Chin

Guilleminault

et al. 2020

JCM

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Background: Inflammation is often considered relating to pediatric obstructive sleep apnea (OSA). We conducted a study investigating cytokines, including Il-17 and Il-23, in children with OSA before and after adenotonsillectomy (T&A), compared with controls. Methods: Children with OSA between age 4 and 12 receiving T&A were prospectively followed. Evaluation before and reevaluation six months after the treatment were done, including polysomnography (PSG), blood tests, and questionnaires. Blood samples were obtained to determine the values of high-sensitivity-C-reactive-protein (HS-CRP); tumor-necrosis-factor-alpha (TNF-α); and interleukin (IL)-1, 6, 10, 12, 17, and 23. We compared the results with an age-matched control group. Results: We included 55 OSA children and 32 controls. Children with OSA presented significant improvement after T&A in complaints, signs, apnea hypopnea index (AHI) (p < 0.001), mean oxygen desaturation index (p < 0.001), and mean oxygen saturation (p = 0.010). Upon entering this study, children with OSA had significantly higher cytokine levels than the controls and significant changes in HS-CRP (p = 0.013), TNF-α (p = 0.057), IL-1β (p = 0.022), IL-10 (p = 0.035), and IL-17 (p = 0.010) after T&A. Children with improved but persistently abnormal AHI did not have all cytokine levels normalized, particularly IL-23 and HS-CRP. Conclusion: Sleep-disordered breathing can persist after T&A and can continue to have a negative inflammatory effect. HS-CRP and IL-23 may serve as blood markers for the persistence of sleep-disordered breathing after T&A.

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Effects of nondipping pattern on systemic inflammation in obstructive sleep apnea

Abstract: In conclusion, nondipping pattern appears to be associated with increased serum IL-2 levels indicating the increased inflammatory response independently from OSAS severity, and this pattern should be evaluated carefully for possible cardiovascular complications.

Cited by 21 publications

References 25 publications

Association of Interleukin-10 gene promoter polymorphisms with obstructive sleep apnea

Association of Interleukin-10 gene promoter polymorphisms with obstructive sleep apnea

Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms

Inflammatory Factors: Nonobese Pediatric Obstructive Sleep Apnea and Adenotonsillectomy

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